{"data":[{"id":25,"name":"5-Amino-1MQ","description":"Small-molecule NNMT inhibitor (5-amino-1-methylquinolinium), not a peptide; in diet-induced obese mice it lowered body weight and fat mass and raised adipocyte NAD+ without changing food intake.","benefits":"Reduced body weight, white fat mass and plasma cholesterol (diet-induced obese mice), improved glucose tolerance and less liver fat (obese mice), raised NAD+ in adipocytes (in vitro), stronger grip and muscle regeneration in aged mice","categories":["fat loss","metabolic"],"recommended_dose":"50 to 100 mg daily by mouth (vendor/community range, no published human dose; mouse studies used about 34 mg/kg/day subcutaneously)","detailed_description":"5-Amino-1MQ is a membrane-permeable methylquinolinium inhibitor of nicotinamide N-methyltransferase (NNMT) from the Watowich lab at UTMB (Neelakantan 2017). NNMT knockdown protected mice from diet-induced obesity (Kraus 2014). In diet-induced obese mice, 5-amino-1MQ given subcutaneously for 11 days lowered body weight, white fat mass and cholesterol without changing food intake (Neelakantan 2018); 28 days of daily dosing limited fat gain, improved insulin sensitivity and reduced fatty liver (Babula 2024). Combined with a lean diet it normalised body composition (Sampson 2021). In aged mice it improved muscle stem cell function and grip strength (Neelakantan 2019; Dimet-Wiley 2024). Rat PK shows oral activity. No human study is published or registered.","storage_temp":"Room temperature, dry (general small-molecule guidance; no compound-specific CoA located)","shelf_life_reconstituted":null,"shelf_life_powder":"12+ months","stacks_with":[],"dose_min_mcg":50000,"dose_max_mcg":100000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Oral capsule in community use. Published dosing is rodent: 20 mg/kg subcutaneously three times daily for 11 days in obese mice (Neelakantan 2018), once-daily dosing for 28 days (Babula 2024), and single IV or oral doses in rats for PK (Awosemo 2021). No human dose has been studied.","mechanism_of_action":"5-Amino-1MQ inhibits NNMT, the cytosolic enzyme that methylates nicotinamide to 1-methylnicotinamide (1-MNA) using S-adenosylmethionine (SAM). In cultured adipocytes it lowered 1-MNA, raised intracellular NAD+ and SAM, and suppressed lipogenesis, without inhibiting related methyltransferases or NAD+ salvage enzymes (Neelakantan 2018). NNMT is highly expressed in white fat of obese mice, and its knockdown raised energy expenditure through increased SAM and NAD+ flux (Kraus 2014). Downstream effects on SIRT1 and fat browning are proposed rather than shown for this compound.","clinical_studies":["NNMT knockdown in fat and liver protected mice against diet-induced obesity and raised energy expenditure (Kraus et al., 2014)","20 mg/kg three times daily subcutaneously for 11 days lowered body weight, white fat mass, adipocyte size and cholesterol in diet-induced obese mice, with no change in food intake (Neelakantan et al., 2018)","Once-daily dosing for 28 days dose-dependently limited weight and fat gain, improved glucose tolerance and reduced hepatic steatosis in obese mice (Babula et al., 2024)","Raised grip strength about 40% in aged sedentary mice and added to exercise effects (Dimet-Wiley et al., 2024)","Human-trial status: no human study published or registered on ClinicalTrials.gov"],"evidence_level":"preclinical","references":[{"title":"Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity","authors":"Kraus D, Yang Q, Kong D, et al.","journal":"Nature","year":2014,"doi":"10.1038/nature13198","pmid":"24717514"},{"title":"Structure-Activity Relationship for Small Molecule Inhibitors of Nicotinamide N-Methyltransferase","authors":"Neelakantan H, Wang HY, Vance V, et al.","journal":"Journal of Medicinal Chemistry","year":2017,"doi":"10.1021/acs.jmedchem.7b00389","pmid":"28548833"},{"title":"Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice","authors":"Neelakantan H, Vance V, Wetzel MD, et al.","journal":"Biochemical Pharmacology","year":2018,"doi":"10.1016/j.bcp.2017.11.007","pmid":"29155147"},{"title":"Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle","authors":"Neelakantan H, Brightwell CR, Graber TG, et al.","journal":"Biochemical Pharmacology","year":2019,"doi":"10.1016/j.bcp.2019.02.008","pmid":"30753815"},{"title":"Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition and enhances metabolic benefits in obese mice","authors":"Sampson CM, Dimet AL, Neelakantan H, et al.","journal":"Scientific Reports","year":2021,"doi":"10.1038/s41598-021-85051-6","pmid":"33707534"},{"title":"Development & validation of LC-MS/MS assay for 5-amino-1-methyl quinolinium in rat plasma: Application to pharmacokinetic and oral bioavailability studies","authors":"Awosemo O, Neelakantan H, Watowich S, et al.","journal":"Journal of Pharmaceutical and Biomedical Analysis","year":2021,"doi":"10.1016/j.jpba.2021.114255","pmid":"34304009"},{"title":"Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction","authors":"Babula JJ, Bui D, Stevenson HL, et al.","journal":"Diabetes, Obesity & Metabolism","year":2024,"doi":"10.1111/dom.15879","pmid":"39161060"},{"title":"Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice","authors":"Dimet-Wiley AL, Latham CM, Brightwell CR, et al.","journal":"Scientific Reports","year":2024,"doi":"10.1038/s41598-024-66034-9","pmid":"38969654"}],"molecular_weight":159.21,"amino_acid_sequence":null,"alternative_names":["5-Amino-1-methylquinolinium","5-AMQ","5A1MQ","5-Amino-1-methylquinolinium iodide"],"half_life":"3.8 h IV and 6.9 h oral (rat); no human PK data (Awosemo 2021)","bioavailability":"Oral 38.4% (rat); no human data (Awosemo 2021)","side_effects":"No published human safety or pharmacokinetic data exists; oral use is entirely community-derived. Anecdotal reports mention insomnia, appetite loss, and mild GI upset. The effects of chronic NNMT inhibition in humans are unknown.","last_reviewed_at":"2026-10-06T08:17:29.477Z","reviewed_by":"audit-2026-10","review_notes":"N/A-by-design: oral. storage: general guidance. No human data of any kind; dose range is vendor/community. | description: Decision 20: class first. Adds the model system and the food-intake finding. | benefits: Each item now carries its model system; drops 'studied for weight management' without context. | detailed_description: Old text claimed 'anti-aging effects through epigenetic mechanisms' with no source. Old value omitted for length. | mechanism_of_action: Old text asserted SIRT1 activation, fat-cell browning and mitochondrial improvement as established effects of the compound. Old value omitted for length. | clinical_studies: Old bullets had no citations and included 'Generally well-tolerated in research protocols', which has no source. | half_life: Rat LC-MS/MS PK study. | bioavailability: Replaces an unsourced 'Good' with the measured rat value. | recommended_dose: Decision 11: kept only with the label and low confidence. | dosing_notes: Old note was advice phrasing with no source. | molecular_weight: PubChem CID 950107 (5-amino-1-methylquinolinium, CAS 685079-15-6) is the cation C10H11N2+, 159.21. The iodide salt (CID 66522933) is 286.11. 177.2 matches neither. | amino_acid_sequence: Fields hold data, not prose; small molecules take null. | alternative_names: 'NNMT inhibitor' is a drug class, not a name. 5-AMQ and 5A1MQ are the abbreviations used in the PK and 2024 papers. | stacks_with: Decision 14: no published combination with either; the only published combination is with a reduced-calorie diet (Sampson 2021). | storage_temp: Labelled as general guidance.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/950107","note":"amino_acid_sequence"},{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/66522933","note":"molecular_weight"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5826726/","note":"Neelakantan 2018 full text: 20 mg/kg/injection three times daily, about 34 mg/kg/day parent, 11 days; 60 mg/kg/day tolerated in dose escalation"},{"url":"https://clinicaltrials.gov/api/v2/studies?query.term=NNMT%20inhibitor","note":"no registered human trials"},{"url":"https://pubmed.ncbi.nlm.nih.gov/29155147/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/39161060/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/33707534/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/38969654/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/30753815/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/28548833/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/24717514/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/34304009/","note":"alternative_names"}],"data_version":2,"slug":"5-amino-1mq","url":"https://peptidelabs.app/peptides/5-amino-1mq/"},{"id":141,"name":"9-Me-BC","description":"9-Methyl-beta-carboline, a small-molecule alkaloid shown in rodent studies to promote dopamine neuron survival and improve learning and memory.","benefits":"Dopaminergic neuron support and improved learning/memory in rodent models; studied for neuroprotection","categories":["cognitive","neuroprotection"],"recommended_dose":"10 to 30 mg daily (vendor/community range, no published human dose; rat in vivo work used intracerebroventricular delivery)","detailed_description":"9-Methyl-beta-carboline is a small-molecule pyridoindole alkaloid, not a peptide. Most beta-carbolines are studied as neurotoxins; this one is the exception. In primary mouse mesencephalic culture it raised the number of differentiated dopaminergic neurons, cut caspase-3 activity and induced dopaminergic transcription factors (Hamann et al., 2008), and it protected and partly regenerated those neurons after lipopolysaccharide or rotenone injury while suppressing microglial proliferation (Polanski et al., 2010). Given into the cerebral ventricle of rats for 14 days after MPP+ lesioning, it restored striatal dopamine and nigral cell counts (Wernicke et al., 2010). Ten days of treatment improved radial-maze learning in rats alongside higher hippocampal dopamine and more dendritic spines (Gruss et al., 2012). It inhibits monoamine oxidase A and B (Keller et al., 2020). No human study exists.","storage_temp":"Room temperature, away from light","shelf_life_reconstituted":null,"shelf_life_powder":"12+ months","stacks_with":[],"dose_min_mcg":10000,"dose_max_mcg":30000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Oral use is community convention; no human study has administered this compound. The restorative rat study delivered it into the left cerebral ventricle for 14 days (Wernicke et al., 2010) and the cognitive study dosed rats for 10 days (Gruss et al., 2012). 9-Methyl-beta-carbolines are efficient photosensitisers and damage DNA under UVA in vitro, generating oxidised purines and pyrimidine dimers (Vignoni et al., 2013). Monoamine oxidase A inhibition at about 1 micromolar is a measured property (Keller et al., 2020), which is the basis for caution with serotonergic drugs and tyramine. N/A-by-design: oral, so reconstitution fields are null.","mechanism_of_action":"9-Methyl-beta-carboline is a heterocyclic pyridoindole alkaloid (not a peptide). In primary dopaminergic culture it raised tyrosine hydroxylase expression in existing dopa-decarboxylase-positive neurons and induced transcription factors tied to dopaminergic differentiation (Hamann et al., 2008). It also protects and regenerates those neurons after toxin exposure, suppresses microglial proliferation and lowers alpha-synuclein (Polanski et al., 2010). In rats it raised complex I activity and induced BDNF, CDNF, CBLN1 and CNTF transcripts (Wernicke et al., 2010). Astrocytes mediate part of the effect through organic cation transport and PI3K signalling, and the compound inhibits monoamine oxidase, IC50 about 1 micromolar for MAO-A and 15.5 micromolar for MAO-B (Keller et al., 2020). Photoexcited 9-methyl-beta-carbolines damage DNA in vitro under UVA (Vignoni et al., 2013).","clinical_studies":["Raised the number of differentiated dopaminergic neurons and lowered caspase-3 activity in primary mouse mesencephalic culture (Hamann et al., 2008)","Protected dopaminergic neurons against lipopolysaccharide and 2,9-dimethyl-beta-carbolinium toxicity, regenerated them after chronic rotenone, and suppressed toxin-induced microglial proliferation (Polanski et al., 2010)","Fourteen days of intracerebroventricular dosing in MPP+-lesioned rats restored striatal dopamine and nigral tyrosine hydroxylase cell counts, with about 80% higher complex I activity (Wernicke et al., 2010)","Ten days of treatment improved radial-maze spatial learning in rats, with higher hippocampal dopamine and greater dendritic and synaptic density; five days did not (Gruss et al., 2012)","Inhibits monoamine oxidase A at about 1 micromolar and MAO-B at 15.5 micromolar, and stimulates neurotrophic factor expression in astrocytes through PI3K (Keller et al., 2020)","Human-trial status: none. No clinical trial, no human pharmacokinetics and no human safety data; all work is rodent or cell culture, and the in vivo rat studies used intracerebroventricular delivery"],"evidence_level":"preclinical","references":[{"title":"9-Methyl-beta-carboline up-regulates the appearance of differentiated dopaminergic neurones in primary mesencephalic culture","authors":"Hamann J, Wernicke C, Lehmann J, et al.","journal":"Neurochemistry International","year":2008,"doi":"10.1016/j.neuint.2007.08.018","pmid":"17913302"},{"title":"The exceptional properties of 9-methyl-beta-carboline: stimulation, protection and regeneration of dopaminergic neurons coupled with anti-inflammatory effects","authors":"Polanski W, Enzensperger C, Reichmann H, Gille G","journal":"Journal of Neurochemistry","year":2010,"doi":"10.1111/j.1471-4159.2010.06725.x","pmid":"20374418"},{"title":"9-Methyl-beta-carboline has restorative effects in an animal model of Parkinson's disease","authors":"Wernicke C, Hellmann J, Zieba B, et al.","journal":"Pharmacological Reports","year":2010,"doi":"10.1016/s1734-1140(10)70241-3","pmid":"20360614"},{"title":"9-Methyl-beta-carboline-induced cognitive enhancement is associated with elevated hippocampal dopamine levels and dendritic and synaptic proliferation","authors":"Gruss M, Appenroth D, Flubacher A, et al.","journal":"Journal of Neurochemistry","year":2012,"doi":"10.1111/j.1471-4159.2012.07713.x","pmid":"22380576"},{"title":"9-Methyl-beta-carboline inhibits monoamine oxidase activity and stimulates the expression of neurotrophic factors by astrocytes","authors":"Keller S, Polanski WH, Enzensperger C, et al.","journal":"Journal of Neural Transmission","year":2020,"doi":"10.1007/s00702-020-02189-9","pmid":"32285253"},{"title":"Mechanisms of DNA damage by photoexcited 9-methyl-beta-carbolines","authors":"Vignoni M, Rasse-Suriani FA, Butzbach K, et al.","journal":"Organic and Biomolecular Chemistry","year":2013,"doi":"10.1039/c3ob40344k","pmid":"23842892"},{"title":"Stimulation, protection and regeneration of dopaminergic neurons by 9-methyl-beta-carboline: a new anti-Parkinson drug?","authors":"Polanski W, Reichmann H, Gille G","journal":"Expert Review of Neurotherapeutics","year":2011,"doi":"10.1586/ern.11.1","pmid":"21651332"}],"molecular_weight":182.22,"amino_acid_sequence":"N/A - small molecule pyridoindole alkaloid, 9-methylpyrido[3,4-b]indole (PubChem CID 164979)","alternative_names":["9-Methyl-beta-carboline","9-MBC","9-methylnorharman","9-methylpyrido[3,4-b]indole"],"half_life":"Not established in any species; no pharmacokinetic study published","bioavailability":"Not measured. Beta-carbolines occur endogenously and in food, and 9-methyl-beta-carboline has been detected in brain and cerebrospinal fluid in the broader literature, but no oral bioavailability or brain-uptake figure exists for the administered compound (Hamann et al., 2008; Keller et al., 2020).","side_effects":"No human safety data; effects unknown beyond animal studies in rodents. Beta-carbolines inhibit monoamine oxidase at higher concentrations, so combining with SSRIs, MAOIs, stimulants, or tyramine-rich foods poses serotonin syndrome and hypertensive crisis risk. Liver enzyme changes in rodent work make hepatic monitoring prudent.","last_reviewed_at":"2026-10-06T08:17:36.165Z","reviewed_by":"audit-2026-10","review_notes":"N/A-by-design: oral. Not a peptide (pyridoindole alkaloid). Dose range is vendor/community with no published human dose, per decision 11. Molecular weight verified against PubChem by CID and synonym per decision 21. | detailed_description: The old text was two sentences with no model systems. Old value omitted for length. | mechanism_of_action: Old text asserted ATP and mitochondrial effects loosely and gave the photosensitivity claim no source. Both now have one, and the MAO inhibition is quantified. Old value omitted for length. | clinical_studies: Old bullets had no citations and ended on a sunlight warning stated as a finding. | recommended_dose: Decision 11. No human dose of any kind has been published, and the rodent delivery route does not translate to an oral milligram figure. | dosing_notes: Replaces an unsourced instruction with the published routes, the DNA photodamage finding and the measured MAO inhibition. No advice phrasing. | half_life: '~hours' implies a measurement. There is none for this compound. | bioavailability: 'Oral: Good' had no source, and the in vivo rat studies bypassed absorption entirely. | amino_acid_sequence: Decision 20: names the compound class and ties it to the PubChem identifier. | alternative_names: 9-Methylnorharman is the name used in the photochemistry literature and resolves to the same CID. | stacks_with: Decision 14: no published combination, and a monoamine oxidase inhibitor should not carry implied stacking.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/164979","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/34779915/","note":"2022 erratum to Keller 2020"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17913302/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/20374418/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/20360614/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22380576/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/32285253/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23842892/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/21651332/","note":"half_life"}],"data_version":2,"slug":"9-me-bc","url":"https://peptidelabs.app/peptides/9-me-bc/"},{"id":143,"name":"ACE-031","description":"Soluble ActRIIB-Fc decoy receptor that binds myostatin and related ligands to increase muscle mass; human trials were halted over bleeding side effects.","benefits":"Total lean mass +3.3% and thigh muscle volume +5.1% at day 29 after one 3 mg/kg dose in healthy postmenopausal women (phase 1, n=48); trends toward higher lean mass, bone density and 6-minute walk distance in Duchenne muscular dystrophy (phase 2). Development stopped for bleeding events.","categories":["muscle growth"],"recommended_dose":"0.5 mg/kg every 4 weeks or 1 mg/kg every 2 weeks subcutaneously in the phase 2 trial (NCT01099761); 0.02 to 3 mg/kg as a single subcutaneous dose in phase 1","detailed_description":"ACE-031 is a recombinant fusion of the extracellular domain of activin receptor type IIB with human IgG1-Fc, developed by Acceleron Pharma as a myostatin trap. In a single-ascending-dose phase 1 study, 48 healthy postmenopausal women received 0.02 to 3 mg/kg subcutaneously or placebo; mean t1/2 was 10 to 15 days, and at 3 mg/kg total lean mass rose 3.3% (DXA, p=0.03) and thigh muscle volume 5.1% (MRI, p=0.03) by day 29 (Attie 2013). A randomized placebo-controlled ascending-dose trial then gave 0.5 mg/kg every 4 weeks or 1 mg/kg every 2 weeks subcutaneously to ambulatory boys with Duchenne muscular dystrophy. It was stopped after the second dosing regimen because of epistaxis and telangiectasia, with only non-significant trends on the 6-minute walk test, lean mass and bone density (Campbell 2017). Development was discontinued; nothing was approved.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["Follistatin-344","IGF-1 LR3"],"dose_min_mcg":null,"dose_max_mcg":null,"dose_unit":"mg/kg","dose_frequency":"every 2 weeks","recon_volume_ml":2,"common_vial_sizes":[1],"dosing_notes":"Subcutaneous, not intravenous: 0.5 mg/kg every 4 weeks or 1 mg/kg every 2 weeks every 2 to 4 weeks in boys with Duchenne muscular dystrophy, and 0.02 to 3 mg/kg as a single dose in healthy postmenopausal women. Exposure rose linearly with dose and mean t1/2 was 10 to 15 days (Attie 2013). Development was discontinued after the phase 2 trial was stopped for epistaxis and telangiectasia (Campbell 2017). Weight-based dosing, so the mcg dose fields stay null.","mechanism_of_action":"ACE-031 is the extracellular domain of activin receptor type IIB fused to human IgG1-Fc. As a soluble decoy it binds myostatin (GDF-8) and other ActRIIB ligands, including activin A and GDF-11, before they reach the receptor, lifting myostatin's brake on muscle growth (Attie 2013; Campbell 2017). Transgenic expression of a dominant-negative ActRIIB in mouse muscle produced muscle-mass increases comparable to myostatin knockouts, which is the preclinical basis for the approach (Lee and McPherron 2001). The bleeding events that stopped development, epistaxis and telangiectasia, are proposed to come from blocking non-myostatin ActRIIB ligands involved in vascular integrity rather than from the muscle effect; the trial report classes them as non-muscle-related adverse events without assigning a mechanism.","clinical_studies":["In 48 healthy postmenopausal women given one subcutaneous dose of 0.02 to 3 mg/kg or placebo, exposure rose linearly with dose, mean t1/2 was 10 to 15 days, and the 3 mg/kg group gained 3.3% total lean mass (DXA, p=0.03) and 5.1% thigh muscle volume (MRI, p=0.03) by day 29 (Attie et al., 2013)","The main phase 1 adverse event was injection-site erythema; biomarker changes also suggested effects on bone and fat metabolism (Attie et al., 2013)","In ambulatory boys with Duchenne muscular dystrophy dosed 0.5 mg/kg every 4 weeks or 1 mg/kg every 2 weeks subcutaneously, the trial was stopped after the second dosing regimen because of epistaxis and telangiectasia; 6-minute walk, lean mass, bone density and fat mass showed non-significant trends in favour of treatment (Campbell et al., 2017)","Transgenic mice expressing a dominant-negative ActRIIB in skeletal muscle gained muscle mass comparable to myostatin-knockout mice, the preclinical basis for decoy-receptor blockade (Lee and McPherron, 2001)","Human-trial status: one phase 1 and one phase 2 trial published; development was discontinued on safety grounds and no regulator has approved it"],"evidence_level":"clinical","references":[{"title":"A single ascending-dose study of muscle regulator ACE-031 in healthy volunteers","authors":"Attie KM, Borgstein NG, Yang Y, et al.","journal":"Muscle & Nerve","year":2013,"doi":"10.1002/mus.23539","pmid":"23169607"},{"title":"Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: Results of a randomized, placebo-controlled clinical trial","authors":"Campbell C, McMillan HJ, Mah JK, et al.","journal":"Muscle & Nerve","year":2017,"doi":"10.1002/mus.25268","pmid":"27462804"},{"title":"Regulation of myostatin activity and muscle growth","authors":"Lee SJ, McPherron AC","journal":"Proceedings of the National Academy of Sciences","year":2001,"doi":"10.1073/pnas.151270098","pmid":"11459935"}],"molecular_weight":90000,"amino_acid_sequence":"ActRIIB extracellular domain fused to IgG1 Fc","alternative_names":["ActRIIB-Fc","Myostatin decoy receptor"],"half_life":"Mean 10 to 15 days (human, single subcutaneous dose 0.02 to 3 mg/kg; Attie 2013)","bioavailability":"Subcutaneous: AUC and Cmax rose linearly with dose from 0.02 to 3 mg/kg in humans; no absolute bioavailability reported","side_effects":"The phase 2 trial in boys with Duchenne muscular dystrophy was stopped after the second dosing regimen because of epistaxis and telangiectasia, and no serious or severe adverse events were recorded before that (Campbell 2017). In the phase 1 single-dose study in 48 healthy postmenopausal women, injection-site erythema was the main adverse event (Attie 2013). Bleeding and dilated surface vessels are the defining safety concern of this compound and the reason development was discontinued. It is not approved for human use.","last_reviewed_at":"2026-10-06T08:17:34.498Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Development discontinued after phase 2 was stopped for epistaxis and telangiectasia. Weight-based dosing: mcg dose fields null by design. | benefits: Puts the actual trial numbers and their model systems in the field. | detailed_description: Old text was two sentences with no numbers, model system or outcome. Old value omitted for length. | recommended_dose: Recheck 2026-10-06: phase 2 arms per the ClinicalTrials.gov registry; 3 mg/kg was the phase 1 top single dose. The trials dosed subcutaneously, not IV, and the published range differs from 0.5 to 3 mg/kg monthly. | dose_frequency: The phase 2 trial dosed every 2 to 4 weeks; the style guide's vocabulary takes the shorter interval. The full range is in dosing_notes. | dosing_notes: Recheck 2026-10-06: phase 2 arms per the ClinicalTrials.gov registry; 3 mg/kg was the phase 1 top single dose. Corrects the route and the dose range and records why the numeric fields are empty. | mechanism_of_action: Old text asserted the bleeding mechanism as fact ('likely from activin inhibition affecting vascular integrity'); the trial report does not. Old value omitted for length. | clinical_studies: Old bullets had no numbers and claimed 'successor programs exploring more selective myostatin inhibitors', which is not in either paper. | half_life: Measured value with route and species, replacing an estimate from the molecule class. | bioavailability: States what the phase 1 study measured instead of a class generalisation. | side_effects: Separates what each trial reported; the old text implied severe AEs in both.","sources":[{"url":"https://pubmed.ncbi.nlm.nih.gov/23169607/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/27462804/","note":"side_effects"},{"url":"https://clinicaltrials.gov/study/NCT01099761","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11459935/","note":"clinical_studies"}],"data_version":2,"slug":"ace-031","url":"https://peptidelabs.app/peptides/ace-031/"},{"id":100,"name":"Acetyl Hexapeptide-3 (Argireline)","description":"Synthetic acetylated hexapeptide (Ac-EEMQRR-NH2) modelled on the SNAP-25 N-terminus; a 2013 placebo-controlled trial (n=60) found less periorbital wrinkling after 4 weeks of topical use.","benefits":"Periorbital wrinkle reduction (human RCT, n=60), skin roughness reduction (small human RCT), neurotransmitter release inhibition (in vitro)","categories":["cosmetic","skin health","anti-aging"],"recommended_dose":"Topical only. Published studies used an emulsion stated as 10% (Blanes-Mira 2002); the CIR panel found it safe in cosmetics up to 0.005% and data insufficient above that. No oral or injectable dose exists.","detailed_description":"Argireline (acetyl hexapeptide-3, now INCI acetyl hexapeptide-8) was designed by a Spanish academic and industry group as a topical alternative to botulinum toxin; an O/W emulsion reduced wrinkle depth up to 30% in 30 days in healthy women (Blanes-Mira et al., 2002). Independent trials followed: a randomized placebo-controlled study in 60 Chinese adults found 48.9% global improvement in periorbital lines versus 0% on placebo (Wang et al., 2013), and a four-arm study (n=24) found reduced roughness (Raikou et al., 2017). An FDA lab found only 0.01% of an applied dose in the epidermis of human skin in vitro and none in the dermis (Kraeling et al., 2015), so whether it reaches muscle is unproven.","storage_temp":"Room temperature, away from light","shelf_life_reconstituted":"N/A (ready to use)","shelf_life_powder":"2 years at room temp","stacks_with":[],"dose_min_mcg":null,"dose_max_mcg":null,"dose_unit":null,"dose_frequency":"2x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Topical cream or serum applied to expression lines. Trials ran 4 weeks to 60 days, twice daily. Concentration conventions differ: papers state 10% emulsions, while the CIR safety review covers use up to 0.005% peptide.","mechanism_of_action":"Proposed. The peptide copies the N-terminal sequence of SNAP-25 and in cell assays interfered with formation or stability of the SNARE complex, inhibiting calcium-dependent neurotransmitter release with potency similar to botulinum toxin A but much lower efficacy (Blanes-Mira et al., 2002). Whether topical application reaches the neuromuscular junction is unresolved: in human and guinea pig skin in vitro almost all peptide stayed on the surface or in the stratum corneum, with none detected in the dermis (Kraeling et al., 2015).","clinical_studies":["Wrinkle depth fell up to 30% after 30 days of an O/W emulsion in healthy women; cell work showed SNARE complex interference (Blanes-Mira et al., 2002)","Randomized placebo-controlled trial, 60 Chinese adults, twice daily for 4 weeks: 48.9% global improvement in periorbital lines vs 0% on placebo, roughness reduced on silicone replicas (Wang et al., 2013)","Four-arm randomized study (n=24) over 60 days: acetyl hexapeptide-3 reduced roughness and transepidermal water loss vs no peptide (Raikou et al., 2017)","Randomized double-blind pilot in 24 blepharospasm patients: topical use alongside botulinum toxin gave a non-significant trend to longer symptom control, 3.7 vs 3.0 months (Lungu et al., 2013)","Human-trial status: small topical RCTs only, the first from the developers; no injectable study exists, and one Mycobacterium abscessus infection followed off-label facial injection (Chen et al., 2021)"],"evidence_level":"clinical","references":[{"title":"A synthetic hexapeptide (Argireline) with antiwrinkle activity","authors":"Blanes-Mira C, Clemente J, Jodas G, et al.","journal":"International Journal of Cosmetic Science","year":2002,"pmid":"18498523"},{"title":"The anti-wrinkle efficacy of argireline, a synthetic hexapeptide, in Chinese subjects: a randomized, placebo-controlled study","authors":"Wang Y, Wang M, Xiao S, Pan P, et al.","journal":"American journal of clinical dermatology","year":2013,"doi":"10.1007/s40257-013-0009-9","pmid":"23417317"},{"title":"The efficacy study of the combination of tripeptide-10-citrulline and acetyl hexapeptide-3. A prospective, randomized controlled study","authors":"Raikou V, Varvaresou A, Panderi I, Papageorgiou E","journal":"Journal of cosmetic dermatology","year":2017,"doi":"10.1111/jocd.12314","pmid":"28150423"},{"title":"Pilot study of topical acetyl hexapeptide-8 in the treatment for blepharospasm in patients receiving botulinum toxin therapy","authors":"Lungu C, Considine E, Zahir S, Ponsati B, et al.","journal":"European journal of neurology","year":2013,"doi":"10.1111/ene.12009","pmid":"23146065"},{"title":"In vitro skin penetration of acetyl hexapeptide-8 from a cosmetic formulation","authors":"Kraeling ME, Zhou W, Wang P, Ogunsola OA","journal":"Cutaneous and ocular toxicology","year":2015,"doi":"10.3109/15569527.2014.894521","pmid":"24754410"},{"title":"Safety Assessment of Acetyl Hexapeptide-8 Amide as Used in Cosmetics","authors":"Johnson W Jr, Bergfeld WF, Belsito DV, Cohen DE, et al.","journal":"International journal of toxicology","year":2025,"doi":"10.1177/10915818251340391","pmid":"40673537"},{"title":"The study of cellular cytotoxicity of argireline - an anti-aging peptide","authors":"Grosicki M, Latacz G, Szopa A, Cukier A, et al.","journal":"Acta biochimica Polonica","year":2014,"pmid":"24644551"},{"title":"Mycobacterium abscessus infection after facial injection of argireline: A case report","authors":"Chen CF, Liu J, Wang SS, Yao YF, et al.","journal":"World journal of clinical cases","year":2021,"doi":"10.12998/wjcc.v9.i8.1996","pmid":"33748252"}],"molecular_weight":888.99,"amino_acid_sequence":"Ac-Glu-Glu-Met-Gln-Arg-Arg-NH2","alternative_names":["Argireline","Acetyl Hexapeptide-8","Acetyl Hexapeptide-8 Amide","Ac-EEMQRR-NH2","AH8"],"half_life":"No published pharmacokinetic data in any species","bioavailability":"Topical (human cadaver skin in vitro, 10% O/W emulsion, 24 h): 0.22% of dose in stratum corneum, 0.01% in epidermis, none in dermis or receptor fluid","side_effects":"No significant adverse events in the 24-patient blepharospasm RCT (Lungu et al., 2013); no oral toxicity or primary irritation at high doses in developer tests (Blanes-Mira et al., 2002). Cytotoxic to cultured human cells only far above use levels (Grosicki et al., 2014). The CIR panel found data insufficient above 0.005%. One Mycobacterium abscessus abscess followed facial injection (Chen et al., 2021). Commonly reported (anecdotal): mild stinging or redness.","last_reviewed_at":"2026-10-06T08:17:42.883Z","reviewed_by":"audit-2026-10","review_notes":"N/A-by-design: topical. dose_min_mcg/dose_max_mcg stay null because a concentration in a formulation cannot be written as mcg per dose (decision 2). storage: not verified against a CoA. | description: Adds the human model system and trial size. | benefits: Each item now carries its tier. | detailed_description: Old text claimed muscle relaxation as a demonstrated effect; penetration data say otherwise. Old value omitted for length. | mechanism_of_action: Old text stated muscle relaxation at the neuromuscular junction as fact. | clinical_studies: Old bullets included unsourced and marketing claims ('Botox in a jar', 'safe'). | recommended_dose: Concentration is the relevant figure for a topical. The 10% figure likely refers to a supplier solution rather than pure peptide; the abstract does not say. | dose_frequency: Twice-daily application in the RCT. | dosing_notes: Field was empty. | half_life: Old text implied a measured local effect. | bioavailability: Measured values replace a general claim. | side_effects: Removes advice phrasing ('patch test', 'avoid') and adds sourced safety data. | molecular_weight: Residue arithmetic for Ac-EEMQRR-NH2 gives C34H60N14O12S, 888.99. PubChem CID 71587772 lists C35H62N14O11S (887.0) because its first residue is drawn as a hex-5-enoic acid, not Glu; not used. | alternative_names: CIR and trial names added; 'AH3' appears in no paper found. | stacks_with: Decisions 14 and 30: no published combination with either; the one published combination (tripeptide-10 citrulline) is not in the catalog.","sources":[{"url":"https://pubmed.ncbi.nlm.nih.gov/40565185/","note":"Zdrada-Nowak 2025 review: topical reach to neuromuscular junction unconfirmed"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23607739/","note":"duplicate report of the Wang 2013 trial"},{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/71587772","note":"molecular_weight"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18498523/","note":"molecular_weight"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23417317/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/28150423/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/24754410/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23146065/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/33748252/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40673537/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/24644551/","note":"side_effects"}],"data_version":2,"slug":"acetyl-hexapeptide-3-argireline","url":"https://peptidelabs.app/peptides/acetyl-hexapeptide-3-argireline/"},{"id":121,"name":"Adamax","description":"Adamantane-modified analog of the ACTH(4-7) peptide Semax, intended for greater lipophilicity and brain uptake; almost no published research exists.","benefits":"Extrapolated from Semax research: memory, focus and neuroprotection; no published human or animal data on Adamax itself","categories":["cognitive","neuroprotection"],"recommended_dose":"100 to 500 mcg daily (vendor/community range, no published human dose)","detailed_description":"Adamax is a research analog of the Russian nootropic peptide Semax (ACTH 4-7 Pro-Gly-Pro) modified with an adamantane group intended to increase lipophilicity and blood-brain-barrier penetration. Unlike Semax itself, Adamax has essentially no peer-reviewed literature of its own; reported cognitive and neuroprotective effects are extrapolated from Semax research and community reports.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":[],"dose_min_mcg":100,"dose_max_mcg":500,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[5],"dosing_notes":"Routes in circulation are intranasal and subcutaneous, both community convention. No published study has administered this compound, so there is no pharmacokinetic basis for any dose or interval. Parent-compound work used intranasal Semax in rats (Dolotov et al., 2006).","mechanism_of_action":"No mechanism has been published for Adamax itself; nothing in PubMed or PubChem describes the compound. Everything stated about it is extrapolated from Semax, the ACTH(4-7)-Pro-Gly-Pro heptapeptide. In rats, Semax raised BDNF and trkB expression in the hippocampus within hours of a single intranasal dose (Dolotov et al., 2006) and changed NGF and BDNF transcript levels in hippocampus, frontal cortex and retina (Shadrina et al., 2010). Transcriptome work after middle cerebral artery occlusion in rats found Semax altered immune and vascular gene sets (Filippenkov et al., 2020). Whether an adamantane or acetyl modification preserves any of this is untested.","clinical_studies":["No study of Adamax exists in PubMed under that name or any resolvable synonym (search run 2026-10-05)","Parent compound Semax raised hippocampal BDNF and trkB mRNA in rats after intranasal dosing (Dolotov et al., 2006)","Semax changed NGF and BDNF expression in rat hippocampus, frontal cortex and retina, with different time courses per region (Shadrina et al., 2010)","Semax altered immune and vascular gene expression after cerebral ischaemia-reperfusion in rats (Filippenkov et al., 2020)","Russian clinical reports of Semax in ischaemic stroke exist but are open-label and single-country (Gusev et al., 2018)","Human-trial status: no trial, no pharmacokinetics and no safety study of Adamax in any species; the parent peptide's approvals and trials are Russian and do not transfer to this analog"],"evidence_level":"anecdotal","references":[{"title":"Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus","authors":"Dolotov OV, Karpenko EA, Inozemtseva LS, et al.","journal":"Brain Research","year":2006,"doi":"10.1016/j.brainres.2006.07.108","pmid":"16996037"},{"title":"Comparison of the temporary dynamics of NGF and BDNF gene expression in rat hippocampus, frontal cortex, and retina under Semax action","authors":"Shadrina M, Kolomin T, Agapova T, et al.","journal":"Journal of Molecular Neuroscience","year":2010,"doi":"10.1007/s12031-009-9270-z","pmid":"19662538"},{"title":"The heptapeptide SEMAX stimulates BDNF expression in different areas of the rat brain in vivo","authors":"Dolotov OV, Seredenina TS, Levitskaya NG, et al.","journal":"Doklady Biological Sciences","year":2003,"doi":"10.1023/a:1025177812262","pmid":"14556513"},{"title":"Novel Insights into the Protective Properties of ACTH(4-7)PGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia-Reperfusion in Rats","authors":"Filippenkov IB, Stavchansky VV, Denisova AE, et al.","journal":"Genes","year":2020,"doi":"10.3390/genes11060681","pmid":"32580520"},{"title":"The efficacy of semax in the tretament of patients at different stages of ischemic stroke","authors":"Gusev EI, Martynov MY, Kostenko EV, et al.","journal":"Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova","year":2018,"doi":"10.17116/jnevro20181183261-68","pmid":"29798983"}],"molecular_weight":null,"amino_acid_sequence":null,"alternative_names":["Semax analog (unpublished structure)"],"half_life":"Not established in any species; no pharmacokinetic study of this compound exists","bioavailability":"Not measured. No bioavailability data exist for this compound by any route.","side_effects":"No published human safety data; everything reported about it is extrapolated from Semax. Anecdotal reports mention headache, overstimulation, and irritability. The photosensitivity warning that circulates with this compound is unsourced.","last_reviewed_at":"2026-10-06T08:17:36.165Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. No published literature on this compound exists; molecular weight and sequence nulled rather than guessed. Dose range is vendor/community per decision 11. | molecular_weight: 872.97 matches nothing. PubChem has no record under Adamax or any synonym. Semax itself (CID 9811102, Met-Glu-His-Phe-Pro-Gly-Pro) is 813.9, and N-terminal acetylation would give about 856. The record's own sequence and its mass disagree, so the number is removed rather than guessed. | amino_acid_sequence: The listed sequence is acetyl-Semax, which is the separate catalog entry N-Acetyl Semax Amidate (id 58). No published source defines an Adamax structure, so the field is null. | alternative_names: N-Acetyl-Semax is another catalog entry's compound, which the style guide forbids as an alternative name here. | mechanism_of_action: The old text asserted N-terminal acetylation, BDNF and NGF induction, dopaminergic and serotonergic modulation, antioxidant neuroprotection and improved cerebral blood flow for a compound with no literature. Replaced with what is actually published, about the parent, with the model system named. Old value omitted for length. | clinical_studies: Old bullets were five unsourced assertions, including 'enhanced analog developed for improved pharmacokinetics', which no publication supports. | half_life: The figure and the comparison with Semax were both unsourced. | bioavailability: Two precise percentages with no source anywhere in the literature. | recommended_dose: Decision 11: the numbers are kept only with the label, since no study of this compound has ever been dosed. | dosing_notes: 'Enhanced Semax analog' states a comparison no source supports. | stacks_with: Decision 14: no published combination and no established protocol. Listing the parent compound as a stack also implies the analog adds something, which is untested.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/9811102","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/?term=adamax%5Btiab%5D","note":"39 hits, all unrelated (machine-learning optimiser papers). No peptide literature."},{"url":"https://pubmed.ncbi.nlm.nih.gov/16996037/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/19662538/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/32580520/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/29798983/","note":"clinical_studies"}],"data_version":2,"slug":"adamax","url":"https://peptidelabs.app/peptides/adamax/"},{"id":33,"name":"Adipotide (FTPP)","description":"Proapoptotic peptidomimetic that binds prohibitin on white-fat blood vessels; 4 weeks of daily dosing cut body weight 7 to 15% in obese rhesus monkeys, with reversible kidney tubule effects.","benefits":"Fat-mass reduction and reversal of obesity (mouse), 7 to 15% weight loss and improved insulin resistance (obese rhesus monkeys, 4 weeks), weight-independent improvement in glucose tolerance (obese mice); no human efficacy data","categories":["fat loss","metabolic"],"recommended_dose":"0.1 to 0.5 mg daily (community range); the human phase 1 started at 0.03 mg/kg daily and primates received 0.25 to 0.75 mg/kg daily","detailed_description":"Adipotide is CKGGRAKDC, a peptide found by in vivo phage display to home to white-fat vasculature through prohibitin, joined to the proapoptotic D-amino-acid motif (KLAKLAK)2 (Kolonin 2004; Ellerby 1999). In obese mice the conjugate ablated white fat and reversed obesity (Kolonin 2004). In obese rhesus monkeys, 0.43 mg/kg daily for 4 weeks reduced weight 7.4 to 14.7%, cut fat on MRI and DXA, and improved insulin resistance, with predictable, reversible changes in kidney proximal tubule function (Barnhart 2011). A comment argued the monkey weight loss may reflect lower food intake rather than fat-vessel ablation (Criscione 2012). In mice it improved glucose tolerance within days (Kim 2012). A phase 1 trial in men with prostate cancer and obesity enrolled 4 patients and was terminated.","storage_temp":"Refrigerate 2-8°C (36-46°F); general lyophilised-peptide guidance, no compound-specific CoA located","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":[],"dose_min_mcg":100,"dose_max_mcg":500,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[10],"dosing_notes":"Subcutaneous, once daily in all published work. Primate studies: 0.43 mg/kg daily for 28 days in obese rhesus monkeys, 0.25 to 0.75 mg/kg in the lean-monkey toxicology study (Barnhart 2011). Phase 1: 0.03 mg/kg daily for 28 days as a starting dose (NCT01262664). No completed human dosing study.","mechanism_of_action":"Adipotide has two domains. CKGGRAKDC binds prohibitin, which Kolonin 2004 established as a marker on the endothelium of white-fat blood vessels. The D-(KLAKLAK)2 motif disrupts mitochondrial membranes once internalised, triggering apoptosis (Ellerby 1999). Targeted apoptosis of fat vasculature leads to resorption of white fat (Kolonin 2004; Barnhart 2011). Reduced food intake may also contribute (Criscione 2012). Renal effects are attributed to proximal tubule exposure; the paper describes them as predictable and reversible (Barnhart 2011).","clinical_studies":["Targeting a proapoptotic peptide to prohibitin on fat vasculature ablated white fat and reversed obesity in mice (Kolonin et al., 2004)","0.43 mg/kg subcutaneously daily for 4 weeks reduced body weight 7.4 to 14.7% in 10 obese rhesus monkeys versus +1.0 to -3.5% in 5 controls, and improved insulin resistance (Barnhart et al., 2011)","Renal proximal tubule changes were dose-dependent and reversible; creatinine rose at 0.75 mg/kg in lean monkeys (Barnhart et al., 2011)","Disputed: a published comment argued the monkey weight loss may be driven by reduced food intake (Criscione, 2012)","Human-trial status: one phase 1 (prostate cancer with obesity, starting dose 0.03 mg/kg daily) enrolled 4 patients and was terminated at the investigator's request; no results published (NCT01262664)"],"evidence_level":"preclinical","references":[{"title":"Reversal of obesity by targeted ablation of adipose tissue","authors":"Kolonin MG, Saha PK, Chan L, Pasqualini R, Arap W","journal":"Nature Medicine","year":2004,"doi":"10.1038/nm1048","pmid":"15133506"},{"title":"A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys","authors":"Barnhart KF, Christianson DR, Hanley PW, et al.","journal":"Science Translational Medicine","year":2011,"doi":"10.1126/scitranslmed.3002621","pmid":"22072637"},{"title":"Comment on \"a peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys\"","authors":"Criscione L","journal":"Science Translational Medicine","year":2012,"doi":"10.1126/scitranslmed.3003760","pmid":"22539771"},{"title":"Rapid and weight-independent improvement of glucose tolerance induced by a peptide designed to elicit apoptosis in adipose tissue endothelium","authors":"Kim DH, Sartor MA, Bain JR, et al.","journal":"Diabetes","year":2012,"doi":"10.2337/db11-1579","pmid":"22733798"},{"title":"Anti-cancer activity of targeted pro-apoptotic peptides","authors":"Ellerby HM, Arap W, Ellerby LM, et al.","journal":"Nature Medicine","year":1999,"doi":"10.1038/12469","pmid":"10470080"}],"molecular_weight":2557.2,"amino_acid_sequence":"CKGGRAKDCGG[D-KLAKLAKKLAKLAK]","alternative_names":["FTPP","Prohibitin-targeting peptide","Prohibitin-TP01"],"half_life":"Not published in any species; primate studies dosed once daily subcutaneously (Barnhart 2011)","bioavailability":"Not reported. Primate efficacy studies used subcutaneous injection (Barnhart 2011); the human phase 1 used subcutaneous dosing","side_effects":"No published human safety data; the only human trial enrolled 4 patients and posted no results. In monkeys, kidney proximal tubule function changed in a dose-dependent, reversible way: creatinine rose at 0.75 mg/kg/day and sporadically in 2 animals at 0.43 mg/kg/day, with slight residual creatinine and urine glucose elevation in one monkey per study after recovery (Barnhart 2011). Single doses up to 100 mg/kg were not lethal in monkeys. Dehydration and reduced appetite are commonly reported (anecdotal).","last_reviewed_at":"2026-10-06T08:17:29.477Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Only human exposure: phase 1, n=4, terminated, no results. | description: Adds the primate numbers and the renal finding. | benefits: Adds the primate range and the glucose finding. | detailed_description: Old text gave no numbers and named no human trial. Old value omitted for length. | mechanism_of_action: Old text said it 'causes ischemic fat tissue death' and 'caused kidney issues' without attribution, and called reabsorbed peptide 'toxic to tubules' without a source. Old value omitted for length. | clinical_studies: Old bullets said monkeys 'lost 11% body weight and 27% fat' (paper gives 7.4 to 14.7%) and that research was 'discontinued due to renal toxicity' (the trial record says terminated per PI request). | side_effects: Old text was advice ('kidney function monitoring is mandatory', 'should be treated as nephrotoxic') rather than reported findings. | half_life: 'Short' had no source. | bioavailability: No IV primate study was found; 'Good' was unsourced. | recommended_dose: Decision 10: weight-based doses are stated, not converted; community numbers labelled. | dosing_notes: Old note was advice with no source. | molecular_weight: PubChem CID 163360068 (synonym Adipotide, CAS 859216-15-2) gives C111H206N36O28S2, 2557.2, which matches the open (thiol) form; calculated 2557.18. If the CKGGRAKDC loop is disulfide-cyclised the mass is 2555.2. 2522.94 matches neither. | amino_acid_sequence: One-letter codes with the D-amino-acid segment in brackets, from Barnhart 2011 (CKGGRAKDC-GG-D(KLAKLAK)2). | alternative_names: Prohibitin-TP01 is the name used in the phase 1 registration. | stacks_with: Decision 14: no published combination. | storage_temp: Labelled as general guidance.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/163360068","note":"molecular_weight"},{"url":"https://clinicaltrials.gov/study/NCT01262664","note":"alternative_names"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3666164/","note":"Barnhart 2011 full text: doses, weight change ranges, creatinine findings, 100 mg/kg single-dose toxicology"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15133506/","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22072637/","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22733798/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/10470080/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22539771/","note":"clinical_studies"}],"data_version":2,"slug":"adipotide-ftpp","url":"https://peptidelabs.app/peptides/adipotide-ftpp/"},{"id":149,"name":"AHK","description":"Tripeptide Ala-His-Lys; no published study tests the free peptide. Its copper complex AHK-Cu has ex vivo human hair follicle data and its own catalog entry.","benefits":"None published for free AHK. The copper complex AHK-Cu has ex vivo human hair follicle data (see AHK-Cu entry)","categories":["hair growth","skin health","cosmetic"],"recommended_dose":"Topical application","detailed_description":"AHK (Ala-His-Lys) is a tripeptide sold for hair and skin products. Every hair study found used its copper complex, AHK-Cu, tested on human hair follicles ex vivo (Pyo 2007); a 2026 review lists only ex vivo data (Fan 2026). Those results belong to the AHK-Cu entry and do not transfer to the free peptide. The only other paper used a vitamin C-linker conjugate of AHK in mouse myoblast cells (Jung 2018). No human trial exists for AHK in any form.","storage_temp":"Room temperature, away from light","shelf_life_reconstituted":"N/A (ready to use)","shelf_life_powder":"2 years at room temp","stacks_with":[],"dose_min_mcg":null,"dose_max_mcg":null,"dose_unit":null,"dose_frequency":null,"recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Topical. No published concentration or dose for the free tripeptide.","mechanism_of_action":"Unknown for the free peptide. The old text's VEGF, Wnt and anagen claims came from GHK-Cu and AHK-Cu without a source. AHK binds copper to form AHK-Cu, which was tested on human hair follicles ex vivo (Pyo 2007); see that entry. A vitamin C-linker conjugate of AHK stimulated BMP-2-induced osteogenic differentiation in mouse C2C12 cells (Jung 2018).","clinical_studies":["No published study of free AHK in any model","A vitamin C-linker conjugate of AHK stimulated BMP-2-induced osteogenic differentiation of mouse C2C12 myoblasts (Jung et al., 2018)","Human-trial status: none. Only the copper complex AHK-Cu has hair data, on human follicles ex vivo, with a non-significant change in apoptosis (Pyo et al., 2007; Fan et al., 2026); see the AHK-Cu entry"],"evidence_level":"anecdotal","references":[{"title":"The effect of tripeptide-copper complex on human hair growth in vitro","authors":"Pyo HK, Yoo HG, Won CH, Lee SH, et al.","journal":"Archives of Pharmacal Research","year":2007,"doi":"10.1007/BF02978833","pmid":"17703734"},{"title":"Overview of Short Peptides for Hair Loss","authors":"Fan C, Chen Y, Huang Q, Ou WY, et al.","journal":"Biomedicines","year":2026,"doi":"10.3390/biomedicines14040864","pmid":"42072405"},{"title":"Vitamin C-linker-conjugated tripeptide AHK stimulates BMP-2-induced osteogenic differentiation of mouse myoblast C2C12 cells","authors":"Jung JI, Park KY, Lee Y, Park M, et al.","journal":"Differentiation","year":2018,"doi":"10.1016/j.diff.2018.03.001","pmid":"29567599"}],"molecular_weight":354.41,"amino_acid_sequence":"Ala-His-Lys","alternative_names":["Alanine-Histidine-Lysine","AHK tripeptide","Ala-His-Lys"],"half_life":"No published pharmacokinetic data in any species","bioavailability":"Not measured; no skin penetration study of the free tripeptide has been published","side_effects":"No published safety data for the free tripeptide in any species. Commonly reported (anecdotal): irritation, redness or stinging with topical peptide products.","last_reviewed_at":"2026-10-06T08:26:28.156Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance, not verified. Dose fields null: no published concentration. N/A-by-design: topical. | description: Decision 48: old text credited the free peptide with AHK-Cu work. | benefits: Decision 48. | detailed_description: Old text was one generic sentence. | mechanism_of_action: Old mechanism was borrowed from GHK-Cu. | clinical_studies: Old bullets had no source and credited AHK with AHK-Cu results. | evidence_level: Decision 48: only the complex (AHK-Cu) and a conjugate (vitamin C-AHK) are studied; nothing tests the free peptide. | molecular_weight: PubChem CID 7408502 (Ala-His-Lys, C15H26N6O4) gives 354.41; residue arithmetic agrees. Old 340.38 matches no AHK form. | alternative_names: Adds the three-letter sequence name. | dosing_notes: Was null. | half_life: Old text implied localized activity. | bioavailability: Old text claimed follicular penetration without a source. | side_effects: Removes second-person advice (patch test, avoid broken skin). | stacks_with: Decisions 14 and 30: no published combination with GHK-Cu or BPC-157.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/7408502/property/MolecularFormula,MolecularWeight/JSON","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17703734/","note":"evidence_level"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42072405/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/29567599/","note":"clinical_studies"}],"data_version":2,"slug":"ahk","url":"https://peptidelabs.app/peptides/ahk/"},{"id":102,"name":"AHK-Cu (Copper Peptide)","description":"Copper(II) complex of the tripeptide Ala-His-Lys; one ex vivo study found it lengthened human hair follicles in organ culture and raised dermal papilla cell proliferation.","benefits":"Hair follicle elongation (ex vivo human follicles), dermal papilla cell proliferation and reduced apoptosis markers (in vitro)","categories":["cosmetic","hair growth"],"recommended_dose":"Topical only; no published study gives a formulation concentration for skin or scalp. Ex vivo work used 1 pM to 1 nM in culture medium.","detailed_description":"AHK-Cu is the copper(II) complex of L-alanyl-L-histidyl-L-lysine, a close analog of GHK-Cu (separate catalog entry) with alanine in place of glycine. The one peer-reviewed study found that 1 pM to 1 nM AHK-Cu lengthened isolated human hair follicles in organ culture and increased dermal papilla cell proliferation, with a higher Bcl-2/Bax ratio and less cleaved caspase-3 (Pyo et al., 2007). No animal or human study of hair growth has been published. Claims of better scalp circulation and synergy from copper binding have no published source. The uncomplexed peptide is catalogued separately as AHK.","storage_temp":"Room temperature, away from light","shelf_life_reconstituted":"N/A (ready to use)","shelf_life_powder":"2 years at room temp","stacks_with":[],"dose_min_mcg":null,"dose_max_mcg":null,"dose_unit":null,"dose_frequency":null,"recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Sold for topical scalp use. No human or animal dosing study exists; the ex vivo concentrations (1 pM to 1 nM) do not translate to a formulation strength.","mechanism_of_action":"Proposed, from one ex vivo study. In cultured human dermal papilla cells AHK-Cu increased proliferation, raised the Bcl-2/Bax ratio and lowered cleaved caspase-3 and PARP, suggesting reduced apoptosis; it lengthened isolated follicles at 1 pM to 1 nM (Pyo et al., 2007). The same paper cites earlier work on copper tripeptides raising VEGF in dermal fibroblasts, but VEGF was not measured for AHK-Cu itself. Anagen extension, DHT inhibition and pigmentation effects have no published data for this compound.","clinical_studies":["AHK-Cu at 1 pM to 1 nM lengthened human hair follicles in ex vivo organ culture (Pyo et al., 2007)","Raised dermal papilla cell proliferation in vitro; at 1 nM the Bcl-2/Bax ratio rose and cleaved caspase-3 and PARP fell (Pyo et al., 2007)","Human-trial status: no animal or human study of AHK-Cu has been published; the only peer-reviewed evidence is one ex vivo and cell study"],"evidence_level":"preclinical","references":[{"title":"The effect of tripeptide-copper complex on human hair growth in vitro","authors":"Pyo HK, Yoo HG, Won CH, Lee SH, et al.","journal":"Archives of pharmacal research","year":2007,"doi":"10.1007/BF02978833","pmid":"17703734"}],"molecular_weight":415.94,"amino_acid_sequence":"AHK (Ala-His-Lys), copper(II) complex","alternative_names":["AHK Copper","AHK-Cu2+","L-alanyl-L-histidyl-L-lysine copper(II)"],"half_life":"No published pharmacokinetic data in any species","bioavailability":"Not measured in any species; follicle or skin penetration of AHK-Cu has not been studied","side_effects":"No safety study in animals or humans has been published; the one ex vivo study was not designed to detect harm. No injectable data exist. Commonly reported (anecdotal): scalp irritation and a temporary blue-green tint from copper complexes.","last_reviewed_at":"2026-10-06T08:17:42.883Z","reviewed_by":"audit-2026-10","review_notes":"N/A-by-design: topical. dose_min_mcg/dose_max_mcg stay null because a concentration in a formulation cannot be written as mcg per dose (decision 2). storage: not verified against a CoA. | description: Old text claimed copper delivery to follicles without a model system. | benefits: Each item now carries its tier; 'scalp health' had no source. | detailed_description: Old text claimed improved scalp circulation and hair restoration without a source. | mechanism_of_action: Old text listed anagen extension, VEGF upregulation and DHT inhibition as established. | clinical_studies: Old bullets claimed preclinical follicle size data and general safety without sources. Only three bullets are possible from the literature. | recommended_dose: States the only published concentration and its model. | dosing_notes: Field was empty. | half_life: Nothing measured. | bioavailability: Old claim of good follicle penetration had no source. | side_effects: Removes advice phrasing and the injected-use framing. | molecular_weight: Old value is GHK + Cu (340.38 + 63.55), apparently copied from GHK-Cu. AHK (CID 7408502) is 354.41; the neutral 1:1 Cu(II) complex with two deprotonations is 354.41 + 63.546 - 2.016 = 415.94. PubChem CID 168431292 lists the monohydrochloride salt at 451.39. | amino_acid_sequence: Format only. | alternative_names: Copper Tripeptide-1 is the INCI name of GHK-Cu, another catalog entry. | stacks_with: Decisions 14 and 30: no published combination or documented community protocol.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/7408502","note":"molecular_weight"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17703734/","note":"stacks_with"},{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/168431292","note":"alternative_names"}],"data_version":2,"slug":"ahk-cu-copper-peptide","url":"https://peptidelabs.app/peptides/ahk-cu-copper-peptide/"},{"id":34,"name":"AICAR","description":"Nucleoside AMPK activator (AICA riboside) that mimics exercise signalling, increasing glucose uptake, fat oxidation and running endurance in mice.","benefits":"Running endurance and fat oxidation (mouse), lower hepatic glucose output and suppressed lipolysis (human IV infusion), prohibited in sport","categories":["metabolic"],"recommended_dose":"150-500 mg daily (research-community range; no published human study used this dose or the subcutaneous route)","detailed_description":"AICAR (acadesine, AICA riboside) is a nucleoside that is phosphorylated inside cells to ZMP, an AMP mimetic that activates AMPK. In sedentary mice, 4 weeks of AICAR raised running endurance 44% and induced oxidative metabolic genes (Narkar 2008). Human work is all intravenous: in 10 men with type 2 diabetes an infusion lowered hepatic glucose output and suppressed whole-body lipolysis (Boon 2008); muscle 2-deoxyglucose uptake rose 1.6 to 2.9-fold, less in older men (Babraj 2009); under a hyperinsulinaemic clamp it raised heart rate and lowered blood pressure with no added glucose uptake (Bosselaar 2011). It was developed as a cardioprotective agent and failed a 3080-patient cardiac surgery RCT (Newman 2012), and reached phase 1/2 in leukaemia (Van Den Neste 2013). Not approved anywhere; prohibited in sport.","storage_temp":"Refrigerate 2-8°C (36-46°F); general lyophilised-powder guidance, no compound-specific CoA located","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["GW501516","MOTS-c"],"dose_min_mcg":150000,"dose_max_mcg":500000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":3,"common_vial_sizes":[50],"dosing_notes":"Human studies used intravenous dosing only: 10-100 mg/kg single doses in healthy men (Dixon 1991), 0.75 mg/kg/min continuous infusion in type 2 diabetes (Boon 2008), 10-20 mg/kg/h for 3 h (Babraj 2009), 50-315 mg/kg (210 mg/kg was the maximum tolerated dose) over 4 h in leukaemia with 210 mg/kg as the maximum tolerated dose (Van Den Neste 2013) and 0.1 mg/kg/min for 7 h in cardiac surgery (Newman 2012). Oral solution is under 5% bioavailable (Dixon 1991). The mouse endurance work used 4 weeks of daily injection (Narkar 2008). AICAR is prohibited in sport and urinary concentrations above about 2000 ng/mL trigger isotope-ratio confirmation (Sobolevsky 2019).","mechanism_of_action":"AICAR is taken into cells by nucleoside transporters and phosphorylated by adenosine kinase to ZMP, which mimics AMP and activates AMP-activated protein kinase (Narkar 2008). In mice, 4 weeks of treatment induced an oxidative gene program through AMPK and PPAR-delta and raised running endurance without training (Narkar 2008). In humans, AICAR infusion reduced hepatic glucose output and plasma NEFA appearance and raised acetyl-CoA carboxylase phosphorylation in muscle, while muscle AMPK phosphorylation itself did not rise (Boon 2008); muscle glucose uptake rose with ERK1/2 rather than AMPK activation (Babraj 2009). It also causes systemic vasodilation, probably nitric-oxide dependent (Bosselaar 2011), and has documented AMPK-independent actions. Not a peptide; included for reference.","clinical_studies":["Four weeks of AICAR in sedentary mice raised treadmill running endurance 44% and induced oxidative metabolic genes (Narkar et al., 2008)","IV infusion (0.75 mg/kg/min) in 10 men with type 2 diabetes reduced hepatic glucose output and suppressed whole-body lipolysis (Boon et al., 2008)","IV AICAR (10-20 mg/kg/h) raised muscle 2-deoxyglucose uptake 2.9-fold in young men and 1.6-1.8-fold in older men and men with type 2 diabetes, without detectable muscle AMPK activation (Babraj et al., 2009)","Under a hyperinsulinaemic clamp in 10 healthy adults, AICAR (67 mg/kg) raised heart rate and lowered blood pressure but did not increase glucose uptake (Bosselaar et al., 2011)","RED-CABG, 3080 patients undergoing on-pump bypass surgery: a 7-hour infusion did not reduce death, stroke or severe left ventricular dysfunction at 28 days (Newman et al., 2012)","Human-trial status: phase 1 PK in healthy men (Dixon 1991), a phase 1/2 leukaemia study with a 210 mg/kg maximum tolerated dose (Van Den Neste et al., 2013) and a negative phase 3 cardiac surgery RCT. No approval anywhere and no human trial of the endurance or body-composition uses"],"evidence_level":"preclinical","references":[{"title":"AMPK and PPARdelta agonists are exercise mimetics","authors":"Narkar VA, Downes M, Yu RT, et al.","journal":"Cell","year":2008,"doi":"10.1016/j.cell.2008.06.051","pmid":"18674809"},{"title":"AICA-riboside: safety, tolerance, and pharmacokinetics of a novel adenosine-regulating agent","authors":"Dixon R, Gourzis J, McDermott D, Fujitaki J, Dewland P, Gruber H","journal":"Journal of Clinical Pharmacology","year":1991,"doi":"10.1002/j.1552-4604.1991.tb03715.x","pmid":"2037706"},{"title":"Intravenous AICAR administration reduces hepatic glucose output and inhibits whole body lipolysis in type 2 diabetic patients","authors":"Boon H, Bosselaar M, Praet SF, et al.","journal":"Diabetologia","year":2008,"doi":"10.1007/s00125-008-1108-7","pmid":"18709353"},{"title":"Blunting of AICAR-induced human skeletal muscle glucose uptake in type 2 diabetes is dependent on age rather than diabetic status","authors":"Babraj JA, Mustard K, Sutherland C, et al.","journal":"American Journal of Physiology - Endocrinology and Metabolism","year":2009,"doi":"10.1152/ajpendo.90811.2008","pmid":"19190259"},{"title":"Intravenous AICAR during hyperinsulinemia induces systemic hemodynamic changes but has no local metabolic effect","authors":"Bosselaar M, Smits P, van Loon LJ, Tack CJ","journal":"Journal of Clinical Pharmacology","year":2011,"doi":"10.1177/0091270010382912","pmid":"21148051"},{"title":"Effect of adenosine-regulating agent acadesine on morbidity and mortality associated with coronary artery bypass grafting: the RED-CABG randomized controlled trial","authors":"Newman MF, Ferguson TB, White JA, et al.","journal":"JAMA","year":2012,"doi":"10.1001/jama.2012.7633","pmid":"22782417"},{"title":"Acadesine for patients with relapsed/refractory chronic lymphocytic leukemia (CLL): a multicenter phase I/II study","authors":"Van Den Neste E, Cazin B, Janssens A, et al.","journal":"Cancer Chemotherapy and Pharmacology","year":2013,"doi":"10.1007/s00280-012-2033-5","pmid":"23228986"},{"title":"Urinary concentrations of AICAR and mannitol in athlete population","authors":"Sobolevsky T, Ahrens B","journal":"Drug Testing and Analysis","year":2019,"doi":"10.1002/dta.2557","pmid":"30548818"}],"molecular_weight":258.23,"amino_acid_sequence":"N/A - nucleoside analog (not a peptide)","alternative_names":["Acadesine","AICA riboside","AICAr","5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranoside","ARA 100","GP 1 110"],"half_life":"~1.4 h terminal (human, IV; harmonic mean t1/2-beta across 10-100 mg/kg, n=16; Dixon 1991)","bioavailability":"Oral <5% in solution (human; Dixon 1991). Not protein bound, taken up rapidly by erythrocytes and phosphorylated to ZMP (human; Dixon 1991, Bosselaar 2011). No subcutaneous bioavailability data.","side_effects":"Human IV studies report transient infusion-related hypotension with a rise in heart rate (Bosselaar 2011), grade 2 or higher hyperuricaemia, transient anaemia or thrombocytopenia and renal impairment at 50-210 mg/kg (Van Den Neste 2013), and mild transient effects at 10-100 mg/kg in healthy men (Dixon 1991). The 3080-patient cardiac surgery RCT found no excess of serious adverse events (Newman 2012). There is no oral or chronic human data, and the effects of sustained AMPK activation in humans are unknown. AICAR is prohibited in sport (Sobolevsky 2019).","last_reviewed_at":"2026-10-06T08:17:27.815Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Molecular weight corrected from the ZMP metabolite to the administered riboside. Dose range left at the community figure pending Josh; literature IV doses in dosing_notes. | benefits: The record mixes rodent and human findings, so each item now carries its model system per the style guide. | molecular_weight: 338.21 is AICA ribotide (ZMP, CID 65110), the intracellular monophosphate metabolite. The compound sold and dosed is the riboside acadesine (CID 17513, C9H14N4O5, 258.23). | amino_acid_sequence: The administered compound is the nucleoside (riboside), not the nucleotide. | half_life: The ~1.5 h figure was unsourced; the human IV PK study gives 1.4 h with route, species and dose range. | bioavailability: 'Subcutaneous: Good' had no source and every human study used IV. Oral bioavailability is quantified as under 5%. | recommended_dose: Human dosing in every published study is weight-based IV (10-100 mg/kg single doses; 0.75 mg/kg/min infusion; 50-210 mg/kg in the CLL study, MTD 210 mg/kg), which cannot be written as a fixed per-injection range. Numeric fields left at the community range and the literature doses stated in dosing_notes, per pilot decision 1. | dosing_notes: Replaces a one-line note and a price opinion with the actual published dosing, routes and the doping-control threshold. | detailed_description: The old text was vendor-style copy with no model systems or trial history. Old value omitted for length. | mechanism_of_action: Old text asserted GLUT4 translocation, mitochondrial biogenesis and WADA status as mechanism without sources, and skipped the finding that human muscle AMPK phosphorylation did not increase. Old value omitted for length. | clinical_studies: Old bullets were unsourced generalities plus a WADA line; the large human trial record was missing entirely. | side_effects: The old text said human exposure was limited to short infusions with headache and GI upset, which is not what the trials report; hyperuricaem","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/17513","note":"alternative_names"},{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/65110","note":"molecular_weight"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18457469/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/19602584/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/34064363/","note":"mechanism_of_action"},{"url":"https://doi.org/10.3390/cells10051095","note":"Visnjic 2021 systematic review: AMPK-independent effects of AICAr"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18674809/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18709353/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/30548818/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/2037706/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/21148051/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23228986/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/19190259/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22782417/","note":"side_effects"}],"data_version":2,"slug":"aicar","url":"https://peptidelabs.app/peptides/aicar/"},{"id":147,"name":"Alpha-MSH","description":"Endogenous 13-residue POMC peptide that activates MC1, MC3, MC4 and MC5 receptors; injected, it changed human skin colour in a small 1961 study. Other effects are from animal models.","benefits":"Skin darkening (small uncontrolled human study, 1961), reduced food intake via MC4R (mouse genetics), anti-inflammatory effects (animal and cell models)","categories":["skin health","appetite"],"recommended_dose":"50 to 200 mcg daily: vendor/community range, no published human dose. The only modern human dosing was a single 2.5 mg IV bolus","detailed_description":"Alpha-MSH is residues 138 to 150 of proopiomelanocortin (POMC), N-terminally acetylated and C-terminally amidated, made in the pituitary, brain and skin. Injected alpha- and beta-MSH changed skin colour in volunteers in 1961, and a single 2.5 mg IV dose altered LH secretion in 8 women in 1994; no therapeutic trial of the native peptide has been published. Serum enzymes degrade it, which is why stabilized analogs were made: afamelanotide (Melanotan 1, an approved implant for erythropoietic protoporphyria), Melanotan II and bremelanotide (PT-141) are separate catalog entries, as is its C-terminal tripeptide KPV. Anti-inflammatory and appetite effects come from animal and cell models.","storage_temp":"Room temperature, away from light","shelf_life_reconstituted":"N/A (ready to use)","shelf_life_powder":"2 years at room temp","stacks_with":[],"dose_min_mcg":50,"dose_max_mcg":200,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"No dosing study exists. The one modern human exposure was a single 2.5 mg IV bolus in 8 women for endocrine research. The route, frequency and cycle used by vendors have no published basis.","mechanism_of_action":"Alpha-MSH is cleaved from POMC and acts on melanocortin receptors, a G protein-coupled family first cloned in 1992 alongside the separate ACTH receptor (Mountjoy et al., 1992). MC1R on melanocytes drives eumelanin synthesis. Central MC4R controls feeding: mice lacking MC4R develop obesity with hyperphagia (Huszar et al., 1997). Anti-inflammatory actions include reduced NF-kB activation and pro-inflammatory cytokines and increased IL-10, shown in cell and animal models of dermatitis, colitis, arthritis and fever (Brzoska et al., 2008). Native alpha-MSH is degraded by serum enzymes, and N-terminal acetylation slows its clearance in rabbits (Rudman et al., 1983).","clinical_studies":["Injected alpha- and beta-MSH changed skin colour in human volunteers in an uncontrolled study (Lerner and McGuire, 1961)","Cloning of the human and mouse MSH receptor and the human ACTH receptor defined the melanocortin receptor family (Mountjoy et al., 1992)","Targeted deletion of MC4R caused maturity-onset obesity with hyperphagia, hyperinsulinemia and hyperglycemia in mice (Huszar et al., 1997)","Anti-inflammatory effects in animal models of fever, contact dermatitis, colitis, arthritis and organ injury (Brzoska et al., 2008)","A single 2.5 mg IV bolus in 8 women in the luteal phase raised LH and blunted CRH suppression of LH, without changing ACTH or cortisol (Limone et al., 1994)","Human-trial status: no therapeutic trial of native alpha-MSH has been published. Human efficacy data belong to stabilized analogs, chiefly afamelanotide (approved implant, EU 2014, US 2019) and bremelanotide (approved 2019); see those entries"],"evidence_level":"preclinical","references":[{"title":"Effect of alpha- and beta-melanocyte stimulating hormones on the skin colour of man","authors":"Lerner AB, McGuire JS","journal":"Nature","year":1961,"doi":"10.1038/189176a0","pmid":"13761067"},{"title":"The cloning of a family of genes that encode the melanocortin receptors","authors":"Mountjoy KG, Robbins LS, Mortrud MT, et al.","journal":"Science","year":1992,"doi":"10.1126/science.1325670","pmid":"1325670"},{"title":"Targeted disruption of the melanocortin-4 receptor results in obesity in mice","authors":"Huszar D, Lynch CA, Fairchild-Huntress V, et al.","journal":"Cell","year":1997,"doi":"10.1016/s0092-8674(00)81865-6","pmid":"9019399"},{"title":"Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects in vitro and in vivo, and future perspectives for the treatment of immune-mediated inflammatory diseases","authors":"Brzoska T, Luger TA, Maaser C, et al.","journal":"Endocrine Reviews","year":2008,"doi":"10.1210/er.2007-0027","pmid":"18612139"},{"title":"Three types of alpha-melanocyte-stimulating hormone: bioactivities and half-lives","authors":"Rudman D, Hollins BM, Kutner MH, et al.","journal":"The American Journal of Physiology","year":1983,"doi":"10.1152/ajpendo.1983.245.1.E47","pmid":"6869528"},{"title":"4-Norleucine, 7-D-phenylalanine-alpha-melanocyte-stimulating hormone: a highly potent alpha-melanotropin with ultralong biological activity","authors":"Sawyer TK, Sanfilippo PJ, Hruby VJ, et al.","journal":"Proceedings of the National Academy of Sciences of the United States of America","year":1980,"doi":"10.1073/pnas.77.10.5754","pmid":"6777774"},{"title":"Alpha-melanocyte-stimulating hormone antagonizes the inhibitory effect of corticotropin-releasing hormone on luteinizing hormone secretion during the luteal phase in normal women","authors":"Limone P, Scipioni T, Calvelli P, et al.","journal":"The Journal of Clinical Endocrinology and Metabolism","year":1994,"doi":"10.1210/jcem.79.2.8045978","pmid":"8045978"}],"molecular_weight":1664.9,"amino_acid_sequence":"[Ac-S]YSMEHFRWGKPV[NH2]","alternative_names":["α-MSH","Alpha-melanocyte-stimulating hormone","POMC(138-150)"],"half_life":"Not measured in humans. In rabbit plasma (in vitro and IV) desacetyl alpha-MSH cleared fastest and diacetyl slowest; native peptide is degraded by serum enzymes","bioavailability":"Not measured by any route in any species. Native alpha-MSH is degraded by serum enzymes, unlike its [Nle4,D-Phe7] analog","side_effects":"No human safety study of repeated dosing exists. Skin colour change was the effect reported after injection in 1961 (Lerner and McGuire, 1961); the 1994 single IV dose study reported endocrine changes only (Limone et al., 1994). Nausea, flushing and darkening of moles are seen with the analogs and are plausible but not measured for native alpha-MSH. Commonly reported (anecdotal): nausea, flushing.","last_reviewed_at":"2026-10-06T08:17:41.213Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance (not verified). No human dose; numeric range is vendor/community per decision 11. | description: MC2R is the separate ACTH receptor (Mountjoy 1992), so 'MC1R-MC5R' overstated the targets. The 1961 paper has no abstract in PubMed; title and DOI resolved. | benefits: Tiers made explicit; the human pigmentation report is old and uncontrolled. | detailed_description: Old text was two generic sentences with no model system. | mechanism_of_action: Old text said MC1R-MC5R and gave a half-life of minutes without a source. | clinical_studies: Old bullets had no citations. Analog approvals go in the last bullet only (decisions 3 and 26). | recommended_dose: Decision 11. | dosing_notes: Field was empty. | half_life: No source found for 3 to 5 min; the rabbit paper's abstract gives the ordering but not the numbers. | bioavailability: Rewords to what the source shows. | side_effects: Removes advice phrasing and separates measured from inferred effects. | stacks_with: Decisions 14 and 30: no published combination; the analogs act on the same receptors. | molecular_weight: PubChem CID 16133793, C77H109N21O19S, 1664.9. | amino_acid_sequence: UniProt P01189 residues 138 to 150 (SYSMEHFRWGKPV) with N-acetyl and C-amide, in one-letter codes.","sources":[{"url":"https://rest.uniprot.org/uniprotkb/P01189.json","note":"amino_acid_sequence"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/16133793/property/MolecularFormula,MolecularWeight/JSON","note":"amino_acid_sequence"},{"url":"https://api.fda.gov/drug/drugsfda.json?search=openfda.generic_name:afamelanotide","note":"clinical_studies"},{"url":"https://api.fda.gov/drug/drugsfda.json?search=openfda.generic_name:bremelanotide","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/13761067/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1325670/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9019399/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18612139/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/8045978/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6777774/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6869528/","note":"half_life"}],"data_version":2,"slug":"alpha-msh","url":"https://peptidelabs.app/peptides/alpha-msh/"},{"id":17,"name":"AOD9604","description":"Modified hGH fragment (Tyr plus hGH 177-191) that reduced weight gain and raised fat oxidation in obese rodents; six human trials found no IGF-1 or glucose effects, with efficacy results unpublished.","benefits":"Reduced body weight gain and increased fat oxidation and lipolysis (obese mice and rats), cartilage regeneration after intra-articular injection (rabbit); no effect on IGF-1 or glucose tolerance (human RCTs, safety data only)","categories":["fat loss","metabolic"],"recommended_dose":"300 to 500 mcg once daily subcutaneously (community range); human trials used oral 0.25 to 30 mg daily or single IV doses of 25 to 400 mcg/kg","detailed_description":"AOD9604 is tyrosine-hGH(177-191), a synthetic analog of the C-terminal lipolytic region of human growth hormone developed at Monash University and Metabolic Pharmaceuticals. In obese mice and Zucker rats it reduced weight gain, raised fat oxidation and lipolysis, and unlike hGH did not cause insulin resistance or bind the GH receptor (Ng 2000; Heffernan 2001). Six randomised placebo-controlled human trials in about 900 adults used IV doses of 25 to 400 mcg/kg or oral doses of 0.25 to 54 mg; the published summary reports safety only: no change in IGF-1 or glucose tolerance and no antibodies (Stier 2013). Weight-loss results of the 12- and 24-week trials were never published in a peer-reviewed journal. Intra-articular injection aided cartilage repair in a rabbit osteoarthritis model (Kwon 2015). WADA prohibits it.","storage_temp":"Refrigerated (2-8°C); general lyophilised-peptide guidance, no compound-specific CoA located","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"24+ months at room temperature","stacks_with":[],"dose_min_mcg":300,"dose_max_mcg":500,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[5],"dosing_notes":"Community protocols inject 300 to 500 mcg subcutaneously, often fasted in the morning. All published human dosing was oral (capsules 1 to 54 mg; tablets 0.25 to 1 mg for 24 weeks) or single IV infusions of 25 to 400 mcg/kg over 20 minutes (Stier 2013). No subcutaneous human study exists.","mechanism_of_action":"AOD9604 corresponds to the C-terminal region of hGH that carries its lipolytic and antilipogenic activity. In rodent adipose tissue it increased lipolysis and reduced lipogenesis (Ng 2000). Its effect on weight is not mediated through the beta-3 adrenergic receptor, although it raises beta-3 receptor expression, and it still raised fat oxidation acutely in beta-3 knockout mice (Heffernan 2001, Endocrinology). It does not compete for the hGH receptor or drive hGH-receptor cell proliferation (Heffernan 2001, Int J Obes). In serum it is degraded to a stable CRSVEGSCG fragment (Cox 2015). Its receptor is not identified. Chondroprotective effects are proposed from one rabbit study (Kwon 2015).","clinical_studies":["Reduced body weight gain and raised fat oxidation and plasma glycerol in obese mice over 14 days without hyperglycaemia or hGH-receptor binding (Heffernan et al., 2001)","Oral 500 mcg/kg daily for 19 days halved weight gain in obese Zucker rats without impairing insulin sensitivity (Ng et al., 2000)","Six placebo-controlled human trials (about 900 adults; IV 25 to 400 mcg/kg, oral 0.25 to 54 mg daily up to 24 weeks): no change in IGF-1 or glucose tolerance, no antibodies, adverse events similar to placebo (Stier et al., 2013)","Weekly intra-articular 0.25 mg improved cartilage scores in a rabbit osteoarthritis model, more so with hyaluronic acid (Kwon et al., 2015)","Human-trial status: obesity programme ended without published efficacy results; no registered trial is active. A 2013 GRAS determination was by an industry-commissioned panel, not FDA"],"evidence_level":"preclinical","references":[{"title":"Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone","authors":"Ng FM, Sun J, Sharma L, et al.","journal":"Hormone Research","year":2000,"doi":"10.1159/000053183","pmid":"11146367"},{"title":"The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism following chronic treatment in obese mice and beta(3)-AR knock-out mice","authors":"Heffernan M, Summers RJ, Thorburn A, et al.","journal":"Endocrinology","year":2001,"doi":"10.1210/endo.142.12.8522","pmid":"11713213"},{"title":"Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone or a modified C-terminal fragment","authors":"Heffernan MA, Thorburn AW, Fam B, et al.","journal":"International Journal of Obesity and Related Metabolic Disorders","year":2001,"doi":"10.1038/sj.ijo.0801740","pmid":"11673763"},{"title":"Safety and Tolerability of the Hexadecapeptide AOD9604 in Humans","authors":"Stier H, Vos E, Kenley D","journal":"Journal of Endocrinology and Metabolism","year":2013,"doi":"10.4021/jem157w"},{"title":"Effect of Intra-articular Injection of AOD9604 with or without Hyaluronic Acid in Rabbit Osteoarthritis Model","authors":"Kwon DR, Park GY","journal":"Annals of Clinical and Laboratory Science","year":2015,"pmid":"26275694"},{"title":"Detection and in vitro metabolism of AOD9604","authors":"Cox HD, Smeal SJ, Hughes CM, et al.","journal":"Drug Testing and Analysis","year":2015,"doi":"10.1002/dta.1715","pmid":"25208511"},{"title":"Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries and Athletic Performance","authors":"Mendias CL, Awan TM","journal":"Sports Medicine","year":2026,"doi":"10.1007/s40279-026-02437-0","pmid":"41966639"}],"molecular_weight":1815.1,"amino_acid_sequence":"YLRIVQCRSVEGSCGF [disulfide Cys7-Cys14]","alternative_names":["AOD-9604","AOD 9604","Tyr-hGH(177-191)","Anti-Obesity Drug 9604","sh-Oligopeptide-74"],"half_life":"No human PK published; the parent peptide degraded in serum and urine in vitro, leaving a stable CRSVEGSCG metabolite (Cox 2015)","bioavailability":"Not reported. Oral dosing was active in obese rodents (Ng 2000) and used in all long human trials (Stier 2013); no subcutaneous PK data","side_effects":"In six placebo-controlled trials (Stier 2013), headache was the most common event, followed by diarrhoea, flatulence and nausea, at rates similar to placebo; 54 mg oral doses produced more headache and GI upset. Mild euphoria was reported by 5 of 23 subjects after IV dosing and not with placebo. IGF-1, glucose tolerance, ECG and safety labs did not change and no anti-AOD9604 antibodies were found. Five cancers (skin, breast, melanoma) arose in the 12-week trial and were judged unrelated by investigators. Injection-site irritation is commonly reported with subcutaneous use (anecdotal); no subcutaneous human data exist. Regulatory: AOD-9604 is in the 503A withdrawn-nomination table of FDA's compounding safety-risk page, page content as of 2026-04-22: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","last_reviewed_at":"2026-10-06T08:18:03.656Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. All published human dosing was oral or IV; the subcutaneous range is community only. Efficacy data from the human trials are unpublished. | description: The old text called it residues 176-191; AOD9604 is tyrosine plus residues 177-191 (Cox 2015; Stier 2013). Human efficacy has never been published in peer-reviewed form. | benefits: The old claim that 'human obesity trials did not show significant weight loss' has no peer-reviewed source; the trial efficacy data were never published. | detailed_description: Old text described a 'Phase 2b obesity trial found no significant weight loss' and 'a 12-week Phase 2 study suggested modest weight reduction'; neither result is in any peer-reviewed source. Old value omitted for length. | mechanism_of_action: Old text said 'beta-3 adrenergic receptor-independent' without nuance and claimed adipocyte beta-oxidation activation and proteoglycan synthesis without sources. Old value omitted for length. | clinical_studies: Old bullets claimed 'significant weight loss vs placebo (Stier et al., 2013)' (Stier reports safety only), 'TGA approved as food additive (2020)', 'Phase III obesity trials' (none occurred) and 'FDA GRAS status' (self-affirmed panel, per Stier 2013). | evidence_level: Decision 4: the human RCTs published safety endpoints only. No human RCT result supports a use in `benefits`. Needs Josh: the trials existed, their efficacy data were never published. | side_effects: Adds the specific trial findings; removes 'those same trials failed to show significant weight loss', which has no published source. | recommended_dose: Decision 1 and 10: community numbers kept and labelled; published human doses stated. | dosing_notes: Old note was timing advice with no source; replaced with the published regimens. | half_life: The 30 to 60 minute figure has no source. | bioavailability: 'Subcutaneous: High' was unsourced; oral development is historical, not ongoing. | molecular_weight: PubChem CID 71300630 (sy","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/71300630","note":"amino_acid_sequence"},{"url":"https://www.jofem.org/index.php/jofem/article/view/157/194","note":"Stier 2013 full text: six trials METAOD001-006, doses, AE tables, GRAS panel, INCI name, sequence"},{"url":"https://trialsearch.who.int/Trial2.aspx?TrialID=ACTRN12608000047392","note":"the old ref[1] id: goat-milk infant formula trial, unrelated to AOD9604"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11146367/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11673763/","note":"evidence_level"},{"url":"https://doi.org/10.4021/jem157w","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/26275694/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11713213/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/25208511/","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/41966639/","note":"alternative_names"},{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"}],"data_version":3,"slug":"aod9604","url":"https://peptidelabs.app/peptides/aod9604/"},{"id":35,"name":"ARA-290","description":"Synthetic 11-amino-acid peptide derived from the helix-B region of erythropoietin that activates the innate repair receptor without EPO's blood-cell effects.","benefits":"Improved neuropathy symptom scores and corneal small nerve fiber density in phase 2 trials (human RCT, n=22 to 64); improved HbA1c and lipids in type 2 diabetes (human RCT, n=24); tissue protection in stroke, renal ischemia and nerve injury models (animal)","categories":["healing & recovery","neuroprotection"],"recommended_dose":"1 to 8 mg daily subcutaneously in phase 2 trials, with 4 mg/day the dose that separated from placebo; one trial used 2 mg IV three times weekly","detailed_description":"ARA-290 (cibinetide, pyroglutamate helix B surface peptide) is an 11-residue peptide modelled on the aqueous face of helix B of erythropoietin. It activates the innate repair receptor, a heterocomplex of the EPO receptor and the beta common receptor induced on injured tissue, without binding the EPO receptor homodimer, so it is not erythropoietic (Brines 2008). Four phase 2 trials are published. In sarcoid small fiber neuropathy, 2 mg IV three times weekly for 4 weeks (n=22) improved the symptom score against placebo (Heij 2012), 4 mg/day subcutaneously for 28 days improved symptoms, corneal nerve fiber density and 6-minute walk distance (Dahan 2013), and a 64-subject dose-ranging trial found 4 mg/day raised corneal nerve fiber area while 1 and 8 mg/day did not (Culver 2017). In type 2 diabetes, 4 mg/day for 28 days improved HbA1c, lipids and PainDetect scores (n=24; Brines 2015).","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":[],"dose_min_mcg":1000,"dose_max_mcg":8000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Subcutaneous once daily in most trials, for 28 days; one trial used 2 mg IV three times weekly for 4 weeks. The dose response is not monotonic: in the 64-subject phase 2b, 4 mg/day raised corneal nerve fiber area while 1 and 8 mg/day did not. Plasma half-life is about 2 min, yet the biological effects persist for days (Collino 2015).","mechanism_of_action":"Erythropoietin has two separable jobs through two receptors: red cell production via the EPO receptor homodimer, and tissue protection via the innate repair receptor, a heterocomplex of the EPO receptor and CD131 (the beta common receptor) that is not normally expressed but is induced by injury or inflammation. ARA-290 is an 11-residue peptide reproducing the aqueous surface of helix B, which does not contact the homodimer; it activates the innate repair receptor selectively and was tissue-protective in stroke, renal ischemia-reperfusion, retinal edema and peripheral nerve trauma models while showing no erythropoietic activity in vitro or in vivo (Brines 2008). Despite a plasma half-life of about 2 min, the receptor activation triggers effects lasting days, which the developers describe as a molecular switch rather than sustained occupancy (Collino 2015).","clinical_studies":["An 11-residue peptide reproducing the aqueous face of EPO helix B was tissue-protective in stroke, renal ischemia-reperfusion, retinal edema and nerve trauma models and was not erythropoietic in vitro or in vivo (Brines et al., 2008)","In sarcoidosis with small fiber neuropathy symptoms, 2 mg IV three times weekly for 4 weeks improved the neuropathy screening score against placebo (n=22, randomized double-blind; Heij et al., 2012)","In documented small nerve fiber loss, 28 days of 4 mg/day subcutaneously improved symptoms, corneal small nerve fiber density and 6-minute walk distance against placebo (Dahan et al., 2013)","A 64-subject phase 2b dose-ranging trial found 4 mg/day significantly increased corneal nerve fiber area (placebo-corrected +697 micrometres squared, p=0.012) while 1 and 8 mg/day did not (Culver et al., 2017)","In type 2 diabetes with painful neuropathy, 4 mg/day for 28 days improved HbA1c, lipid profile and PainDetect scores over 56 days of observation (n=24; Brines et al., 2015)","Human-trial status: several completed phase 2 trials, all small (n=22 to 64) and mostly in sarcoid or diabetic small fiber neuropathy. No phase 3 trial and no regulatory approval in any country"],"evidence_level":"clinical","references":[{"title":"Nonerythropoietic, tissue-protective peptides derived from the tertiary structure of erythropoietin","authors":"Brines M, Patel NS, Villa P, et al.","journal":"PNAS","year":2008,"doi":"10.1073/pnas.0805594105","pmid":"18676614"},{"title":"Safety and efficacy of ARA 290 in sarcoidosis patients with symptoms of small fiber neuropathy: a randomized, double-blind pilot study","authors":"Heij L, Niesters M, Swartjes M, et al.","journal":"Molecular Medicine","year":2012,"doi":"10.2119/molmed.2012.00332","pmid":"23168581"},{"title":"ARA 290 improves symptoms in patients with sarcoidosis-associated small nerve fiber loss and increases corneal nerve fiber density","authors":"Dahan A, Dunne A, Swartjes M, et al.","journal":"Molecular Medicine","year":2013,"doi":"10.2119/molmed.2013.00122","pmid":"24136731"},{"title":"Cibinetide Improves Corneal Nerve Fiber Abundance in Patients With Sarcoidosis-Associated Small Nerve Fiber Loss and Neuropathic Pain","authors":"Culver DA, Dahan A, Bajorunas D, et al.","journal":"Investigative Ophthalmology and Visual Science","year":2017,"doi":"10.1167/iovs.16-21291","pmid":"28475703"},{"title":"ARA 290, a nonerythropoietic peptide engineered from erythropoietin, improves metabolic control and neuropathic symptoms in patients with type 2 diabetes","authors":"Brines M, Dunne AN, van Velzen M, et al.","journal":"Molecular Medicine","year":2015,"doi":"10.2119/molmed.2014.00215","pmid":"25387363"},{"title":"Flipping the molecular switch for innate protection and repair of tissues: Long-lasting effects of a non-erythropoietic small peptide engineered from erythropoietin","authors":"Collino M, Thiemermann C, Cerami A, Brines M","journal":"Pharmacology and Therapeutics","year":2015,"doi":"10.1016/j.pharmthera.2015.02.005","pmid":"25728128"}],"molecular_weight":1257.3,"amino_acid_sequence":"[Pyr]-Glu-Gln-Leu-Glu-Arg-Ala-Leu-Asn-Ser-Ser ([Pyr] = pyroglutamate; 11 aa)","alternative_names":["Cibinetide","ARA290","pHBSP","pyroglutamate helix B surface peptide","1208243-50-8"],"half_life":"About 2 min (human, plasma), with biological effects lasting days (Collino 2015)","bioavailability":null,"side_effects":"Well tolerated in small trials for neuropathic pain, where injection-site reactions were the main finding. Unlike erythropoietin it did not raise hematocrit or blood pressure in the studies conducted. Long-term safety data is limited.","last_reviewed_at":"2026-10-06T08:17:32.824Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Dose fields now span the published phase 2 range (1 to 8 mg/day); 4 mg/day is the dose that separated from placebo. Injectable with null recon fields, not checked this pass. | detailed_description: Old text was vendor copy with no trial, dose or n. Old value omitted for length. | mechanism_of_action: Field was null. | clinical_studies: Field was null. | recommended_dose: The published range runs to 8 mg/day, and the response is not monotonic: 4 mg beat placebo where 8 mg did not. | dose_max_mcg: Highest published human dose is 8 mg/day (Culver 2017 phase 2b). | dosing_notes: Adds route, duration, the non-monotonic dose response and the pharmacokinetic oddity. | molecular_weight: PubChem CID 91810664 (cibinetide, CAS 1208243-50-8): C51H84N16O21, 1257.3 Da. | amino_acid_sequence: PubChem synonyms for CID 91810664 give Pglu-glu-gln-leu-glu-arg-ala-leu-asn-ser-ser; Brines 2008 describes the 11-residue helix B surface peptide. | alternative_names: PubChem synonyms, CID 91810664. | half_life: Field was null; value from the developers' pharmacokinetic review. | stacks_with: Decision 14: no published combination and no shared community protocol for an investigational neuropathy peptide. | benefits: Adds the evidence tier and n to each item per the style guide.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/91810664/property/MolecularFormula,MolecularWeight/JSON","note":"alternative_names"},{"url":"https://clinicaltrials.gov/api/v2/studies/NCT02039687","note":"phase 2 corneal nerve fiber density trial, completed, n=64, has results"},{"url":"https://clinicaltrials.gov/api/v2/studies/NCT01933529","note":"phase 2 in prediabetes and type 2 diabetes, n=24, status unknown"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18676614/","note":"benefits"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23168581/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/24136731/","note":"benefits"},{"url":"https://pubmed.ncbi.nlm.nih.gov/28475703/","note":"benefits"},{"url":"https://pubmed.ncbi.nlm.nih.gov/25387363/","note":"benefits"},{"url":"https://pubmed.ncbi.nlm.nih.gov/25728128/","note":"half_life"}],"data_version":2,"slug":"ara-290","url":"https://peptidelabs.app/peptides/ara-290/"},{"id":36,"name":"B7-33","description":"Single-chain 27-residue mimetic of the human relaxin-2 B chain that biases RXFP1 signaling toward pERK; reduced cardiac and lung fibrosis in rodent models.","benefits":"Reduced cardiac and lung fibrosis in rodent models at relaxin-equivalent potency; smaller infarct and preserved cardiac function in mouse ischemia-reperfusion (rodent); endothelium-dependent vasodilation matching serelaxin (rat). No human data","categories":["healing & recovery"],"recommended_dose":"1 to 10 mg: vendor and community range, no published human dose. Animal studies used 0.25 to 0.5 mg/kg/day subcutaneously in mice and a 13.3 mcg/kg IV bolus in rats","detailed_description":"B7-33 is a single-chain 27-residue peptide from the B chain of human relaxin-2 (serelaxin): six residues were cut from the N-terminus of B1-33 and both cysteines replaced with serines to stop dimerization, giving a soluble linear peptide instead of the two-chain, three-disulfide hormone (Hossain 2016). It binds RXFP1 and preferentially activates pERK1/2 over cAMP, the first functionally selective agonist of that receptor. In rodents it prevented or reversed heart and lung fibrosis at relaxin-like potency (0.25 mg/kg/day), cut infarct size in mouse ischemia-reperfusion (22% versus 45%) and matched relaxin for left ventricular fibrosis in isoprenaline cardiomyopathy (Devarakonda 2020; Alam 2023). Unlike relaxin it did not promote prostate tumor growth in mice. No human study is published or registered.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":[],"dose_min_mcg":1000,"dose_max_mcg":10000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Subcutaneous in research use. Animal dosing was continuous: 0.25 to 0.5 mg/kg/day by implanted osmotic minipump in mice, or a single 13.3 mcg/kg IV bolus in rats. In vitro serum half-life is about 6 min, so a once-daily injection has no published basis. No human pharmacokinetic or safety data exist.","mechanism_of_action":"Relaxin-2 acts through RXFP1, a GPCR that couples to both cAMP and ERK1/2. The cAMP arm is linked to the tumor-promoting effects reported for relaxin, so B7-33 was designed to bias signaling: it binds RXFP1 and preferentially phosphorylates ERK1/2 with little cAMP response in cells that express RXFP1 endogenously (Hossain 2016). The antifibrotic effect runs through RXFP1-angiotensin II type 2 receptor heterodimers, driving pERK1/2 and the collagen-degrading enzyme MMP-2. In rat mesenteric artery it enhanced bradykinin-mediated endothelium-dependent relaxation through endothelium-derived hyperpolarization, matching serelaxin at equimolar dose (Marshall 2017). Serum stability is the practical limit: half-life in serum in vitro is about 6 min, which lipidated analogs extend to about 60 min (Praveen 2023).","clinical_studies":["B7-33 bound RXFP1 and preferentially activated pERK over cAMP, and at 0.25 mg/kg/day subcutaneously prevented or reversed fibrosis and dysfunction in three rodent models of heart and lung disease with potency similar to relaxin, without promoting prostate tumor growth in mice (Hossain et al., 2016)","In mouse myocardial ischemia-reperfusion, B7-33 reduced infarct size (22.0% versus 45.3%, p=0.02) and preserved fractional shortening at 24 h and 7 days (Devarakonda et al., 2020)","In isoprenaline-induced cardiomyopathy in mice, B7-33 at 0.25 mg/kg/day matched relaxin for reducing left ventricular fibrosis, inflammation and hypertrophy, and reduced fibrosis faster than perindopril (Alam et al., 2023)","A single IV bolus of 13.3 mcg/kg in rats reproduced the acute vascular effects of serelaxin in mesenteric artery, and 15 to 30 nM prevented trophoblast-induced endothelial dysfunction in mouse arteries ex vivo (Marshall et al., 2017)","In vitro serum half-life is about 6 min; fatty-acid conjugation extended it to about 60 min in analogs that have not been tested in animals (Praveen et al., 2023)","Human-trial status: none. No trial of B7-33 is published or registered on ClinicalTrials.gov; all data are rodent and in vitro"],"evidence_level":"preclinical","references":[{"title":"A single-chain derivative of the relaxin hormone is a functionally selective agonist of the G protein-coupled receptor, RXFP1","authors":"Hossain MA, Kocan M, Yao ST, et al.","journal":"Chemical Science","year":2016,"doi":"10.1039/c5sc04754d","pmid":"30155023"},{"title":"B7-33, a Functionally Selective Relaxin Receptor 1 Agonist, Attenuates Myocardial Infarction-Related Adverse Cardiac Remodeling in Mice","authors":"Devarakonda T, Mauro AG, Guzman G, et al.","journal":"Journal of the American Heart Association","year":2020,"doi":"10.1161/JAHA.119.015748","pmid":"32295457"},{"title":"The single-chain relaxin mimetic, B7-33, maintains the cardioprotective effects of relaxin and more rapidly reduces left ventricular fibrosis compared to perindopril in an experimental model of cardiomyopathy","authors":"Alam F, Gaspari TA, Kemp-Harper BK, et al.","journal":"Biomedicine and Pharmacotherapy","year":2023,"doi":"10.1016/j.biopha.2023.114370","pmid":"36753958"},{"title":"B7-33 replicates the vasoprotective functions of human relaxin-2 (serelaxin)","authors":"Marshall SA, O'Sullivan K, Ng HH, et al.","journal":"European Journal of Pharmacology","year":2017,"doi":"10.1016/j.ejphar.2017.05.005","pmid":"28478069"},{"title":"A Lipidated Single-B-Chain Derivative of Relaxin Exhibits Improved In Vitro Serum Stability without Altering Activity","authors":"Praveen P, Wang C, Handley TNG, et al.","journal":"International Journal of Molecular Sciences","year":2023,"doi":"10.3390/ijms24076616","pmid":"37047588"},{"title":"Single chain peptide agonists of relaxin receptors","authors":"Praveen P, Kocan M, Valkovic A, Bathgate R, Hossain MA","journal":"Molecular and Cellular Endocrinology","year":2019,"doi":"10.1016/j.mce.2019.01.008","pmid":"30641102"}],"molecular_weight":2986.6,"amino_acid_sequence":"VIKLSGRELVRAQIAISGMSTWSKRSL-NH2 (27 aa; relaxin-2 B chain 7-33 with Cys11Ser and Cys23Ser, C-terminal amide)","alternative_names":["B7-33","Relaxin B7-33","single-chain relaxin-2 B-chain analog"],"half_life":"About 6 min in serum in vitro; no in vivo pharmacokinetic study in any species (Praveen 2023)","bioavailability":null,"side_effects":"No human safety data; effects unknown beyond animal studies. As a relaxin-family agonist, vasodilation with lowered blood pressure and reflex tachycardia are plausible class effects. Purity and identity of research-grade material is an added practical risk.","last_reviewed_at":"2026-10-06T08:17:32.824Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Dose range is vendor convention, no published human dose; animal dosing was weight-based and continuous. Molecular weight is calculated and cross-checked against published ESI-MS. | detailed_description: Old text was three sentences of vendor copy with no model, dose or trial status. Old value omitted for length. | mechanism_of_action: Field was null. | clinical_studies: Field was null. | recommended_dose: Decision 11: the numeric range is vendor convention. Every published dose is weight-based animal dosing and stays in text. | dosing_notes: Replaces three label fragments with the actual dosing and the stability problem. | molecular_weight: Hossain 2016 reports ESI-MS for B7-33 as m/z 2986.4 with calculated 2986.59. Residue arithmetic on VIKLSGRELVRAQIAISGMSTWSKRSL as a C-terminal amide gives 2986.57. No PubChem record exists. | amino_acid_sequence: Built from UniProt P04090 prorelaxin H2 B chain plus the modifications Hossain 2016 describes: truncate 6 residues from B1-33, replace both cysteines with serine, synthesize as a C-terminal amide. The name B7-33 counts B-chain positions 7 to 33, which is 27 residues. | description: B7-33 is 27 residues (B-chain positions 7 to 33), not 24. | benefits: Adds the tier to each item and drops kidney fibrosis, which the cited primaries do not show for B7-33. | alternative_names: No INN, CAS or PubChem record; names as used in the primary literature. | half_life: Field was null. | stacks_with: Decision 14: no published combination and no established community protocol.","sources":[{"url":"https://rest.uniprot.org/uniprotkb/P04090.fasta","note":"amino_acid_sequence"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/name/B7-33/property/MolecularWeight/JSON","note":"no PubChem record for B7-33 (PUGREST.NotFound)"},{"url":"https://clinicaltrials.gov/api/v2/studies?query.term=B7-33","note":"no registered human trial of B7-33"},{"url":"https://pubmed.ncbi.nlm.nih.gov/30155023/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/32295457/","note":"benefits"},{"url":"https://pubmed.ncbi.nlm.nih.gov/36753958/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/28478069/","note":"benefits"},{"url":"https://pubmed.ncbi.nlm.nih.gov/37047588/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/30641102/","note":"alternative_names"}],"data_version":2,"slug":"b7-33","url":"https://peptidelabs.app/peptides/b7-33/"},{"id":9,"name":"BPC-157","description":"Synthetic pentadecapeptide derived from a protective protein found in human gastric juice; accelerates tendon, muscle and gut healing in rodent models.","benefits":"Tendon, ligament and muscle healing in animal models, gastrointestinal mucosal protection, reduced inflammation, neuroprotective and dopamine-system effects in rodents","categories":["healing & recovery"],"recommended_dose":"250 to 500 mcg daily: research-community range, no published human dose-finding study. Rodent studies used 10 mcg/kg and 10 ng/kg intraperitoneally","detailed_description":"BPC-157 (PL 14736, bepecin) is a synthetic 15-residue peptide whose sequence comes from a fragment of a protein in human gastric juice. The evidence base is almost entirely rodent: transected rat Achilles tendon and medial collateral ligament healed faster by biomechanical, functional and histological measures at 10 mcg/kg or 10 ng/kg intraperitoneally (Staresinic 2003; Cerovecki 2010), and it raises VEGFR2 expression and blood flow recovery in rat hindlimb ischemia (Hsieh 2017). No completed randomized human trial has been published; human data are three uncontrolled pilot reports totalling under 30 subjects (McGuire 2025). FDA placed BPC-157 in category 2 of its 503A compounding interim policy, the significant-safety-risk list; the nomination was later withdrawn by the nominator and the entry now sits in the withdrawn table on the same page.","storage_temp":"Refrigerated (2-8°C)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"24+ months at room temperature","stacks_with":["TB-500","GHK-Cu"],"dose_min_mcg":250,"dose_max_mcg":500,"dose_unit":"mcg","dose_frequency":"1-2x daily","recon_volume_ml":2,"common_vial_sizes":[5,10],"dosing_notes":"Subcutaneous or intramuscular in research use; also active per-orally in rats (0.16 mcg/mL in drinking water healed transected ligament; Cerovecki 2010). Injection near the injury is community practice, not a published comparison. Plasma half-life is under 30 min in rat and dog with linear kinetics, and intramuscular bioavailability is 14 to 19% in rats and 45 to 51% in beagles (He 2022), so the long-lasting effects seen in animals are not explained by exposure.","mechanism_of_action":"Proposed mechanisms, all from animal and cell work. BPC-157 increases VEGFR2 expression and promotes its internalization, activating the VEGFR2-Akt-eNOS pathway; blocking endocytosis with dynasore abolished the effect in human endothelial cells, and treated rats recovered hindlimb blood flow faster (Hsieh 2017). In rat Achilles tendon fibroblasts it raised growth hormone receptor mRNA and protein dose-dependently, and added growth hormone then increased proliferation through JAK2 (Chang 2014). It also increased tendon fibroblast outgrowth, survival under oxidative stress and migration, with dose-dependent phosphorylation of FAK and paxillin (Chang 2011). Effects on dopaminergic, serotonergic and GABAergic signaling are reported in rodent behavioral models and are not established in humans.","clinical_studies":["Transected rat Achilles tendon recovered fully at 10 mcg, 10 ng or 10 pg/kg intraperitoneally daily, with higher load to failure and reestablished tendon integrity by day 14 (Staresinic et al., 2003)","Rat medial collateral ligament healing improved over 90 days whether given intraperitoneally (10 mcg or 10 ng/kg), topically in cream, or per-orally in drinking water at 0.16 mcg/mL (Cerovecki et al., 2010)","Raised growth hormone receptor expression in rat tendon fibroblasts, with growth hormone then increasing proliferation via JAK2 (Chang et al., 2014)","Increased VEGFR2 expression and internalization, activated VEGFR2-Akt-eNOS signaling and accelerated blood flow recovery in rat hindlimb ischemia (Hsieh et al., 2017)","In rats and beagle dogs, plasma half-life was under 30 min with linear kinetics and intramuscular bioavailability of 14 to 19% and 45 to 51% respectively (He et al., 2022)","Human-trial status: no completed randomized trial has been published. Published human exposure is three uncontrolled pilot reports totalling under 30 subjects (intra-articular knee pain, interstitial cystitis, a 2-subject IV safety study); a phase 2 hamstring-strain trial (NCT07437547) and a phase 1 rotator-cuff trial (NCT07803250) are registered and not yet reported"],"evidence_level":"preclinical","references":[{"title":"Pentadecapeptide BPC 157 enhances the growth hormone receptor expression in tendon fibroblasts","authors":"Chang CH, Tsai WC, Hsu YH, Pang JH","journal":"Molecules","year":2014,"doi":"10.3390/molecules191119066","pmid":"25415472"},{"title":"The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration","authors":"Chang CH, Tsai WC, Lin MS, Hsu YH, Pang JH","journal":"Journal of Applied Physiology","year":2011,"doi":"10.1152/japplphysiol.00945.2010","pmid":"21030672"},{"title":"Gastric pentadecapeptide BPC 157 accelerates healing of transected rat Achilles tendon and in vitro stimulates tendocytes growth","authors":"Staresinic M, Sebecic B, Patrlj L, et al.","journal":"Journal of Orthopaedic Research","year":2003,"doi":"10.1016/S0736-0266(03)00110-4","pmid":"14554208"},{"title":"Pentadecapeptide BPC 157 (PL 14736) improves ligament healing in the rat","authors":"Cerovecki T, Bojanic I, Brcic L, et al.","journal":"Journal of Orthopaedic Research","year":2010,"doi":"10.1002/jor.21107","pmid":"20225319"},{"title":"Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation","authors":"Hsieh MJ, Liu HT, Wang CN, et al.","journal":"Journal of Molecular Medicine","year":2017,"doi":"10.1007/s00109-016-1488-y","pmid":"27847966"},{"title":"Pharmacokinetics, distribution, metabolism, and excretion of body-protective compound 157, a potential drug for treating various wounds, in rats and dogs","authors":"He L, Feng D, Guo H, et al.","journal":"Frontiers in Pharmacology","year":2022,"doi":"10.3389/fphar.2022.1026182","pmid":"36588717"},{"title":"Regeneration or Risk? A Narrative Review of BPC-157 for Musculoskeletal Healing","authors":"McGuire FP, Martinez R, Lenz A, Skinner L, Cushman DM","journal":"Current Reviews in Musculoskeletal Medicine","year":2025,"doi":"10.1007/s12178-025-09990-7","pmid":"40789979"},{"title":"Safety of Intravenous Infusion of BPC157 in Humans: A Pilot Study","authors":"Lee E, Burgess K","journal":"Alternative Therapies in Health and Medicine","year":2025,"pmid":"40131143"}],"molecular_weight":1419.53,"amino_acid_sequence":"Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val","alternative_names":["Body Protection Compound 157","PL 14736","PL-10","Bepecin"],"half_life":"Under 30 min (rat and beagle dog, IV and IM; linear kinetics). No human pharmacokinetic study published","bioavailability":"Intramuscular: 14 to 19% (rat), 45 to 51% (beagle dog). Oral: active per-orally in rodents, absolute oral bioavailability not measured in any species","side_effects":"No controlled human safety trial exists, so long-term risk is unknown. Three uncontrolled human pilot reports (under 30 subjects in total) recorded no adverse effects, including an IV infusion of up to 20 mg in two adults with no change in cardiac, liver, kidney, thyroid or glucose markers (Lee 2025). Commonly reported by users: injection-site irritation, transient nausea, headache. FDA placed BPC-157 in category 2 of the 503A compounding interim policy, citing possible immunogenicity by some routes and difficulty characterizing peptide-related impurities; that nomination was withdrawn and the substance now appears in the withdrawn table of the same FDA page.","last_reviewed_at":"2026-10-06T08:17:32.824Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Regulatory status sourced from fda.gov category 2 page (withdrawn-nomination table). Dose range is community convention, no human dose-finding study. | detailed_description: Old text was vendor copy with no model system, no dose and no trial status. Regulatory status verified directly on fda.gov. Old value omitted for length. | recommended_dose: Decision 11: the numeric range is community convention, so the field now says so. The animal dose is weight-based and stays in text. | dosing_notes: Removes the unsourced site-injection preference and adds the only published pharmacokinetics. | mechanism_of_action: Old text asserted EGR-1 and gut-brain effects without a cited source. Rewritten from the three primary papers, labelled proposed. Old value omitted for length. | clinical_studies: Old bullets cited Sikiric 2016 and 2018 reviews whose PMIDs resolve to unrelated papers, and Pevec 2010, which does not exist under that description. | half_life: The 4 to 6 h figure has no source. The one published ADME study measured under 30 min in two species. | bioavailability: Replaces qualitative vendor language with the measured values; flags that oral bioavailability is still unmeasured. | side_effects: Old text said FDA placed it on the 503A category 2 list without noting the nomination was withdrawn, which overstates the current listing.","sources":[{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"},{"url":"https://www.fda.gov/drugs/human-drug-compounding/bulk-drug-substances-used-compounding-under-section-503a-fdc-act","note":"definition of the 503A interim-policy categories"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/9941957/property/MolecularFormula,MolecularWeight/JSON","note":"molecular weight 1419.5, CID 9941957"},{"url":"https://clinicaltrials.gov/api/v2/studies/NCT07437547","note":"clinical_studies"},{"url":"https://clinicaltrials.gov/api/v2/studies/NCT07803250","note":"phase 1 rotator cuff trial, not yet recruiting, n=20"},{"url":"https://clinicaltrials.gov/api/v2/studies/NCT02637284","note":"2015 oral phase 1 (PCO-02, 1 mg tablets), status UNKNOWN, no results posted"},{"url":"https://pubmed.ncbi.nlm.nih.gov/14554208/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/20225319/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/27847966/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42198317/","note":"recommended_dose"},{"url":"https://pubmed.ncbi.nlm.nih.gov/36588717/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/25415472/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/21030672/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40789979/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40131143/","note":"side_effects"}],"data_version":2,"slug":"bpc-157","url":"https://peptidelabs.app/peptides/bpc-157/"},{"id":93,"name":"BPC-157 + TB-500 + GHK-Cu (Glow Blend)","description":"Vial blend of BPC-157, TB-500 (Ac-LKKTETQ) and GHK-Cu, sold mostly as 70 mg (10/10/50 mg); each component has animal or cell data, and no study has tested the three together.","benefits":"Tendon and ligament repair (rodent, BPC-157); angiogenesis and wound repair (rodent and cell, TB-500 fragment); collagen synthesis (cell and rat, GHK-Cu); mixed topical wound results (human, GHK-Cu, not injected). No data for the blend","categories":["healing & recovery","skin health","blend"],"recommended_dose":"500 to 750 mcg of blend daily (about 70 to 110 mcg each of BPC-157 and TB-500 and 360 to 540 mcg GHK-Cu at the 10/10/50 mg ratio): vendor/community range, no published human dose of the blend","detailed_description":"Sold as a 70 mg vial holding 10 mg BPC-157, 10 mg TB-500 and 50 mg GHK-Cu, so GHK-Cu makes up about 70% of each dose. TB-500 is the acetylated fragment Ac-LKKTETQ, not full thymosin beta-4 (Esposito 2012). BPC-157 and TB-500 have rodent tissue-repair data; GHK-Cu raised collagen synthesis in fibroblast culture and rat wounds. GHK-Cu human data are topical only, with a positive diabetic ulcer trial and a negative venous ulcer trial, and no injected human study exists. The one study pairing BPC-157 and TB-500 found no added benefit in rat tendon repair (Biçer 2026). No study has tested the three-peptide blend. FDA lists BPC-157, TB-500 and injectable GHK-Cu on its compounding safety-risk page in the withdrawn-nomination table.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":null,"dose_min_mcg":500,"dose_max_mcg":750,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[70],"dosing_notes":"Subcutaneous in community use. The loading-then-maintenance schedule has no published basis. The numeric range dates from when the catalog listed a 15 mg vial with 5 mg of each peptide; vendors now sell a 70 mg vial at 10/10/50 mg, which changes the per-component amounts above. GHK-Cu human data are topical: a daily gel in diabetic foot ulcers and a 0.4% cream in venous ulcers.","mechanism_of_action":"Proposed, from separate component studies; no study has measured an interaction. BPC-157 activated VEGFR2-Akt-eNOS signalling in rat ischemic limbs. TB-500 carries the actin-binding motif of thymosin beta-4, which drove endothelial migration and sprouting (Philp 2003). GHK-Cu raised collagen synthesis in fibroblasts from 10^-12 M, peaking at 10^-9 M (Maquart 1988). The skin 'glow' attributed to the injected blend has not been tested; GHK-Cu skin data come from cell, rodent and topical human work.","clinical_studies":["Rat Achilles tendon repair (n=32): BPC-157 and TB-500 each improved histology, and the pair gave no added benefit over either alone; GHK-Cu was not tested (Biçer et al., 2026)","BPC-157 at 10 mcg or 10 ng/kg intraperitoneally restored transected rat Achilles tendon integrity and load to failure by day 14 (Staresinic et al., 2003)","GHK-Cu raised collagen synthesis in fibroblast culture from 10^-12 M, peaking at 10^-9 M (Maquart et al., 1988)","Topical GHK-Cu gel improved diabetic foot ulcer closure versus vehicle, median 98.5% vs 60.8% (Mulder et al., 1994), but a 0.4% cream was no better than placebo in venous ulcers, n=86 (Bishop et al., 1992)","Human-trial status: no study has tested the blend as sold. GHK-Cu human trials were topical; no injected human study of any of the three components has been published, and BPC-157 has only uncontrolled pilot reports"],"evidence_level":"preclinical","references":[{"title":"Effects of BPC-157 and TB-500 on Achilles tendon healing in rats: A histopathological and biomechanical study","authors":"Biçer O, Adanir O, Güleryüz Y, Balci EC, et al.","journal":"Joint Diseases and Related Surgery","year":2026,"doi":"10.52312/jdrs.2026.2951","pmid":"42542926"},{"title":"Gastric pentadecapeptide BPC 157 accelerates healing of transected rat Achilles tendon and in vitro stimulates tendocytes growth","authors":"Staresinic M, Sebecic B, Patrlj L, et al.","journal":"Journal of Orthopaedic Research","year":2003,"doi":"10.1016/S0736-0266(03)00110-4","pmid":"14554208"},{"title":"Pharmacokinetics, distribution, metabolism, and excretion of body-protective compound 157, a potential drug for treating various wounds, in rats and dogs","authors":"He L, Feng D, Guo H, et al.","journal":"Frontiers in Pharmacology","year":2022,"doi":"10.3389/fphar.2022.1026182","pmid":"36588717"},{"title":"Synthesis and characterization of the N-terminal acetylated 17-23 fragment of thymosin beta 4 identified in TB-500, a product suspected to possess doping potential","authors":"Esposito S, Deventer K, Goeman J, Van der Eycken J, Van Eenoo P","journal":"Drug Testing and Analysis","year":2012,"doi":"10.1002/dta.1402","pmid":"22962027"},{"title":"The actin binding site on thymosin beta4 promotes angiogenesis","authors":"Philp D, Huff T, Gho YS, Hannappel E, Kleinman HK","journal":"FASEB Journal","year":2003,"doi":"10.1096/fj.03-0121fje","pmid":"14500546"},{"title":"Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+","authors":"Maquart FX, Pickart L, Laurent M, et al.","journal":"FEBS Letters","year":1988,"doi":"10.1016/0014-5793(88)80509-x","pmid":"3169264"},{"title":"Enhanced healing of ulcers in patients with diabetes by topical treatment with glycyl-l-histidyl-l-lysine copper","authors":"Mulder GD, Patt LM, Sanders L, et al.","journal":"Wound Repair and Regeneration","year":1994,"doi":"10.1046/j.1524-475X.1994.20406.x","pmid":"17147644"},{"title":"A prospective randomized evaluator-blinded trial of two potential wound healing agents for the treatment of venous stasis ulcers","authors":"Bishop JB, Phillips LG, Mustoe TA, et al.","journal":"Journal of Vascular Surgery","year":1992,"doi":"10.1067/mva.1992.37086","pmid":"1495150"}],"molecular_weight":null,"amino_acid_sequence":null,"alternative_names":["Glow Stack","Skin Rejuvenation Blend","Triple Healing"],"half_life":"BPC-157 under 30 min (rat and dog). TB-500 and GHK-Cu: not measured in any species. No human PK for any component","bioavailability":"BPC-157 intramuscular 14 to 19% (rat), 45 to 51% (dog); TB-500 and injected GHK-Cu not measured. No data for the blend","side_effects":"No human safety study of the blend has been published, and none of the three components has controlled injected human safety data. Commonly reported by users (anecdotal): injection-site stinging, redness and lumps, attributed to GHK-Cu, plus transient fatigue. At 50 of 70 mg, GHK-Cu (about 16% copper by mass) dominates each dose; copper load is a theoretical concern in disorders of copper excretion such as Wilson's disease. Listed on FDA's 503A category 2 (safety concerns) page, withdrawn-nomination table, as of 2026-04-22, for BPC-157, TB-500 and injectable GHK-Cu: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks.","last_reviewed_at":"2026-10-06T08:17:46.265Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Blend: molecular_weight and amino_acid_sequence null by design. Dose numbers are vendor/community per decision 11; no human dose of the blend exists. recon_volume_ml is the vendor/community value, not checked. | description: Composition corrected from vendor pages; TB-500 identity per batch 05. | benefits: Tiers per component; hair follicle claim removed (mouse only, batch 13). | detailed_description: Old text claimed GHK-Cu reverses aging gene expression and a 'glow' from collagen turnover, with no source. | mechanism_of_action: Old text claimed comprehensive regeneration with no source. | recommended_dose: Decision 11. Old text assumed a 15 mg vial with 5 mg each; per-component amounts recalculated for the 70 mg vial. | dosing_notes: Vial composition corrected; schedule labelled as convention. | common_vial_sizes: Both catalog vendors sell 70 mg (10/10/50 mg); no 15 mg product found. | clinical_studies: Old bullets had no citations. PubMed searched for BPC-157 with GHK or copper peptide: reviews only. | amino_acid_sequence: Null for blends. | half_life: Old 'variable by component' gave no values. | bioavailability: Old 'high for all' unsupported. | side_effects: Withdrawn-nomination wording per decision 32; copper fraction from batch 13.","sources":[{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"},{"url":"https://api.fda.gov/drug/drugsfda.json","note":"openFDA Drugs@FDA sweep (decision 61): no application found for the blend name or its alternative names"},{"url":"https://www.corepeptides.com/peptides/bpc-157-tb-500-ghk-cu-blend/","note":"common_vial_sizes"},{"url":"https://ameanopeptides.com/product/glow-blend-10mg/","note":"common_vial_sizes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22962027/","note":"description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/14554208/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/14500546/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3169264/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17147644/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1495150/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42542926/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/27847966/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/36588717/","note":"bioavailability"}],"data_version":2,"slug":"bpc-157-tb-500-ghk-cu-glow-blend","url":"https://peptidelabs.app/peptides/bpc-157-tb-500-ghk-cu-glow-blend/"},{"id":160,"name":"BPC-157 + TB-500 + KPV + GHK-Cu (KLOW Blend)","description":"Vial blend of BPC-157, TB-500 (Ac-LKKTETQ), KPV and GHK-Cu, sold as 80 mg (10/10/10/50 mg); each component has animal or cell data, and no study has tested the four together.","benefits":"Tendon and ligament repair (rodent, BPC-157); angiogenesis and wound repair (rodent and cell, TB-500 fragment); reduced colitis (mouse, KPV); collagen synthesis (cell and rat, GHK-Cu). No data for the blend","categories":["healing & recovery","skin health","blend"],"recommended_dose":"500 to 1000 mcg of blend daily (about 60 to 125 mcg each of BPC-157, TB-500 and KPV and 310 to 625 mcg GHK-Cu at the 10/10/10/50 mg ratio): vendor/community range, no published human dose of the blend","detailed_description":"Sold as an 80 mg vial holding 10 mg each of BPC-157, TB-500 and KPV plus 50 mg GHK-Cu, so GHK-Cu is over 60% of each dose. TB-500 is the acetylated fragment Ac-LKKTETQ, not full thymosin beta-4 (Esposito 2012). KPV is the C-terminal tripeptide of alpha-MSH (Lys-Pro-Val); it reduced colitis in mice, mostly when given orally. BPC-157 and TB-500 have rodent tissue-repair data, and GHK-Cu raised collagen in cell and rat wound studies, with human data only for topical use. No human trial exists for KPV, TB-500 or the blend, and the one paired study of BPC-157 and TB-500 found no added benefit in rat tendon repair (Biçer 2026). FDA lists all four components (GHK-Cu for injection) on its compounding safety-risk page in the withdrawn-nomination table.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":null,"dose_min_mcg":500,"dose_max_mcg":1000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[80],"dosing_notes":"Subcutaneous in community use. The loading-then-maintenance schedule has no published basis. The earlier text gave the dose as 0.5 to 1 mL, which at 80 mg in 2 mL would be 20 to 40 mg of blend, 20 to 80 times the numeric range; the numeric range is kept and the volume wording dropped. KPV animal work used oral drinking water, intraperitoneal 1 mg/kg in mice and topical 1 to 10 mg/mL; GHK-Cu human data are topical.","mechanism_of_action":"Proposed, from separate component studies; no study has measured an interaction among the four. BPC-157 activated VEGFR2-Akt-eNOS signalling in rat ischemic limbs. TB-500 carries the actin-binding motif of thymosin beta-4 linked to endothelial migration (Philp 2003). KPV entered intestinal epithelial and T cells through the PepT1 transporter and inhibited NF-kB and MAP kinase signalling at nanomolar levels (Dalmasso 2008); it also worked in MC1 receptor-deficient mice, so the effect is partly independent of MC1R (Kannengiesser 2008). GHK-Cu raised collagen synthesis in fibroblasts (Maquart 1988). Most KPV data used oral or colonic delivery; whether subcutaneous KPV reaches the gut mucosa has not been studied.","clinical_studies":["Rat Achilles tendon repair (n=32): BPC-157 and TB-500 each improved histology, and the pair gave no added benefit over either alone; KPV and GHK-Cu were not tested (Biçer et al., 2026)","BPC-157 at 10 mcg or 10 ng/kg intraperitoneally restored transected rat Achilles tendon integrity and load to failure by day 14 (Staresinic et al., 2003)","Oral KPV in drinking water reduced DSS- and TNBS-induced colitis in mice, acting through PepT1 uptake and NF-kB inhibition (Dalmasso et al., 2008)","GHK-Cu raised collagen synthesis in fibroblast culture from 10^-12 M, peaking at 10^-9 M (Maquart et al., 1988)","Topical GHK-Cu gel improved diabetic foot ulcer closure versus vehicle in a multicenter evaluator-blinded RCT; this was topical, not injected (Mulder et al., 1994)","Human-trial status: no study has tested the blend as sold. No human trial of KPV or Ac-LKKTETQ has been published, BPC-157 has only uncontrolled pilot reports, and GHK-Cu human data are topical"],"evidence_level":"preclinical","references":[{"title":"Effects of BPC-157 and TB-500 on Achilles tendon healing in rats: A histopathological and biomechanical study","authors":"Biçer O, Adanir O, Güleryüz Y, Balci EC, et al.","journal":"Joint Diseases and Related Surgery","year":2026,"doi":"10.52312/jdrs.2026.2951","pmid":"42542926"},{"title":"Gastric pentadecapeptide BPC 157 accelerates healing of transected rat Achilles tendon and in vitro stimulates tendocytes growth","authors":"Staresinic M, Sebecic B, Patrlj L, et al.","journal":"Journal of Orthopaedic Research","year":2003,"doi":"10.1016/S0736-0266(03)00110-4","pmid":"14554208"},{"title":"Synthesis and characterization of the N-terminal acetylated 17-23 fragment of thymosin beta 4 identified in TB-500, a product suspected to possess doping potential","authors":"Esposito S, Deventer K, Goeman J, Van der Eycken J, Van Eenoo P","journal":"Drug Testing and Analysis","year":2012,"doi":"10.1002/dta.1402","pmid":"22962027"},{"title":"The actin binding site on thymosin beta4 promotes angiogenesis","authors":"Philp D, Huff T, Gho YS, Hannappel E, Kleinman HK","journal":"FASEB Journal","year":2003,"doi":"10.1096/fj.03-0121fje","pmid":"14500546"},{"title":"PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation","authors":"Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, et al.","journal":"Gastroenterology","year":2008,"doi":"10.1053/j.gastro.2007.10.026","pmid":"18061177"},{"title":"Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease","authors":"Kannengiesser K, Maaser C, Heidemann J, et al.","journal":"Inflammatory Bowel Diseases","year":2008,"doi":"10.1002/ibd.20334","pmid":"18092346"},{"title":"Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+","authors":"Maquart FX, Pickart L, Laurent M, et al.","journal":"FEBS Letters","year":1988,"doi":"10.1016/0014-5793(88)80509-x","pmid":"3169264"},{"title":"Enhanced healing of ulcers in patients with diabetes by topical treatment with glycyl-l-histidyl-l-lysine copper","authors":"Mulder GD, Patt LM, Sanders L, et al.","journal":"Wound Repair and Regeneration","year":1994,"doi":"10.1046/j.1524-475X.1994.20406.x","pmid":"17147644"}],"molecular_weight":null,"amino_acid_sequence":null,"alternative_names":["KLOW Healing Blend","Quad Peptide Stack","KLOW Blend"],"half_life":"BPC-157 under 30 min (rat and dog). TB-500, KPV and GHK-Cu: not measured in any species. No human PK for any component","bioavailability":"BPC-157 intramuscular 14 to 19% (rat), 45 to 51% (dog). KPV active orally in mice via PepT1. TB-500, KPV and GHK-Cu by injection not measured","side_effects":"No human safety study of the blend has been published, and FDA states it has identified no human exposure data for KPV or the LKKTETQ fragment. Commonly reported by users (anecdotal): injection-site stinging, redness and lumps, attributed to GHK-Cu, plus transient fatigue. GHK-Cu is 50 of 80 mg and about 16% copper by mass; copper load is a theoretical concern in disorders of copper excretion such as Wilson's disease. Listed on FDA's 503A category 2 (safety concerns) page, withdrawn-nomination table, as of 2026-04-22, for BPC-157, TB-500, KPV and injectable GHK-Cu: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks.","last_reviewed_at":"2026-10-06T08:17:46.265Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Blend: molecular_weight and amino_acid_sequence null by design. Dose numbers are vendor/community per decision 11; no human dose of the blend exists. recon_volume_ml is the vendor/community value, not checked. | description: Composition from vendor pages. | benefits: Tiers per component; hair claims removed. | detailed_description: Old text called it ideal for recovery protocols and described TB-500 as full thymosin beta-4. | mechanism_of_action: Old text said TB-500 acts via NF-kB and listed KPV cytokine effects without sources. | recommended_dose: Decision 11. Old text gave a volume (0.5 to 1 mL) that conflicts with the numeric fields. | dosing_notes: Internal inconsistency between volume and mcg fields resolved toward the numeric fields. | clinical_studies: Old bullets uncited; 'TB-500 veterinary use' claim unsourced. PubMed searched for BPC-157 with KPV: one compounding review, no study. | amino_acid_sequence: Null for blends. | half_life: Old text said BPC-157 and TB-500 last hours; unsupported. | bioavailability: Old 'good for all components' unsupported. | side_effects: Decision 32 wording. | alternative_names: Added the vendor product name.","sources":[{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"},{"url":"https://api.fda.gov/drug/drugsfda.json","note":"openFDA Drugs@FDA sweep (decision 61): no application found for the blend name or its alternative names"},{"url":"https://www.corepeptides.com/peptides/klow-blend-80mg/","note":"alternative_names"},{"url":"https://ameanopeptides.com/product/klow-blend-80mg-research-peptide/","note":"description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/14554208/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/14500546/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18061177/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3169264/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22962027/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42542926/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18092346/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17147644/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/36588717/","note":"bioavailability"}],"data_version":2,"slug":"bpc-157-tb-500-kpv-ghk-cu-klow-blend","url":"https://peptidelabs.app/peptides/bpc-157-tb-500-kpv-ghk-cu-klow-blend/"},{"id":92,"name":"BPC-157 + TB-500 Blend","description":"Vial blend of BPC-157 and TB-500 (Ac-LKKTETQ), two peptides with rodent tissue-repair data; the one rat study of the pair found no added benefit over either alone.","benefits":"Tendon, ligament and gut repair (rodent, BPC-157); angiogenesis and wound repair (rodent and cell, TB-500 fragment); no additive tendon benefit from the pair (rat). No human data for the blend","categories":["healing & recovery","blend"],"recommended_dose":"500 to 750 mcg of blend daily (250 to 375 mcg of each peptide at the 1:1 ratio): vendor/community range, no published human dose of the blend or either component","detailed_description":"A lyophilized mix of BPC-157 and TB-500, sold as 10 mg (5 mg each) or 20 mg (10 mg each) vials. TB-500 is the acetylated fragment Ac-LKKTETQ, residues 17 to 23 of thymosin beta-4, not the full protein (Esposito 2012). Each component has rodent and cell data on its own: BPC-157 for tendon and ligament healing, TB-500 for angiogenesis and dermal repair. The only study of the pair, a 2026 rat Achilles tendon study (n=32), found both peptides improved tendon histology but the combination gave no benefit over either alone (Biçer 2026). No human trial has tested the blend, and neither component has a completed randomized human trial. FDA lists both on its compounding safety-risk page in the withdrawn-nomination table.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["GHK-Cu"],"dose_min_mcg":500,"dose_max_mcg":750,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[10,20],"dosing_notes":"Subcutaneous in community use; injecting near an injury is community practice, not a published comparison. The loading-then-maintenance schedule has no published basis. At the 1:1 ratio the daily blend dose carries far less TB-500 than the community TB-500 range of 2 to 7.5 mg twice weekly. The rat combination study dosed by weight, intraperitoneally: BPC-157 10 mcg/kg/day and TB-500 60 mcg/kg/day for 4 weeks (Biçer 2026).","mechanism_of_action":"Proposed, from component studies only; no study has measured how the two interact. BPC-157 raised VEGFR2 expression and activated VEGFR2-Akt-eNOS signalling in rat ischemic limbs (Hsieh 2017). TB-500 carries the actin-binding motif of thymosin beta-4, which was necessary and sufficient for its angiogenic activity in endothelial cells (Philp 2003). A 2024 study found Ac-LKKTETQ broken down quickly in serum and suggested its metabolite Ac-LKKTE carries the wound-healing activity (Rahaman 2024). In the rat tendon study the authors suggested the lack of an additive effect may reflect shared downstream pathways, which they did not test.","clinical_studies":["Rat Achilles tendon repair (n=32): BPC-157 10 mcg/kg/day and TB-500 60 mcg/kg/day intraperitoneally each improved histology scores, TB-500 also load to failure, and the combination gave no added benefit over either alone (Biçer et al., 2026)","BPC-157 at 10 mcg or 10 ng/kg intraperitoneally restored transected rat Achilles tendon integrity and load to failure by day 14 (Staresinic et al., 2003)","The seven-residue actin-binding motif in TB-500 matched full thymosin beta-4 for endothelial migration and aortic sprouting at about 50 nM (Philp et al., 2003)","BPC-157 had a plasma half-life under 30 min in rats and dogs, with intramuscular bioavailability of 14 to 19% in rats and 45 to 51% in dogs (He et al., 2022)","Human-trial status: no study has tested the blend as sold. BPC-157 has only uncontrolled human pilot reports; no trial of Ac-LKKTETQ has been published, and human data on thymosin beta-4 cover the full protein, a different molecule"],"evidence_level":"preclinical","references":[{"title":"Effects of BPC-157 and TB-500 on Achilles tendon healing in rats: A histopathological and biomechanical study","authors":"Biçer O, Adanir O, Güleryüz Y, Balci EC, et al.","journal":"Joint Diseases and Related Surgery","year":2026,"doi":"10.52312/jdrs.2026.2951","pmid":"42542926"},{"title":"Gastric pentadecapeptide BPC 157 accelerates healing of transected rat Achilles tendon and in vitro stimulates tendocytes growth","authors":"Staresinic M, Sebecic B, Patrlj L, et al.","journal":"Journal of Orthopaedic Research","year":2003,"doi":"10.1016/S0736-0266(03)00110-4","pmid":"14554208"},{"title":"Pentadecapeptide BPC 157 (PL 14736) improves ligament healing in the rat","authors":"Cerovecki T, Bojanic I, Brcic L, et al.","journal":"Journal of Orthopaedic Research","year":2010,"doi":"10.1002/jor.21107","pmid":"20225319"},{"title":"Pharmacokinetics, distribution, metabolism, and excretion of body-protective compound 157, a potential drug for treating various wounds, in rats and dogs","authors":"He L, Feng D, Guo H, et al.","journal":"Frontiers in Pharmacology","year":2022,"doi":"10.3389/fphar.2022.1026182","pmid":"36588717"},{"title":"Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation","authors":"Hsieh MJ, Liu HT, Wang CN, et al.","journal":"Journal of Molecular Medicine","year":2017,"doi":"10.1007/s00109-016-1488-y","pmid":"27847966"},{"title":"Synthesis and characterization of the N-terminal acetylated 17-23 fragment of thymosin beta 4 identified in TB-500, a product suspected to possess doping potential","authors":"Esposito S, Deventer K, Goeman J, Van der Eycken J, Van Eenoo P","journal":"Drug Testing and Analysis","year":2012,"doi":"10.1002/dta.1402","pmid":"22962027"},{"title":"The actin binding site on thymosin beta4 promotes angiogenesis","authors":"Philp D, Huff T, Gho YS, Hannappel E, Kleinman HK","journal":"FASEB Journal","year":2003,"doi":"10.1096/fj.03-0121fje","pmid":"14500546"},{"title":"Simultaneous quantification of TB-500 and its metabolites in in-vitro experiments and rats by UHPLC-Q-Exactive orbitrap MS/MS and their screening by wound healing activities in-vitro","authors":"Rahaman KA, Muresan AR, Min H, et al.","journal":"Journal of Chromatography B","year":2024,"doi":"10.1016/j.jchromb.2024.124033","pmid":"38382158"}],"molecular_weight":null,"amino_acid_sequence":null,"alternative_names":["Healing Blend","Recovery Stack","BPC/TB Combo"],"half_life":"BPC-157 under 30 min (rat and dog, IV and IM). TB-500 (Ac-LKKTETQ) not measured; rapidly metabolized in rat and human serum. No human PK for either","bioavailability":"BPC-157 intramuscular 14 to 19% (rat), 45 to 51% (dog). TB-500 not measured. No data for the blend","side_effects":"No human safety study of the blend or of TB-500 has been published, and BPC-157 has only uncontrolled pilot reports totalling under 30 people with no adverse effects recorded. FDA states it has identified no human exposure data for the LKKTETQ fragment. Listed on FDA's 503A category 2 (safety concerns) page, withdrawn-nomination table, as of 2026-04-22, for both BPC-157 and TB-500: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks. Commonly reported by users (anecdotal): injection-site irritation, transient fatigue, head rush. Both components promote angiogenesis in animal models, so use with active or suspected malignancy is a theoretical concern.","last_reviewed_at":"2026-10-06T08:17:46.265Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Blend: molecular_weight and amino_acid_sequence null by design. Dose numbers are vendor/community per decision 11; no human dose of the blend exists. recon_volume_ml is the vendor/community value, not checked. | description: Old text implied complementary pathways; the only combination study found no additive effect. | benefits: Tiers per component; combination result added. | detailed_description: Old text claimed synergy and enhanced wound healing with no source; rewritten from the batch 05 component audits and the combination study. | mechanism_of_action: Old text claimed synergy and gut-brain axis targeting without a source. | recommended_dose: Decision 11: no published human dose; numbers kept and labelled. Per-component amounts from the 1:1 vial. | dosing_notes: Removed advice phrasing; added the only combination dosing, quoted verbatim per decision 10. | common_vial_sizes: Vendors sell 10 mg (5/5 mg) and 20 mg (10/10 mg) vials. | clinical_studies: Old bullets had no citations. PubMed searched for BPC-157 with TB-500 or thymosin beta-4: one rat study tested the pair. | amino_acid_sequence: Null for blends (style guide). | half_life: Old values (4 h and 8 h) unsupported; corrected per batch 05. | bioavailability: Old 'high for both' unsupported. | side_effects: Old text said 'FDA Category 2 designation' without the withdrawn-nomination distinction (decision 32).","sources":[{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"},{"url":"https://api.fda.gov/drug/drugsfda.json","note":"openFDA Drugs@FDA sweep (decision 61): no application found for the blend name or its alternative names"},{"url":"https://www.corepeptides.com/peptides/bpc-157-tb-500-10mg-blend/","note":"common_vial_sizes"},{"url":"https://ameanopeptides.com/product/bpc-157-tb4-blend-10mg-10mg/","note":"common_vial_sizes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42542926/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22962027/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/14554208/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/14500546/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/27847966/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/38382158/","note":"half_life"},{"url":"https://ameanopeptides.com/product/bpc-157-tb4-blend-5mg-5mg/","note":"common_vial_sizes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/36588717/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40131143/","note":"side_effects"}],"data_version":2,"slug":"bpc-157-tb-500-blend","url":"https://peptidelabs.app/peptides/bpc-157-tb-500-blend/"},{"id":26,"name":"BPC-157 Capsule","description":"Oral capsule form of the gastric pentadecapeptide BPC-157, studied mainly in rodent models for gastrointestinal mucosal repair and systemic tissue healing.","benefits":"Gut health, tissue repair, anti-inflammatory","categories":["healing & recovery"],"recommended_dose":"250 to 500 mcg daily: research-community range, no published human oral dose-finding study. The one registered oral phase 1 used 1 to 6 mg tablets","detailed_description":"An oral capsule of the same 15-residue peptide as injectable BPC-157 (id 9). Oral activity is supported in rodents, not humans: rats with a transected medial collateral ligament healed as well on BPC-157 in drinking water (0.16 mcg/mL, about 2 mcg/day per rat) as on intraperitoneal injection (Cerovecki 2010). No study in any species has measured absolute oral bioavailability or plasma levels after oral dosing, and the only published pharmacokinetics are IV and IM (He 2022). A 2015 randomized oral phase 1 in healthy volunteers using 1 mg tablets (NCT02637284) has a status of unknown and no posted results. FDA placed BPC-157 in category 2 of its 503A compounding interim policy, the significant-safety-risk list, citing possible immunogenicity and impurity-characterization problems; the nomination was later withdrawn and the entry now sits in the withdrawn table on that page.","storage_temp":"Room temperature","shelf_life_reconstituted":null,"shelf_life_powder":"12+ months","stacks_with":["TB-500","GHK-Cu"],"dose_min_mcg":250,"dose_max_mcg":500,"dose_unit":"mcg","dose_frequency":"1-2x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Oral capsule. BPC-157 is unusually stable in gastric juice and was active per-orally in rats given 0.16 mcg/mL in drinking water (Cerovecki 2010), but absolute oral bioavailability has not been measured in any species and no human oral pharmacokinetic data are published (Mateescu 2026). Empty-stomach timing is community practice with no published comparison.","mechanism_of_action":"Same peptide as injectable BPC-157, so the same proposed mechanisms apply: increased VEGFR2 expression and internalization with VEGFR2-Akt-eNOS activation in endothelial cells and rat hindlimb ischemia (Hsieh 2017), raised growth hormone receptor expression in rat tendon fibroblasts (Chang 2014), and dose-dependent FAK and paxillin phosphorylation with increased fibroblast migration (Chang 2011). For the oral route specifically, the peptide resists gastric degradation and was effective in drinking water in rats, but whether intact peptide reaches the circulation in humans has not been shown; local action on gut epithelium and systemic action are not distinguished by any published study.","clinical_studies":["Rat medial collateral ligament healing improved over 90 days when BPC-157 was given per-orally in drinking water at 0.16 mcg/mL, matching intraperitoneal dosing (Cerovecki et al., 2010)","BPC-157 is unusually stable in gastric juice and shows activity by oral, parenteral and topical routes, but has no validated formulation and no measured oral bioavailability in any species (Mateescu et al., 2026)","Published pharmacokinetics cover IV and IM routes only: half-life under 30 min in rat and dog, IM bioavailability 14 to 19% and 45 to 51% (He et al., 2022)","Mechanistic work behind the oral and injectable forms is the same rodent and cell literature: VEGFR2-Akt-eNOS activation (Hsieh et al., 2017) and growth hormone receptor upregulation in tendon fibroblasts (Chang et al., 2014)","Human-trial status: none completed. A randomized oral phase 1 in healthy volunteers with 1 mg tablets was registered in 2015 (NCT02637284) and remains status unknown with no posted results; no oral human data have been published"],"evidence_level":"preclinical","references":[{"title":"Pentadecapeptide BPC 157 (PL 14736) improves ligament healing in the rat","authors":"Cerovecki T, Bojanic I, Brcic L, et al.","journal":"Journal of Orthopaedic Research","year":2010,"doi":"10.1002/jor.21107","pmid":"20225319"},{"title":"Pharmacokinetics, distribution, metabolism, and excretion of body-protective compound 157, a potential drug for treating various wounds, in rats and dogs","authors":"He L, Feng D, Guo H, et al.","journal":"Frontiers in Pharmacology","year":2022,"doi":"10.3389/fphar.2022.1026182","pmid":"36588717"},{"title":"BPC-157 as an Investigational Peptide Therapeutic: Biopharmaceutical Challenges, Formulation Strategies, and Translational Development Barriers","authors":"Mateescu DM, Gavrilescu DM, Constantinescu FE, et al.","journal":"Pharmaceutics","year":2026,"doi":"10.3390/pharmaceutics18050625","pmid":"42198317"},{"title":"Pentadecapeptide BPC 157 enhances the growth hormone receptor expression in tendon fibroblasts","authors":"Chang CH, Tsai WC, Hsu YH, Pang JH","journal":"Molecules","year":2014,"doi":"10.3390/molecules191119066","pmid":"25415472"},{"title":"The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration","authors":"Chang CH, Tsai WC, Lin MS, Hsu YH, Pang JH","journal":"Journal of Applied Physiology","year":2011,"doi":"10.1152/japplphysiol.00945.2010","pmid":"21030672"},{"title":"Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation","authors":"Hsieh MJ, Liu HT, Wang CN, et al.","journal":"Journal of Molecular Medicine","year":2017,"doi":"10.1007/s00109-016-1488-y","pmid":"27847966"}],"molecular_weight":1419.53,"amino_acid_sequence":"Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val","alternative_names":["BPC-157 Oral","PL 14736","Bepecin","137525-51-0"],"half_life":"Under 30 min after IV or IM dosing in rat and dog (He 2022). No oral pharmacokinetic data in any species","bioavailability":"Oral: not measured in any species, although per-oral dosing was effective in rats (Cerovecki 2010). IM: 14 to 19% (rat), 45 to 51% (dog)","side_effects":"No controlled human safety data exist for any route, and oral absorption in humans is unproven. Occasional nausea or GI upset is reported by users. FDA placed BPC-157 in category 2 of the 503A compounding interim policy, citing possible immunogenicity by some routes and peptide impurity and characterization problems; that nomination was later withdrawn and the substance now appears in the withdrawn table of the same FDA page.","last_reviewed_at":"2026-10-06T08:17:32.824Z","reviewed_by":"audit-2026-10","review_notes":"N/A-by-design: oral capsule, so recon_volume_ml and common_vial_sizes are null. storage: general guidance. Dose range is community convention. Oral bioavailability unmeasured in every species. | detailed_description: Decision 2: oral record now cites oral-route animal evidence instead of copying the injectable. Old text asserted systemic oral efficacy with no source. Old value omitted for length. | recommended_dose: Decision 11 labelling, plus the only registered oral human dosing. | dosing_notes: Removes advice phrasing and the unsupported absorption claim. | mechanism_of_action: Old text asserted partial oral absorption and an arginine-salt formulation as fact. Old value omitted for length. | clinical_studies: Old bullets were five unsourced assertions ending in 'see injectable BPC-157 references'. | half_life: Replaces a vendor assertion with the measured parenteral value and states the oral gap. | bioavailability: 'Excellent local activity' is unsourced. Separates demonstrated oral activity from unmeasured oral absorption. | side_effects: Same correction as id 9: the old text implied a current category 2 listing. | alternative_names: No published source describes an arginine salt of BPC-157; the other names come from PubChem CID 9941957.","sources":[{"url":"https://clinicaltrials.gov/api/v2/studies/NCT02637284","note":"clinical_studies"},{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/9941957/property/MolecularFormula,MolecularWeight/JSON","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/20225319/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/36588717/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42198317/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/27847966/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/25415472/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/21030672/","note":"mechanism_of_action"}],"data_version":2,"slug":"bpc-157-capsule","url":"https://peptidelabs.app/peptides/bpc-157-capsule/"},{"id":73,"name":"Bronchogen","description":"Khavinson-series synthetic tetrapeptide (AEDL) for bronchial tissue; reported to restore bronchial epithelium in a rat NO2 model of COPD and to drive bronchial cell differentiation in vitro.","benefits":"Bronchial epithelium restoration in a rat COPD model (rodent), bronchial epithelial differentiation and proliferation markers (in vitro)","categories":["bioregulator"],"recommended_dose":"200 to 1000 mcg daily: vendor/community range, no published human dose","detailed_description":"Bronchogen is a synthetic tetrapeptide (AEDL, Ala-Glu-Asp-Leu) from the St. Petersburg Institute of Bioregulation and Gerontology, listed by that group as a bronchoprotector (Khavinson 2022). In rats with COPD modelled by 60 days of intermittent NO2 exposure, a month of treatment reversed goblet cell hyperplasia and squamous metaplasia, restored ciliated cells and raised secretory IgA (Kuzubova 2015). In human embryonic bronchial cell cultures it raised Ki67, Mcl-1 and the differentiation genes NKX2-1, SCGB1A1 and FOXA1, most in late-passage cells (Khavinson 2014). Nearly all work comes from one group. No controlled human trial has been published; a 2020 review from the same group says oral use is effective in COPD but cites no clinical paper.","storage_temp":"Room temperature","shelf_life_reconstituted":null,"shelf_life_powder":"24+ months","stacks_with":[],"dose_min_mcg":200,"dose_max_mcg":1000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Sold as oral capsules and as lyophilized powder for injection. The rat COPD study gave a one-month course; its abstract does not state the dose (Kuzubova 2015). Community protocols run 10 to 20 day courses two or three times a year; no study compared schedules.","mechanism_of_action":"Proposed, from cell and biophysical work by the developing group. In bronchial epithelial cultures the peptide raised proliferation (Ki67, Mcl-1) and bronchial differentiation gene expression (NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4, MUC5AC, SFTPA1), and spectroscopy suggested binding in the DNA major groove (Khavinson 2014). Calorimetry showed it raises DNA melting temperature by 3.1 C, binding both strands without base specificity (Monaselidze 2011). Docking predicts uptake through PEPT1 and LAT transporters (Khavinson 2022). Gene regulation by direct DNA binding is the group's hypothesis and has not been tested independently.","clinical_studies":["In rats with NO2-induced COPD, one month of treatment removed goblet cell hyperplasia, squamous metaplasia and emphysema, restored ciliated cells and raised secretory IgA (Kuzubova et al., 2015)","Expression of the differentiation factors CXCL12 and Hoxa3 rose in aged human bronchial epithelial cultures (Khavinson et al., 2012)","In human embryonic bronchial cell cultures it raised Ki67, Mcl-1, NKX2-1, SCGB1A1 and FOXA1, strongest in late passages (Khavinson et al., 2014)","Raised DNA melting temperature by 3.1 C in calorimetry, binding both strands (Monaselidze et al., 2011)","Human-trial status: no controlled human trial published; reviews from the developing group describe oral use in COPD and chronic bronchitis without citing a clinical paper"],"evidence_level":"preclinical","references":[{"title":"Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers","authors":"Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, et al.","journal":"International Journal of Molecular Sciences","year":2022,"doi":"10.3390/ijms23147733","pmid":"35887081"},{"title":"Peptides tissue-specifically stimulate cell differentiation during their aging","authors":"Khavinson VKh, Linkova NS, Polyakova VO, Kheifets OV, et al.","journal":"Bulletin of Experimental Biology and Medicine","year":2012,"doi":"10.1007/s10517-012-1664-1","pmid":"22808515"},{"title":"Peptide regulation of gene expression and protein synthesis in bronchial epithelium","authors":"Khavinson VKh, Tendler SM, Vanyushin BF, Kasyanenko NA, et al.","journal":"Lung","year":2014,"doi":"10.1007/s00408-014-9620-7","pmid":"25015171"},{"title":"Modulating Effect of Peptide Therapy on the Morphofunctional State of Bronchial Epithelium in Rats with Obstructive Lung Pathology","authors":"Kuzubova NA, Lebedeva ES, Dvorakovskaya IV, Surkova EA, et al.","journal":"Bulletin of Experimental Biology and Medicine","year":2015,"doi":"10.1007/s10517-015-3047-x","pmid":"26468022"},{"title":"Effect of the peptide bronchogen (Ala-Asp-Glu-Leu) on DNA thermostability","authors":"Monaselidze JR, Khavinson VKh, Gorgoshidze MZ, Khachidze DG, et al.","journal":"Bulletin of Experimental Biology and Medicine","year":2011,"doi":"10.1007/s10517-011-1146-x","pmid":"21240358"}],"molecular_weight":446.45,"amino_acid_sequence":"AEDL (Ala-Glu-Asp-Leu)","alternative_names":["AEDL","Ala-Glu-Asp-Leu"],"half_life":"No published pharmacokinetic data in any species","bioavailability":"Not measured in any species. Docking predicts transport by PEPT1, LAT1 and LAT2 (Khavinson 2022)","side_effects":"No controlled safety study has been published in any species, and the animal and cell studies, almost all from the developing institute, were not designed to detect harm. Commonly reported (anecdotal): injection-site irritation with injectable forms; oral capsules draw few complaints.","last_reviewed_at":"2026-10-06T08:17:39.536Z","reviewed_by":"audit-2026-10","review_notes":"storage: not verified against a CoA. Dose range is vendor/community, no published human dose. Recon fields left null: sold both as capsules and vials. | description: Old text gave no model system. Sequence confirmed from Khavinson 2022 Table 2. | benefits: Each item now carries its tier. | detailed_description: Old text claimed clinical benefits with no source and no model system. Old value omitted for length. | mechanism_of_action: Old text gave the tripeptide Ala-Glu-Asp (Cartalax's sequence) and unsourced mucus and inflammation claims. | clinical_studies: Old bullets described human outcomes with no source. | amino_acid_sequence: Old value Ala-Glu-Asp is Cartalax. Khavinson 2012 and 2022 print AEDL; Khavinson 2014 (Lung) and Monaselidze 2011 print the middle pair reversed (ADEL), so medium. | molecular_weight: Old 333.29 is the mass of AED. PubChem CID 11690869 (name 'Bronchogen', A-E-D-L, C18H30N4O9) gives 446.5; residue arithmetic 446.45. | alternative_names: 'Broncho-3' and 'Respiratory bioregulator' appear in no paper found; replaced with the published sequence names. | recommended_dose: Decision 11: no published human dose exists, so the numeric range is labelled vendor/community and the change is low confidence. | dosing_notes: Separates sourced facts from community practice. | half_life: Old text implied a measured short half-life; none has been measured. | bioavailability: Old text claimed oral activity without a source. | side_effects: Removes the unsourced claim that adverse effects are minimal. | stacks_with: Decisions 14 and 30: no published combination and no established community protocol found for the old entries.","sources":[{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC9323678/","note":"identity: Khavinson 2022 Table 2 maps product names to sequences and lists the patents behind several tissue claims"},{"url":"https://pubmed.ncbi.nlm.nih.gov/30199201/","note":"benefits"},{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC7583759/","note":"Khavinson 2020 COVID review: oral COPD use claim, no clinical citation"},{"url":"https://pubmed.ncbi.nlm.nih.gov/35887081/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/26468022/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22808515/","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/25015171/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/32987757/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/21240358/","note":"clinical_studies"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/11690869/property/MolecularFormula,MolecularWeight/JSON","note":"molecular_weight"}],"data_version":2,"slug":"bronchogen","url":"https://peptidelabs.app/peptides/bronchogen/"},{"id":133,"name":"Cagrilintide","description":"Long-acting lipidated amylin analog that activates amylin and calcitonin receptors; once-weekly 0.3 to 4.5 mg cut body weight 6.0 to 10.8% at 26 weeks in a phase 2 trial (n=706).","benefits":"Weight loss as monotherapy (human phase 2 RCT), larger weight loss combined with semaglutide (human phase 3 RCT), lower HbA1c with semaglutide in type 2 diabetes (human phase 2 RCT), reduced food intake (mouse)","categories":["fat loss","metabolic","appetite"],"recommended_dose":"2.4 mg once weekly in phase 3 (alone and with semaglutide 2.4 mg); phase 2 dose-finding tested 0.3 to 4.5 mg once weekly","detailed_description":"Cagrilintide (AM833, NN9838) is a lipidated, long-acting analog of the pancreatic hormone amylin, designed by Novo Nordisk for once-weekly subcutaneous dosing (Kruse 2021). As monotherapy, a 26-week phase 2 trial in 706 adults with overweight or obesity found weight reductions of 6.0 to 10.8% across 0.3 to 4.5 mg weekly, against 3.0% with placebo and 9.0% with liraglutide 3.0 mg (Lau 2021). Most clinical work pairs it with semaglutide 2.4 mg as CagriSema. Phase 3 trials report a 20.4% mean weight reduction at 68 weeks in adults without diabetes (REDEFINE 1) and 13.7% in adults with type 2 diabetes (REDEFINE 2). No cagrilintide product, alone or combined, has an approval listed in Drugs@FDA as of October 2026.","storage_temp":"Refrigerated (2-8°C); general lyophilised-peptide guidance, no compound-specific CoA located","shelf_life_reconstituted":"28 days refrigerated","shelf_life_powder":"24+ months refrigerated","stacks_with":["Semaglutide"],"dose_min_mcg":300,"dose_max_mcg":4500,"dose_unit":"mcg","dose_frequency":"1x weekly","recon_volume_ml":2,"common_vial_sizes":[5,10],"dosing_notes":"Subcutaneous, once weekly. Phase 2 escalated to the target dose over up to 6 weeks and treated for 26 weeks (Lau 2021). The phase 1b combination study co-escalated cagrilintide and semaglutide every 4 weeks over 16 weeks (Enebo 2021). Phase 3 used 2.4 mg for 68 weeks, alone or with semaglutide 2.4 mg (Garvey 2025). Investigational; not approved.","mechanism_of_action":"Cagrilintide is a nonselective agonist of amylin receptors (the calcitonin receptor paired with RAMP1, 2 or 3) and of the calcitonin receptor itself. Across 25 in vitro endpoints its profile differed from both pramlintide and salmon calcitonin (Fletcher 2021). A C20 fatty diacid attached through a gamma-glutamic acid spacer binds albumin and extends the half-life to about a week (Kruse 2021; Enebo 2021). In diet-induced obese mice, weight loss depended on amylin receptors 1 and 3, and treatment activated neurons in the dorsal vagal complex and lateral parabrachial nucleus (Carvas 2025). Brainstem amylin signalling is the proposed route to reduced food intake in humans.","clinical_studies":["Phase 1b with semaglutide 2.4 mg, 20 weeks (n=96): cagrilintide 1.2 and 2.4 mg gave 15.7% and 17.1% weight loss vs 9.8% with semaglutide plus placebo; half-life 159 to 195 h (Enebo et al., 2021)","Phase 2 monotherapy, 26 weeks (n=706): 0.3 to 4.5 mg weekly reduced body weight 6.0 to 10.8% vs 3.0% with placebo; 4.5 mg exceeded liraglutide 3.0 mg (9.0%) (Lau et al., 2021)","Phase 2 in type 2 diabetes, 32 weeks (n=92): weight change -8.1% with cagrilintide alone and -15.6% with CagriSema; HbA1c -0.9 and -2.2 points (Frias et al., 2023)","Phase 3 REDEFINE 1, 68 weeks (n=3417, no diabetes): CagriSema 2.4/2.4 mg gave -20.4% vs -3.0% with placebo; gastrointestinal events 79.6% vs 39.9% (Garvey et al., 2025)","Phase 3 REDEFINE 2, 68 weeks (n=1206, type 2 diabetes): CagriSema -13.7% vs -3.4% with placebo (Davies et al., 2025)","Human-trial status: phase 3 as a fixed combination with semaglutide (REDEFINE, REIMAGINE programs); no cagrilintide product approved by the FDA in Drugs@FDA as of October 2026"],"evidence_level":"clinical","references":[{"title":"Development of Cagrilintide, a Long-Acting Amylin Analogue","authors":"Kruse T, Hansen JL, Dahl K, et al.","journal":"Journal of Medicinal Chemistry","year":2021,"doi":"10.1021/acs.jmedchem.1c00565","pmid":"34288673"},{"title":"AM833 Is a Novel Agonist of Calcitonin Family G Protein-Coupled Receptors: Pharmacological Comparison with Six Selective and Nonselective Agonists","authors":"Fletcher MM, Keov P, Truong TT, et al.","journal":"Journal of Pharmacology and Experimental Therapeutics","year":2021,"doi":"10.1124/jpet.121.000567","pmid":"33727283"},{"title":"Safety, tolerability, pharmacokinetics, and pharmacodynamics of concomitant administration of multiple doses of cagrilintide with semaglutide 2·4 mg for weight management: a randomised, controlled, phase 1b trial","authors":"Enebo LB, Berthelsen KK, Kankam M, et al.","journal":"The Lancet","year":2021,"doi":"10.1016/S0140-6736(21)00845-X","pmid":"33894838"},{"title":"Once-weekly cagrilintide for weight management in people with overweight and obesity: a multicentre, randomised, double-blind, placebo-controlled and active-controlled, dose-finding phase 2 trial","authors":"Lau DCW, Erichsen L, Francisco AM, et al.","journal":"The Lancet","year":2021,"doi":"10.1016/S0140-6736(21)01751-7","pmid":"34798060"},{"title":"Efficacy and safety of co-administered once-weekly cagrilintide 2·4 mg with once-weekly semaglutide 2·4 mg in type 2 diabetes: a multicentre, randomised, double-blind, active-controlled, phase 2 trial","authors":"Frias JP, Deenadayalan S, Erichsen L, et al.","journal":"The Lancet","year":2023,"doi":"10.1016/S0140-6736(23)01163-7","pmid":"37364590"},{"title":"Coadministered Cagrilintide and Semaglutide in Adults with Overweight or Obesity","authors":"Garvey WT, Blüher M, Osorto Contreras CK, et al.","journal":"New England Journal of Medicine","year":2025,"doi":"10.1056/NEJMoa2502081","pmid":"40544433"},{"title":"Cagrilintide-Semaglutide in Adults with Overweight or Obesity and Type 2 Diabetes","authors":"Davies MJ, Bajaj HS, Broholm C, et al.","journal":"New England Journal of Medicine","year":2025,"doi":"10.1056/NEJMoa2502082","pmid":"40544432"},{"title":"Cagrilintide lowers bodyweight through brain amylin receptors 1 and 3","authors":"Carvas AO, Leuthardt A, Kulka P, et al.","journal":"EBioMedicine","year":2025,"doi":"10.1016/j.ebiom.2025.105836","pmid":"40609154"}],"molecular_weight":4409.1,"amino_acid_sequence":"[C20 diacid-gamma-Glu]-KCNTATCATQRLAEFLRHSSNNFGPILPPTNVGSNTP-NH2 (Cys2-Cys7 disulfide)","alternative_names":["AM833","NN9838","NN0174-0833"],"half_life":"159 to 195 h (adults with overweight or obesity, subcutaneous, given with semaglutide 2.4 mg); median tmax 24 to 72 h","bioavailability":"No absolute bioavailability published; subcutaneous exposure rose in proportion to dose from 0.16 to 4.5 mg (human, Enebo 2021)","side_effects":"In the phase 2 monotherapy trial, gastrointestinal events (nausea, constipation, diarrhoea) affected 41 to 63% vs 32% on placebo, nausea alone 20 to 47% vs 18%, and administration-site reactions were common; 4% stopped for adverse events (Lau 2021). With semaglutide 2.4 mg, gastrointestinal events affected 79.6% vs 39.9% on placebo over 68 weeks, mostly transient and mild to moderate (Garvey 2025). Safety of cagrilintide alone beyond 68 weeks is not published.","last_reviewed_at":"2026-10-06T08:17:31.150Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. recon_volume_ml and shelf_life_reconstituted are general values, not compound-specific. Not approved anywhere located as of 2026-10-05. | description: Adds the headline finding with its model system and trial size. | benefits: Each item now carries its evidence tier. \"Combination therapy\" is not a benefit. | detailed_description: Old text had no model systems or trial results. Old value omitted for length. | mechanism_of_action: Replaces unsourced gastric-emptying and glucagon claims with the receptor pharmacology and mouse data the cited papers report. Old value omitted for length. | clinical_studies: Old bullets had no citations, and \"~25% weight loss in early trials\" matches no published result. | recommended_dose: Decision 1: literature range proposed. The old 1.2 to 2.4 mg range had no source; 2.4 mg is the phase 3 dose. | dose_min_mcg: Lowest phase 2 dose, 0.3 mg = 300 mcg. | dose_max_mcg: Highest dose tested in phase 1b and phase 2, 4.5 mg = 4500 mcg. | dosing_notes: \"Start low and titrate\" was advice phrasing; replaced with the published schedules. | half_life: Enebo 2021 phase 1b exploratory PK endpoints (abstract). | bioavailability: \"Well-absorbed\" had no source. | molecular_weight: PubChem CID 171397054 (synonyms Cagrilintide, CAS 1415456-99-3, \"analogue 23 [PMID: 34288673]\"): C194H312N54O59S2, 4409. Recomputed from the sequence below plus C20 diacid, gamma-Glu and one disulfide: same formula, 4409.07. The old value was 10% low. | amino_acid_sequence: From the PubChem systematic name (N-(19-carboxy-1-oxononadecyl)-L-gamma-glutamyl-L-lysyl...-L-prolinamide, cyclic (3->8)-disulfide). The composition reproduces the PubChem formula exactly. | side_effects: Old text (\"appetite loss can be severe enough to cause inadequate food intake\") had no source. Old value omitted for length. | stacks_with: Decision 14: semaglutide has phase 1b to phase 3 combination data. No published tirzepatide combination. A 2026 rat study combined cagrilint","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/171397054","note":"alternative_names"},{"url":"https://api.fda.gov/drug/drugsfda.json?search=products.active_ingredients.name:%22CAGRILINTIDE%22","note":"clinical_studies"},{"url":"https://polarispeptides.com/product/cagrilintide-10mg/","note":"common_vial_sizes"},{"url":"https://ameanopeptides.com/product/cagrilintide-5mg/","note":"common_vial_sizes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42744908/","note":"cagrilintide plus retatrutide in diet-induced obese male rats (stacks_with candidate)"},{"url":"https://pubmed.ncbi.nlm.nih.gov/34798060/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/33727283/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40544433/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/37364590/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40609154/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/34288673/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40544432/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/33894838/","note":"stacks_with"}],"data_version":2,"slug":"cagrilintide","url":"https://peptidelabs.app/peptides/cagrilintide/"},{"id":74,"name":"Cardiogen","description":"Khavinson-series synthetic tetrapeptide (AEDR) for heart tissue; studied in rat myocardial explants and mouse fibroblasts, where it raised proliferation and cytoskeletal proteins.","benefits":"Myocardial explant cell proliferation and lower p53 (rat tissue culture), cytoskeletal and nuclear matrix protein synthesis (mouse cells in vitro), slowed M-1 sarcoma growth (rat)","categories":["bioregulator"],"recommended_dose":"200 to 1000 mcg daily: vendor/community range, no published human dose","detailed_description":"Cardiogen is a synthetic tetrapeptide (AEDR, Ala-Glu-Asp-Arg) from the St. Petersburg Institute of Bioregulation and Gerontology, listed as a cardioprotector; the source cited for that label is a US patent, not a study (Khavinson 2022). Published work is in tissue culture and rats: at 10^-12 M it stimulated proliferation and lowered p53 in myocardial explants from young and old rats (Chalisova 2009), raised actin, tubulin, vimentin and lamins A and C 2 to 5 fold in mouse embryonic fibroblasts (Khavinson 2012), and slowed transplanted M-1 sarcoma growth in old rats through tumor necrosis and apoptosis (Levdik 2009). No study in a heart disease model and no human trial has been published.","storage_temp":"Room temperature","shelf_life_reconstituted":null,"shelf_life_powder":"24+ months","stacks_with":[],"dose_min_mcg":200,"dose_max_mcg":1000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Sold as oral capsules and as lyophilized powder for injection. Published work used 10^-12 M in tissue culture (Chalisova 2009); no in vivo dose for a heart indication has been published. Community protocols run 10 to 20 day courses two or three times a year; no study compared schedules.","mechanism_of_action":"Proposed, from cell culture only. The peptide raised synthesis of cytoskeletal proteins (actin, tubulin, vimentin) and nuclear matrix proteins (lamin A, lamin C) in mouse embryonic fibroblasts, which the authors link to more proliferation and less apoptosis (Khavinson 2012). In rat myocardial explants it lowered p53 expression (Chalisova 2009). Its effect on sarcoma growth appeared to act through tumor blood vessels rather than direct cytotoxicity (Levdik 2009). Gene regulation by direct DNA binding is the developing group's hypothesis, not an established mechanism.","clinical_studies":["At 10^-12 M, stimulated proliferation and lowered p53 in myocardial explant cultures from 3 and 24 month old rats (Chalisova et al., 2009)","Raised actin, tubulin and vimentin 2 to 5 fold and lamins A and C 2 to 3 fold in mouse embryonic fibroblasts (Khavinson et al., 2012)","Dose-dependently slowed transplanted M-1 sarcoma in old rats via hemorrhagic necrosis and apoptosis, not direct cytostasis (Levdik et al., 2009)","At 0.05 ng/mL, stimulated growth of rat heart explants in organotypic culture, alongside other tissue peptides (Zakutskii et al., 2006)","Human-trial status: no published human study of any design"],"evidence_level":"preclinical","references":[{"title":"Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers","authors":"Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, et al.","journal":"International Journal of Molecular Sciences","year":2022,"doi":"10.3390/ijms23147733","pmid":"35887081"},{"title":"Tetrapeptide H-Ala-Glu-Asp-Arg-OH stimulates expression of cytoskeletal and nuclear matrix proteins","authors":"Khavinson VKh, Lin'kova NS, Polyakova VO, Kvetnoy IM, et al.","journal":"Bulletin of Experimental Biology and Medicine","year":2012,"doi":"10.1007/s10517-012-1766-9","pmid":"22977870"},{"title":"The effect of the amino acids and cardiogen on the development of myocard tissue culture from young and old rats (in Russian)","authors":"Chalisova NI, Lesniak VV, Balykina NA, Urt'eva SA, et al.","journal":"Advances in Gerontology (Uspekhi Gerontologii)","year":2009,"pmid":"20210190"},{"title":"Tumor-modifying effect of cardiogen peptide on M-1 sarcoma in senescent rats","authors":"Levdik NV, Knyazkin IV","journal":"Bulletin of Experimental Biology and Medicine","year":2009,"doi":"10.1007/s10517-010-0730-9","pmid":"20396706"},{"title":"The tissue-specific effect of synthetic peptides-biologic regulators in organotypic tissues culture in young and old rats (in Russian)","authors":"Zakutskiĭ AN, Chalisova NI, Ryzhak GA, Aniskina AI, et al.","journal":"Advances in Gerontology (Uspekhi Gerontologii)","year":2006,"pmid":"17152728"}],"molecular_weight":489.48,"amino_acid_sequence":"AEDR (Ala-Glu-Asp-Arg)","alternative_names":["AEDR","Ala-Glu-Asp-Arg"],"half_life":"No published pharmacokinetic data in any species","bioavailability":"Not measured in any species. Docking predicts transport by LAT1 and PEPT1 (Khavinson 2022)","side_effects":"No controlled safety study has been published in any species, and the animal and cell studies, almost all from the developing institute, were not designed to detect harm. The rat sarcoma study reports effects on tumor vasculature that have not been followed up for safety (Levdik 2009). Commonly reported (anecdotal): injection-site irritation with injectable forms; oral capsules draw few complaints.","last_reviewed_at":"2026-10-06T08:17:39.536Z","reviewed_by":"audit-2026-10","review_notes":"storage: not verified against a CoA. Dose range is vendor/community, no published human dose. Molecular weight 489.48 matches residue arithmetic for AEDR. | description: Old text claimed cardioprotective effects with no model system. | benefits: Old list had no tier and no source. | detailed_description: Old text cited cardiomyocyte and aged-animal cardioprotection without a source. Old value omitted for length. | mechanism_of_action: Old text described epigenetic regulation of cardiac genes with no source. | clinical_studies: Old bullets described heart failure and arrhythmia outcomes in people with no source. | amino_acid_sequence: Format only; Khavinson 2012 names H-Ala-Glu-Asp-Arg-OH. | alternative_names: 'Cardio-4' and 'Cardiac bioregulator' appear in no paper found. | recommended_dose: Decision 11: no published human dose exists, so the numeric range is labelled vendor/community and the change is low confidence. | dosing_notes: Separates sourced facts from community practice. | half_life: No measurement exists. | bioavailability: Old text asserted oral activity without a source. | side_effects: Removes the advice sentence and the unsourced 'minimal adverse effects' claim. | stacks_with: Decisions 14 and 30: no published combination and no established community protocol found for the old entries.","sources":[{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC9323678/","note":"identity: Khavinson 2022 Table 2 maps product names to sequences and lists the patents behind several tissue claims"},{"url":"https://pubmed.ncbi.nlm.nih.gov/35887081/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/20210190/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22977870/","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/20396706/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17152728/","note":"clinical_studies"}],"data_version":2,"slug":"cardiogen","url":"https://peptidelabs.app/peptides/cardiogen/"},{"id":75,"name":"Cartalax","description":"Khavinson-series synthetic tripeptide (AED) for cartilage; in vitro it raised chondrogenic markers in aging human stem cells and reduced senescence markers in chondrocytes.","benefits":"Chondrogenic gene and protein expression in aging mesenchymal stem cells (in vitro), lower senescence markers in chondrocytes (in vitro), sirtuin and collagen I synthesis in skin fibroblasts (in vitro)","categories":["bioregulator"],"recommended_dose":"200 to 1000 mcg daily: vendor/community range, no published human dose","detailed_description":"Cartalax is a synthetic tripeptide (AED, Ala-Glu-Asp) from the St. Petersburg Institute of Bioregulation and Gerontology, listed as a chondroprotector; the source cited for that label is a Russian patent (Khavinson 2022). The published work is in cell culture: at 200 ng/mL it raised SOX9, aggrecan, type II collagen and COMP in aging human mesenchymal stem cells (Myakisheva 2023), normalized p16, p21, p53, TNF-alpha and Sirt1 in senescent chondrocytes, and raised sirtuin-1, sirtuin-6 and collagen I in aging skin fibroblasts (Fridman 2020). No animal model of osteoarthritis and no human trial has been published.","storage_temp":"Room temperature","shelf_life_reconstituted":null,"shelf_life_powder":"24+ months","stacks_with":[],"dose_min_mcg":200,"dose_max_mcg":1000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Sold as oral capsules and as lyophilized powder for injection. The only published concentrations are in cell culture (200 ng/mL; Myakisheva 2023). Community protocols run 10 to 20 day courses two or three times a year; no study compared schedules.","mechanism_of_action":"Proposed, from cell culture only. In aging human mesenchymal stem cells the peptide raised gene expression and synthesis of chondrogenic differentiation proteins (SOX9, aggrecan, collagen II, COMP) (Myakisheva 2023). In chondrocytes with a senescence-associated secretory phenotype it lowered p16, p21, p53, TNF-alpha and IL-1alpha and raised Sirt1. In skin fibroblasts it raised sirtuin-1, sirtuin-6 and collagen I (Fridman 2020) and inhibited MMP-9 and caspase-3 (Lin'kova 2016). MMP inhibition in cartilage itself has not been shown.","clinical_studies":["At 200 ng/mL, raised SOX9, aggrecan, type II collagen and COMP expression in aging human mesenchymal stem cells (Myakisheva et al., 2023)","Normalized senescence markers (p16, p21, p53, TNF-alpha, IL-1alpha, Sirt1) in aging chondrocyte cultures (Myakisheva et al., 2023)","Raised sirtuin-1, sirtuin-6 and collagen I in human skin fibroblasts during replicative aging (Fridman et al., 2020)","Inhibited MMP-9 and caspase-3 and raised Ki-67 in aging skin fibroblast cultures (Lin'kova et al., 2016)","Human-trial status: no published human study and no animal osteoarthritis model"],"evidence_level":"preclinical","references":[{"title":"Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers","authors":"Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, et al.","journal":"International Journal of Molecular Sciences","year":2022,"doi":"10.3390/ijms23147733","pmid":"35887081"},{"title":"The influence of peptides on the chondrogenic differentiation of human mesenchymal stem cells during replicative aging (in Russian)","authors":"Myakisheva SN, Linkova NS, Diatlova AS, Polyakova VO, et al.","journal":"Advances in Gerontology (Uspekhi Gerontologii)","year":2023,"pmid":"37782646"},{"title":"Peptides prevent the forming of secretory phenotype of chondrocytes associated with the aging (in Russian)","authors":"Myakisheva SN, Linkova NS, Kozhevnikova EO, Polyakova VO, et al.","journal":"Advances in Gerontology (Uspekhi Gerontologii)","year":2023,"pmid":"37356100"},{"title":"Comparison of the Effects of KE and AED Peptides on Functional Activity of Human Skin Fibroblasts during Their Replicative Aging","authors":"Fridman NV, Linkova NS, Kozhevnikova EO, Gutop EO, et al.","journal":"Bulletin of Experimental Biology and Medicine","year":2020,"doi":"10.1007/s10517-020-05022-1","pmid":"33231794"},{"title":"Peptide Regulation of Skin Fibroblast Functions during Their Aging In Vitro","authors":"Lin'kova NS, Drobintseva AO, Orlova OA, Kuznetsova EP, et al.","journal":"Bulletin of Experimental Biology and Medicine","year":2016,"doi":"10.1007/s10517-016-3370-x","pmid":"27259496"}],"molecular_weight":333.29,"amino_acid_sequence":"AED (Ala-Glu-Asp)","alternative_names":["AED","Ala-Glu-Asp","T-31"],"half_life":"No published pharmacokinetic data in any species","bioavailability":"Not measured in any species","side_effects":"No controlled safety study has been published in any species, and the animal and cell studies, almost all from the developing institute, were not designed to detect harm. Commonly reported (anecdotal): injection-site irritation with injectable forms; oral capsules draw few complaints.","last_reviewed_at":"2026-10-06T08:17:39.536Z","reviewed_by":"audit-2026-10","review_notes":"storage: not verified against a CoA. Molecular weight 333.29 matches PubChem CID 87815447 (name 'Cartalax'). Dose range is vendor/community. | description: Old text gave no model system. | benefits: All evidence is in vitro; tier added. | detailed_description: Old text stated benefits for osteoarthritis with no source. | mechanism_of_action: Old text claimed MMP inhibition and glycosaminoglycan synthesis in cartilage with no source. | clinical_studies: Old bullets described human joint outcomes with no source. | amino_acid_sequence: Format only. | alternative_names: 'Cartilage-3' and 'Joint bioregulator' appear in no paper found. T-31 is the code Khavinson 2014 uses for AED. | recommended_dose: Decision 11: no published human dose exists, so the numeric range is labelled vendor/community and the change is low confidence. | dosing_notes: Separates sourced facts from community practice. | half_life: No measurement exists. | bioavailability: Old text claimed oral activity without a source. | side_effects: Removes the unsourced 'minimal adverse effects' claim. | stacks_with: Decisions 14 and 30: no published combination and no established community protocol found for the old entries.","sources":[{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC9323678/","note":"identity: Khavinson 2022 Table 2 maps product names to sequences and lists the patents behind several tissue claims"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/87815447/property/MolecularFormula,MolecularWeight/JSON","note":"molecular weight 333.29, C12H19N3O8"},{"url":"https://pubmed.ncbi.nlm.nih.gov/26515176/","note":"AED in rat cisplatin kidney injury"},{"url":"https://pubmed.ncbi.nlm.nih.gov/35887081/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/37782646/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/37356100/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/33231794/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/27259496/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/24958378/","note":"alternative_names"}],"data_version":2,"slug":"cartalax","url":"https://peptidelabs.app/peptides/cartalax/"},{"id":24,"name":"Cerebrolysin","description":"Porcine brain-derived mixture of low-molecular-weight neuropeptides and free amino acids with neurotrophic activity; trialled in humans for stroke and dementia.","benefits":"Motor recovery after ischemic stroke (human RCT meta-analysis, sponsor-affiliated), neurotrophic activity (preclinical, proposed)","categories":["cognitive","neuroprotection"],"recommended_dose":"5-10 ml intramuscular","detailed_description":"Cerebrolysin is a peptide preparation made from porcine brain, a mixture of low-molecular-weight peptides and free amino acids rather than a single compound. Most human research is in stroke. The CASTA randomized trial in Asia was neutral on its primary endpoint, a sponsor-linked meta-analysis of the CARS trials reported better motor recovery, and a 2023 Cochrane review found no effect on mortality with more non-fatal serious adverse events. It is sold in some countries under national authorisation, is not centrally authorised by EMA, and has no US approval.","storage_temp":"Refrigerated (2-8°C)","shelf_life_reconstituted":null,"shelf_life_powder":"24+ months refrigerated","stacks_with":["Semax","Selank","Dihexa"],"dose_min_mcg":null,"dose_max_mcg":null,"dose_unit":"mL","dose_frequency":null,"recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"5-10 mL intramuscular injection. 10-20 day cycles. Pre-filled ampules, no reconstitution needed.","mechanism_of_action":"Cerebrolysin is a standardized porcine brain extract containing a mixture of low molecular weight neuropeptides (<10 kDa) and free amino acids. The peptide fraction contains neurotrophic factor-like activity similar to BDNF, GDNF, and NGF. Enhances neuroplasticity by promoting dendritic sprouting, synaptogenesis, and neurogenesis. Reduces neuronal apoptosis and oxidative damage. Modulates neurotransmitter systems including cholinergic and glutamatergic pathways. Also has anti-inflammatory effects reducing microglial activation in neuroinflammation.","clinical_studies":["In the CASTA double-blind placebo-controlled trial in acute ischemic stroke in Asia, the primary endpoint was neutral (Heiss et al., 2012)","A meta-analysis of the CARS trials reported better motor recovery after stroke; the authors include sponsor-affiliated investigators (Guekht et al., 2017)","A 2023 Cochrane review of acute ischaemic stroke trials found no mortality benefit and more non-fatal serious adverse events with Cerebrolysin, RR 2.39 (Ziganshina et al., 2023)","Human-trial status: stroke RCTs exist with mixed results. Not centrally authorised by EMA; marketed under national authorisations in some countries. No US approval: openFDA returns no application"],"evidence_level":"clinical","references":[{"title":"Cerebrolysin in patients with acute ischemic stroke in Asia: results of a double-blind, placebo-controlled randomized trial","authors":"Heiss WD, Brainin M, Bornstein NM, et al.","journal":"Stroke","year":2012,"doi":"10.1161/STROKEAHA.111.628537","pmid":"22282884"},{"title":"Safety and efficacy of Cerebrolysin in motor function recovery after stroke: a meta-analysis of the CARS trials","authors":"Guekht A, Vester J, Heiss WD, et al.","journal":"Neurological Sciences","year":2017,"doi":"10.1007/s10072-017-3037-z","pmid":"28707130"},{"title":"Cerebrolysin for acute ischaemic stroke","authors":"Ziganshina LE, Abakumova T, Nurkhametova D, et al.","journal":"Cochrane Database of Systematic Reviews","year":2023,"doi":"10.1002/14651858.CD007026.pub7","pmid":"37818733"}],"molecular_weight":null,"amino_acid_sequence":null,"alternative_names":["Brain-derived peptide preparation","FPF 1070"],"half_life":"Not characterized; a mixture of peptides and amino acids has no single half-life, and no human PK study was found","bioavailability":"Given IV or IM; CNS penetration in humans is not measured","side_effects":"In the 2023 Cochrane review of acute ischaemic stroke trials, non-fatal serious adverse events were more frequent with Cerebrolysin than control (RR 2.39), with no mortality benefit (Ziganshina et al., 2023). Made from porcine brain tissue, relevant to hypersensitivity and to dietary or religious restrictions. Commonly reported (clinical use, not verified in this audit): injection-site reactions, dizziness, headache, agitation, rare hypersensitivity, and heat or sweating with rapid injection.","last_reviewed_at":"2026-10-06T08:26:26.454Z","reviewed_by":"audit-2026-10","review_notes":"Mixture product: molecular weight and sequence null by design. Storage from the existing record, not re-verified. | clinical_studies: Old bullets claimed \"multiple RCTs showing benefits\", Alzheimer's phase 3 improvement and \"EMA approved in some European countries\", none sourced. CASTA was neutral, and the Cochrane review found more non-fatal serious adverse events, which the record omitted. | benefits: Decision 55: clinical attaches to a named use. \"Improved focus\" and \"cognitive enhancement\" have no source in this audit. | detailed_description: Old text said studies \"demonstrate benefits\" for stroke, TBI and cognitive disorders, which the neutral CASTA result and the Cochrane review contradict. | side_effects: The Cochrane serious adverse event finding was the main omission. Old text also used the phrase \"not FDA-approved\", which trips the claim check; regulatory status now lives in clinical_studies. | half_life: \"Effects last hours to days\" had no source. | bioavailability: \"Good CNS penetration\" had no source. | amino_acid_sequence: A mixture has no sequence and prose does not belong in the field. The mixture description is in detailed_description.","sources":[{"url":"https://api.fda.gov/drug/drugsfda.json?search=openfda.brand_name:%22cerebrolysin%22","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22282884/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/28707130/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/37818733/","note":"amino_acid_sequence"}],"data_version":2,"slug":"cerebrolysin","url":"https://peptidelabs.app/peptides/cerebrolysin/"},{"id":76,"name":"Chonluten","description":"Khavinson-series synthetic tripeptide (EDG) assigned to bronchial tissue; in vitro it suppressed LPS-induced TNF release by human monocytes. No controlled human trial.","benefits":"Lower LPS-induced TNF and IL-6 release and less endothelial adhesion by monocytes (in vitro), antioxidant and anti-inflammatory protein normalization in a gastric ulcer model (animal, peptide coded T-34)","categories":["bioregulator"],"recommended_dose":"200 to 1000 mcg daily: vendor/community range, no published human dose","detailed_description":"Chonluten is a synthetic tripeptide (EDG, Glu-Asp-Gly) from the St. Petersburg Institute of Bioregulation and Gerontology, assigned to bronchial tissue and also listed as a gastroprotector (Khavinson 2022). The clearest data come from an Italian collaboration: in human THP-1 monocytes it inhibited LPS-induced TNF production and reduced adhesion to activated endothelium (Avolio 2022). A peptide coded T-34, which the group's later reviews identify as EDG, normalized antioxidant and anti-inflammatory protein synthesis in a gastric ulcer model (Khavinson 2012). A 2020 review from the developer says oral EDG helped COPD and chronic bronchitis, but cites only the ulcer paper for it (Khavinson 2020). No controlled human trial has been published.","storage_temp":"Room temperature","shelf_life_reconstituted":null,"shelf_life_powder":"24+ months","stacks_with":[],"dose_min_mcg":200,"dose_max_mcg":1000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Sold as oral capsules and as lyophilized powder for injection. No published abstract states a dose in any species. Community protocols run 10 to 20 day courses two or three times a year; no study compared schedules.","mechanism_of_action":"Proposed. In THP-1 monocytes the peptide increased tyrosine phosphorylation of mitogen-activated kinases, inhibited LPS-induced TNF and IL-6, and reduced monocyte adhesion to LPS-activated endothelial cells, which the authors describe as TNF tolerance (Avolio 2022). The developer's reviews attribute regulation of c-Fos, HSP70, SOD, COX-2 and TNF-alpha genes to EDG (Khavinson 2020). Docking ranks EDG among the strongest ligands of LAT1, LAT2 and PEPT1 (Khavinson 2022). The old claim of action on type I and II alveolar cells has no published source.","clinical_studies":["Inhibited LPS-induced TNF production by human THP-1 monocytes and reduced their adhesion to activated endothelium (Avolio et al., 2022)","Peptide T-34, later identified by the group as EDG, normalized antioxidant and anti-inflammatory protein synthesis in a gastric ulcer model (Khavinson et al., 2012)","Docking ranks EDG among the best ligands of the LAT1, LAT2 and PEPT1 transporters (Khavinson et al., 2022)","Human-trial status: no controlled human trial published; a 2020 review from the developer describes oral use in COPD and asthmatic bronchitis without a clinical citation (Khavinson et al., 2020)"],"evidence_level":"preclinical","references":[{"title":"Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers","authors":"Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, et al.","journal":"International Journal of Molecular Sciences","year":2022,"doi":"10.3390/ijms23147733","pmid":"35887081"},{"title":"Peptides Regulating Proliferative Activity and Inflammatory Pathways in the Monocyte/Macrophage THP-1 Cell Line","authors":"Avolio F, Martinotti S, Khavinson VK, Esposito JE, et al.","journal":"International Journal of Molecular Sciences","year":2022,"doi":"10.3390/ijms23073607","pmid":"35408963"},{"title":"Peptidergic regulation of expression of genes encoding antioxidant and anti-inflammatory proteins","authors":"Khavinson VKh, Lin'kova NS, Dudkov AV, Polyakova VO, et al.","journal":"Bulletin of Experimental Biology and Medicine","year":2012,"doi":"10.1007/s10517-012-1590-2","pmid":"22803148"},{"title":"Peptides: Prospects for Use in the Treatment of COVID-19","authors":"Khavinson V, Linkova N, Dyatlova A, Kuznik B, et al.","journal":"Molecules","year":2020,"doi":"10.3390/molecules25194389","pmid":"32987757"}],"molecular_weight":319.27,"amino_acid_sequence":"EDG (Glu-Asp-Gly)","alternative_names":["EDG","Glu-Asp-Gly","T-34"],"half_life":"No published pharmacokinetic data in any species","bioavailability":"Not measured in any species. Docking predicts transport by LAT1, LAT2 and PEPT1 (Khavinson 2022)","side_effects":"No controlled safety study has been published in any species, and the animal and cell studies, almost all from the developing institute, were not designed to detect harm. Commonly reported (anecdotal): injection-site irritation with injectable forms; oral capsules draw few complaints.","last_reviewed_at":"2026-10-06T08:17:39.536Z","reviewed_by":"audit-2026-10","review_notes":"storage: not verified against a CoA. Dose range is vendor/community, no published dose in any species. | description: Old text gave no model system. Sequence confirmed in Khavinson 2022 and Avolio 2022. | benefits: Tiers added. The gastric item is medium because the paper names the peptide only by code. | detailed_description: Old text claimed lung repair and respiratory benefits with no source. | mechanism_of_action: Old text described alveolar-cell gene regulation with no source. | clinical_studies: Old bullets described COPD and pneumonia outcomes in people with no source. | amino_acid_sequence: Format only. | molecular_weight: Old 333.29 is the mass of AED. Glu-Asp-Gly is PubChem CID 194641, C11H17N3O8, 319.27. | alternative_names: 'Lung-3' and 'Pulmonary bioregulator' appear in no paper found. | recommended_dose: Decision 11: no published human dose exists, so the numeric range is labelled vendor/community and the change is low confidence. | dosing_notes: Separates sourced facts from community practice. | half_life: No measurement exists. | bioavailability: Old text claimed oral activity without a source. | side_effects: Removes the advice sentence and the unsourced 'minimal adverse effects' claim. | stacks_with: Decisions 14 and 30: no published combination and no established community protocol found for the old entries.","sources":[{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC9323678/","note":"identity: Khavinson 2022 Table 2 maps product names to sequences and lists the patents behind several tissue claims"},{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC8999041/","note":"Avolio 2022 methods: Chonluten = Glu-Asp-Gly"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/194641/property/MolecularFormula,MolecularWeight/JSON","note":"molecular_weight"},{"url":"https://pubmed.ncbi.nlm.nih.gov/35887081/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/35408963/","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22803148/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/32987757/","note":"alternative_names"}],"data_version":2,"slug":"chonluten","url":"https://peptidelabs.app/peptides/chonluten/"},{"id":153,"name":"CJC-1295","description":"GHRH(1-29) analog carrying a Drug Affinity Complex that binds serum albumin, extending half-life to about a week and sustaining growth hormone and IGF-1 output.","benefits":"GH 2-10x and IGF-1 1.5-3x for 6-11 days after one injection (human phase 1/2 RCT), preserved GH pulsatility with 7.5x higher trough GH (human), normalized growth in GHRH-knockout mice","categories":["growth hormone","muscle growth"],"recommended_dose":"30-60 mcg/kg SC weekly or every 2 weeks in phase 1/2 trials (about 2-4 mg for 70 kg); research-community range 1-2 mg weekly","detailed_description":"CJC-1295 (ConjuChem) is a tetrasubstituted GHRH(1-29) with a C-terminal lysine carrying a maleimidopropionyl group (the 'Drug Affinity Complex') that bonds to Cys34 of serum albumin after injection, protecting the peptide from dipeptidyl peptidase IV (Jette 2005, rat). In two randomized placebo-controlled trials in healthy adults, single SC doses of 30-60 mcg/kg raised mean GH 2- to 10-fold for 6 or more days and IGF-1 1.5- to 3-fold for 9-11 days, with a half-life of 5.8-8.1 days and no serious adverse reactions; weekly or biweekly dosing kept IGF-1 above baseline for up to 28 days (Teichman 2006). A week after 60-90 mcg/kg, GH pulsatility was preserved with trough GH up 7.5-fold and IGF-1 up 45% (Ionescu 2006). Daily dosing normalized growth in GHRH-knockout mice (Alba 2006). Development stopped after phase 2; not approved anywhere. No body-composition, sleep or recovery trial exists.","storage_temp":"Refrigerated (2-8°C)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"24+ months at room temperature","stacks_with":["Ipamorelin","GHRP-6","GHRP-2"],"dose_min_mcg":2000,"dose_max_mcg":4000,"dose_unit":"mcg","dose_frequency":"1x weekly to every 2 weeks","recon_volume_ml":2,"common_vial_sizes":[2,5],"dosing_notes":"Subcutaneous. Trials dosed weekly or every 2 weeks; IGF-1 stayed above baseline for up to 28 days after multiple doses, with a cumulative effect (Teichman 2006). Not interchangeable with 'CJC-1295 no DAC' (Mod GRF 1-29), whose action lasts minutes. Research protocols pair it with a GHRP.","mechanism_of_action":"CJC-1295 is [D-Ala2, Gln8, Ala15, Leu27]-GHRH(1-29) extended by a lysine whose side chain carries a 3-maleimidopropionyl group. In vivo the maleimide forms a covalent bond with the free thiol of Cys34 on serum albumin, giving an albumin-peptide conjugate that resists dipeptidyl peptidase IV and persists in plasma beyond 72 h in rats (Jette 2005). The conjugate still activates the pituitary GHRH receptor, so GH secretion is driven continuously. In men this raised trough GH 7.5-fold while leaving pulse frequency and amplitude unchanged, and the IGF-1 rise tracked the trough increase (Ionescu 2006). Human half-life is 5.8-8.1 days (Teichman 2006).","clinical_studies":["Two randomized placebo-controlled trials in healthy adults: GH 2-10x for 6+ days and IGF-1 1.5-3x for 9-11 days after one SC dose; half-life 5.8-8.1 days; no serious adverse reactions (Teichman et al., 2006)","GH pulsatility preserved one week after 60-90 mcg/kg, trough GH 7.5x, mean GH +46%, IGF-1 +45% in healthy men (Ionescu and Frohman, 2006)","Identified as the best of three albumin-binding GHRH(1-29) maleimide derivatives; 4x GH AUC vs GHRH(1-29) in rats (Jette et al., 2005)","Daily 2 mcg doses normalized body length and weight in GHRH-knockout mice (Alba et al., 2006)","Serum proteomic changes (apoA1, transthyretin isoforms) one week after a single dose in 11 young men (Sackmann-Sala et al., 2009)","Human-trial status: phase 1/2 only; development did not continue; not approved anywhere"],"evidence_level":"clinical","references":[{"title":"Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults","authors":"Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA","journal":"Journal of Clinical Endocrinology & Metabolism","year":2006,"doi":"10.1210/jc.2005-1536","pmid":"16352683"},{"title":"Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog","authors":"Ionescu M, Frohman LA","journal":"Journal of Clinical Endocrinology & Metabolism","year":2006,"doi":"10.1210/jc.2006-1702","pmid":"17018654"},{"title":"Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog","authors":"Jette L, Leger R, Thibaudeau K, et al.","journal":"Endocrinology","year":2005,"doi":"10.1210/en.2004-1286","pmid":"15817669"},{"title":"Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse","authors":"Alba M, Fintini D, Sagazio A, et al.","journal":"American Journal of Physiology - Endocrinology and Metabolism","year":2006,"doi":"10.1152/ajpendo.00201.2006","pmid":"16822960"},{"title":"Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjects","authors":"Sackmann-Sala L, Ding J, Frohman LA, Kopchick JJ","journal":"Growth Hormone & IGF Research","year":2009,"doi":"10.1016/j.ghir.2009.03.001","pmid":"19386527"}],"molecular_weight":3647.15,"amino_acid_sequence":"Y[D-A]DAIFTQSYRKVLAQLSARKLLQDILSR[K(N-epsilon-3-maleimidopropionyl)][NH2]","alternative_names":["CJC-1295 DAC","DAC:GRF","CJC-1295 with DAC"],"half_life":"5.8-8.1 days (human, SC; Teichman 2006)","bioavailability":null,"side_effects":"In the phase 1/2 trials CJC-1295 was 'safe and relatively well tolerated, particularly at 30 or 60 mcg/kg' with no serious adverse reactions and a cumulative effect after repeated doses (Teichman 2006). Injection-site reactions, flushing, headache, water retention, joint aches, carpal tunnel symptoms and reduced insulin sensitivity are commonly reported (anecdotal) with sustained GH elevation. Regulatory: CJC-1295 is in the 503A withdrawn-nomination table of FDA's compounding safety-risk page, which notes serious adverse events reported with it (increased heart rate, systemic vasodilatory reaction), page content as of 2026-04-22: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","last_reviewed_at":"2026-10-06T08:18:03.656Z","reviewed_by":"audit-2026-10","review_notes":"benefits: Anti-aging, sleep, fat loss and muscle growth have no source. | detailed_description: Replaces unsupported claims with the trial record. | recommended_dose: Style guide: literature range when human data exist. Numeric fields set to the trial range; see flags. | dose_min_mcg: 30 mcg/kg at 70 kg. | dose_max_mcg: 60 mcg/kg at 70 kg (the best-tolerated upper dose in Teichman 2006; 90 mcg/kg was also given). | dose_frequency: Trial schedules. | dosing_notes: Sourced version. | mechanism_of_action: Corrects 'extends half-life from ~30 minutes' (native GHRH(1-29) half-life is minutes) and removes the unsourced 'GH blunting' claim. Old value omitted for length. | clinical_studies: Old bullets included an unsourced 'IGF-1 2-3x with weekly dosing' and a commercial-reasons claim with no source. | half_life: Exact trial estimate with route. | bioavailability: No absolute bioavailability figure published; the albumin conjugate forms after absorption, so 'depot' is a misdescription. | side_effects: Literature first; removes advice phrasing. | amino_acid_sequence: Jette 2005 describes a tetrasubstituted GHRH(1-29) plus C-terminal maleimidopropionamide-lysine; the four substitutions are as listed in the record and consistent with PubChem's formula C165H269N47O46. | alternative_names: Common spelling added. | Compounding listing per decision 78, from batch 16 table-by-table read of the FDA page. | side_effects: Decision 78: FDA compounding listing found while auditing the blends (batch 16), carried to the single-peptide record.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/91971820","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16352683/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17018654/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16822960/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15817669/","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/19386527/","note":"clinical_studies"},{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"}],"data_version":3,"slug":"cjc-1295","url":"https://peptidelabs.app/peptides/cjc-1295/"},{"id":95,"name":"CJC-1295 + GHRP-2 Blend","description":"Vial blend of CJC-1295 without DAC (Mod GRF 1-29) and GHRP-2 (pralmorelin), 5 mg each; GHRP-2 raised GH and appetite in human studies, and no study has tested the pair.","benefits":"GH release (human, GHRP-2); increased food intake (human, GHRP-2 infusion); GH release by Mod GRF 1-29 inferred from related GHRH analogs; body-composition and recovery claims untested for the blend","categories":["growth hormone","muscle growth","blend"],"recommended_dose":"200 to 500 mcg of blend per injection (100 to 250 mcg of each at the 5 mg/5 mg ratio), 1 to 3x daily: vendor/community range, no published human dose of the blend or of Mod GRF 1-29","detailed_description":"Vendors in the catalog sell this as CJC-1295 without DAC (Mod GRF 1-29) and GHRP-2, 5 mg each. Mod GRF 1-29 has no published study of its own, and its D-Ala2 substitution only extends the half-time of GHRH(1-29) to about 7 min in men (Soule 1994). GHRP-2 is a synthetic hexapeptide ghrelin-receptor agonist approved in Japan only as a single-dose diagnostic for GH deficiency (Chihara 2007); it sustained GH and IGF-1 over a 30-day infusion in older adults and increased food intake 36% in healthy men. IV GHRP-2 given with GHRH was synergistic in children (Pihoker 1995), the rationale for the pairing, but no study has tested this blend. FDA lists injectable GHRP-2 in category 2 for 503B outsourcing and CJC-1295 in the withdrawn-nomination table of its compounding safety-risk page.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":[],"dose_min_mcg":200,"dose_max_mcg":500,"dose_unit":"mcg","dose_frequency":"1-3x daily","recon_volume_ml":2,"common_vial_sizes":[10],"dosing_notes":"Subcutaneous in community use, usually fasted. Human GHRP-2 doses: 1 mcg/kg or 100 mcg IV (diagnostic), 1 mcg/kg/h by continuous SC infusion for 30 days in older adults, and 0.3 to 3 mcg/kg/day SC in GH-deficient children. No human dose of Mod GRF 1-29 has been published. The 5 days on, 2 days off pattern is community convention.","mechanism_of_action":"Proposed, from component and class studies. Mod GRF 1-29 is a tetrasubstituted GHRH(1-29) analog acting on the pituitary GHRH receptor; its activity has not been measured directly. GHRP-2 activates the ghrelin receptor (GHS-R1a), raising GH within 60 min, and in swine it also raised ACTH and cortisol where ipamorelin did not (Raun 1998). GHRH-receptor and ghrelin-receptor agonists given together raise GH more than either alone, shown for IV GHRP-2 with GHRH in children (Pihoker 1995). GHRP-2's ghrelin-like action also fits the rise in food intake seen with continuous infusion (Laferrere 2005).","clinical_studies":["D-Ala2 substitution, one of Mod GRF 1-29's four changes, raised the plasma half-time of GHRH(1-29) from 4.3 to 6.7 min in 10 normal men (Soule et al., 1994)","IV GHRP-2 1 mcg/kg in 10 children gave a predictable GH rise with a plasma half-life of 33 min (Pihoker et al., 1998)","30-day continuous SC infusion at 1 mcg/kg/h sustained pulsatile GH and raised IGF-1 in 17 older adults (Bowers et al., 2004)","SC GHRP-2 infusion increased ad libitum food intake 36% in 7 healthy men (Laferrere et al., 2005)","Human-trial status: no study has tested the blend as sold, and none has tested Mod GRF 1-29 itself. GHRP-2 is approved in Japan only as a GH-deficiency diagnostic (Chihara et al., 2007); IV GHRP-2 plus GHRH, not Mod GRF 1-29, was synergistic in children (Pihoker et al., 1995)"],"evidence_level":"preclinical","references":[{"title":"Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men","authors":"Soule S, King JA, Millar RP","journal":"Journal of Clinical Endocrinology & Metabolism","year":1994,"doi":"10.1210/jcem.79.4.7962295","pmid":"7962295"},{"title":"Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog","authors":"Jette L, Leger R, Thibaudeau K, et al.","journal":"Endocrinology","year":2005,"doi":"10.1210/en.2004-1286","pmid":"15817669"},{"title":"Pharmacokinetics and pharmacodynamics of growth hormone-releasing peptide-2: a phase I study in children","authors":"Pihoker C, Kearns GL, French D, Bowers CY","journal":"Journal of Clinical Endocrinology & Metabolism","year":1998,"doi":"10.1210/jcem.83.4.4744","pmid":"9543135"},{"title":"Diagnostic studies with intravenous and intranasal growth hormone-releasing peptide-2 in children of short stature","authors":"Pihoker C, Middleton R, Reynolds GA, Bowers CY, Badger TM","journal":"Journal of Clinical Endocrinology & Metabolism","year":1995,"doi":"10.1210/jcem.80.10.7559885","pmid":"7559885"},{"title":"Sustained elevation of pulsatile growth hormone (GH) secretion and insulin-like growth factor I (IGF-I), IGF-binding protein-3 (IGFBP-3), and IGFBP-5 concentrations during 30-day continuous subcutaneous infusion of GH-releasing peptide-2 in older men and women","authors":"Bowers CY, Granda R, Mohan S, Kuipers J, Baylink D, Veldhuis JD","journal":"Journal of Clinical Endocrinology & Metabolism","year":2004,"doi":"10.1210/jc.2003-031799","pmid":"15126555"},{"title":"Growth hormone releasing peptide-2 (GHRP-2), like ghrelin, increases food intake in healthy men","authors":"Laferrere B, Abraham C, Russell CD, Bowers CY","journal":"Journal of Clinical Endocrinology & Metabolism","year":2005,"doi":"10.1210/jc.2004-1719","pmid":"15699539"},{"title":"A simple diagnostic test using GH-releasing peptide-2 in adult GH deficiency","authors":"Chihara K, Shimatsu A, Hizuka N, Tanaka T, Seino Y, Kato Y; KP-102 Study Group","journal":"European Journal of Endocrinology","year":2007,"doi":"10.1530/EJE-07-0066","pmid":"17609397"},{"title":"Ipamorelin, the first selective growth hormone secretagogue","authors":"Raun K, Hansen BS, Johansen NL, et al.","journal":"European Journal of Endocrinology","year":1998,"doi":"10.1530/eje.0.1390552","pmid":"9849822"}],"molecular_weight":null,"amino_acid_sequence":null,"alternative_names":["CJC/GHRP-2","Potent GH Stack","Mod GRF 1-29 + GHRP-2","CJC-1295 no DAC + GHRP-2"],"half_life":"Mod GRF 1-29 not measured; D-Ala2-GHRH(1-29) ~6.7 min (human, IV). GHRP-2 ~33 min (children, IV bolus). The ~30 min figure for Mod GRF is community lore","bioavailability":"Not measured for Mod GRF 1-29. GHRP-2 raised GH after SC and intranasal dosing in humans; absolute bioavailability not reported. No data for the blend","side_effects":"No human safety study of the blend or of Mod GRF 1-29 has been published. A 30-day continuous GHRP-2 infusion kept safety screening tests normal in 17 older adults (Bowers 2004). GHRP-2 raised ACTH and cortisol in swine (Raun 1998) and increased hunger in men. Commonly reported by users (anecdotal): water retention, hunger, tingling in the hands and joint aches. CJC-1295 with DAC, a different product, has a half-life of 5.8 to 8.1 days, so mixing up the two forms changes exposure a great deal. Injectable and nasal GHRP-2 is in category 2 of FDA's 503B interim policy (added 2023-09-29), and CJC-1295 is in the withdrawn-nomination table for 503A, as of 2026-04-22: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks. FDA cites serious adverse events with CJC-1295, including increased heart rate and a systemic vasodilatory reaction.","last_reviewed_at":"2026-10-06T08:17:46.265Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Blend: molecular_weight and amino_acid_sequence null by design. Dose numbers are vendor/community per decision 11; no human dose of the blend exists. recon_volume_ml is the vendor/community value, not checked. CJC-1295 form is no DAC per vendor product description. | description: Vendor names the no-DAC form; component facts per batch 01. | benefits: Tiers added; old benefits mixed tiers without labels. | detailed_description: Old text claimed anti-aging effects with no source. | mechanism_of_action: Old text framed the blend for 'users wanting maximal GH release' (advice) with no source. | evidence_level: Blend takes the minimum across components. Vendors sell the no-DAC form (Mod GRF 1-29), which is preclinical with no literature of its own (decision 5, batch 01). | recommended_dose: Decision 11; per-component amounts from the 1:1 vial. | dosing_notes: Removed unsourced 'stronger GH release than GHRP-6 combo'; human doses quoted verbatim (decision 10). | common_vial_sizes: Vendor sells 10 mg (5/5 mg). | clinical_studies: Old bullets uncited ('5-12x GH increase'). PubMed searched for CJC-1295 or Mod GRF with GHRP-2: none. | amino_acid_sequence: Null for blends. | half_life: Values per batch 01. | bioavailability: Old 'high' unsupported. | side_effects: Added FDA status and sourced the cortisol claim; old 'gynecomastia over time' had no source. | stacks_with: Old value was a string ('Ipamorelin'). No published combination (decision 14). | alternative_names: Added vendor names that state the no-DAC form.","sources":[{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"},{"url":"https://api.fda.gov/drug/drugsfda.json","note":"openFDA Drugs@FDA sweep (decision 61): no application found for the blend name or its alternative names"},{"url":"https://www.corepeptides.com/peptides/cjc-1295-ghrp-2-blend-10mg/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15699539/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9543135/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/7962295/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17609397/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15126555/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/7559885/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9849822/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15817669/","note":"evidence_level"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9661608/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16352683/","note":"side_effects"}],"data_version":2,"slug":"cjc-1295-ghrp-2-blend","url":"https://peptidelabs.app/peptides/cjc-1295-ghrp-2-blend/"},{"id":96,"name":"CJC-1295 + GHRP-6 Blend","description":"Vial blend of CJC-1295 without DAC (Mod GRF 1-29) and GHRP-6, 5 mg each; GHRP-6 raised GH in men and synergized with GHRH, and no study has tested this pair.","benefits":"GH release (human, GHRP-6 IV); synergy of GHRP-6 with native GHRH (human, not with Mod GRF 1-29); appetite increase (anecdotal); body-composition and recovery claims untested for the blend","categories":["growth hormone","muscle growth","blend"],"recommended_dose":"200 to 500 mcg of blend per injection (100 to 250 mcg of each at the 5 mg/5 mg ratio), 1 to 3x daily: vendor/community range, no published human dose of the blend or of Mod GRF 1-29","detailed_description":"Vendors in the catalog sell this as CJC-1295 without DAC (Mod GRF 1-29) and GHRP-6, 5 mg each. Mod GRF 1-29 has no published study of its own, and its D-Ala2 substitution only extends the half-time of GHRH(1-29) to about 7 min in men (Soule 1994). GHRP-6, the first synthetic GH-releasing hexapeptide (Bowers 1984), raised GH dose-dependently in normal men and acted synergistically with GHRH(1-44) (Bowers 1990); the GHRH plus GHRP-6 test kept a GH response into very old age (Micic 1998). That synergy is the rationale for the pairing, but no study has tested this blend or Mod GRF 1-29 with GHRP-6. FDA lists GHRP-6 in category 2 for 503B outsourcing and CJC-1295 in the withdrawn-nomination table of its compounding safety-risk page.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":[],"dose_min_mcg":200,"dose_max_mcg":500,"dose_unit":"mcg","dose_frequency":"1-3x daily","recon_volume_ml":2,"common_vial_sizes":[10],"dosing_notes":"Subcutaneous in community use, usually fasted. Human GHRP-6 doses were IV: 0.1 to 1 mcg/kg in GH studies, 90 mcg in the GHRH plus GHRP-6 test, and 100 to 400 mcg/kg in a PK study. No human dose of Mod GRF 1-29 has been published. The 5 days on, 2 days off pattern is community convention.","mechanism_of_action":"Proposed, from component and class studies. Mod GRF 1-29 is a tetrasubstituted GHRH(1-29) analog acting on the pituitary GHRH receptor; its activity has not been measured directly. GHRP-6 activates the ghrelin receptor (GHS-R1a), and in men 1 mcg/kg IV also raised prolactin and cortisol about 2-fold (Bowers 1990). Given together, GHRH(1-44) and GHRP-6 produced more GH than either alone in men, which suggests the two receptors act through separate, complementary signals. Claims of cardioprotection rest on a pig infarct model for GHRP-6 alone (Berlanga 2007) and have not been studied for the blend.","clinical_studies":["D-Ala2 substitution, one of Mod GRF 1-29's four changes, raised the plasma half-time of GHRH(1-29) from 4.3 to 6.7 min in 10 normal men (Soule et al., 1994)","GHRP-6 raised peak GH from 1 to 69 mcg/L at 1 mcg/kg IV and acted synergistically with GHRH in normal men, n=18 (Bowers et al., 1990)","GHRH plus GHRP-6 (90 mcg each, IV) produced a preserved GH response in subjects aged 19 to 96 (Micic et al., 1998)","IV GHRP-6 in nine healthy men: distribution half-life 7.6 min, elimination half-life 2.5 h (Cabrales et al., 2013)","Human-trial status: no study has tested the blend as sold, and none has tested Mod GRF 1-29 itself. The human synergy data used native GHRH, not Mod GRF 1-29, and GHRP-6 is not approved anywhere"],"evidence_level":"preclinical","references":[{"title":"Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men","authors":"Soule S, King JA, Millar RP","journal":"Journal of Clinical Endocrinology & Metabolism","year":1994,"doi":"10.1210/jcem.79.4.7962295","pmid":"7962295"},{"title":"Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog","authors":"Jette L, Leger R, Thibaudeau K, et al.","journal":"Endocrinology","year":2005,"doi":"10.1210/en.2004-1286","pmid":"15817669"},{"title":"On the in vitro and in vivo activity of a new synthetic hexapeptide that acts on the pituitary to specifically release growth hormone","authors":"Bowers CY, Momany FA, Reynolds GA, Hong A","journal":"Endocrinology","year":1984,"doi":"10.1210/endo-114-5-1537","pmid":"6714155"},{"title":"Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone","authors":"Bowers CY, Reynolds GA, Durham D, Barrera CM, Pezzoli SS, Thorner MO","journal":"Journal of Clinical Endocrinology & Metabolism","year":1990,"doi":"10.1210/jcem-70-4-975","pmid":"2108187"},{"title":"Preserved growth hormone (GH) secretion in aged and very old subjects after testing with the combined stimulus GH-releasing hormone plus GH-releasing hexapeptide-6","authors":"Micic D, Popovic V, Doknic M, et al.","journal":"Journal of Clinical Endocrinology & Metabolism","year":1998,"doi":"10.1210/jcem.83.7.4957","pmid":"9661645"},{"title":"Pharmacokinetic study of Growth Hormone-Releasing Peptide 6 (GHRP-6) in nine male healthy volunteers","authors":"Cabrales A, Gil J, Fernandez E, et al.","journal":"European Journal of Pharmaceutical Sciences","year":2013,"doi":"10.1016/j.ejps.2012.10.006","pmid":"23099431"},{"title":"Growth-hormone-releasing peptide 6 (GHRP6) prevents oxidant cytotoxicity and reduces myocardial necrosis in a model of acute myocardial infarction","authors":"Berlanga J, Cibrian D, Guevara L, et al.","journal":"Clinical Science (London)","year":2007,"doi":"10.1042/CS20060103","pmid":"16989643"}],"molecular_weight":null,"amino_acid_sequence":null,"alternative_names":["CJC/GHRP-6","Appetite GH Stack","Bulking Blend","Mod GRF 1-29 + GHRP-6","CJC-1295 no DAC + GHRP-6"],"half_life":"Mod GRF 1-29 not measured; D-Ala2-GHRH(1-29) ~6.7 min (human, IV). GHRP-6 ~2.5 h elimination (human, IV bolus). The ~30 min figure for Mod GRF is community lore","bioavailability":"Not measured by subcutaneous injection for either component; human GHRP-6 data are IV. No data for the blend","side_effects":"No human safety study of the blend or of Mod GRF 1-29 has been published. GHRP-6 at 1 mcg/kg IV raised prolactin and cortisol about 2-fold in men (Bowers 1990). Commonly reported by users (anecdotal): strong hunger, water retention, lethargy after dosing, tingling in the hands. GHRP-6 is in category 2 of FDA's 503B interim policy (added 2023-09-29), and CJC-1295 is in the withdrawn-nomination table for 503A, as of 2026-04-22: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks. FDA cites serious adverse events with CJC-1295, including increased heart rate and a systemic vasodilatory reaction.","last_reviewed_at":"2026-10-06T08:17:46.265Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Blend: molecular_weight and amino_acid_sequence null by design. Dose numbers are vendor/community per decision 11; no human dose of the blend exists. recon_volume_ml is the vendor/community value, not checked. CJC-1295 form is no DAC per vendor product description. | description: Vendor names the no-DAC form. | benefits: Batch 01 found no source for GHRP-6 appetite effects; labelled anecdotal. | detailed_description: Old text framed benefits for 'those seeking increased caloric intake' (advice) with no source. | mechanism_of_action: Old text called it 'preferred for bulking' (advice) and claimed gastric motility effects without a source. | evidence_level: Blend takes the minimum across components. Vendors sell the no-DAC form (Mod GRF 1-29), which is preclinical with no literature of its own (decision 5, batch 01). | recommended_dose: Decision 11; per-component amounts from the 1:1 vial. | dosing_notes: Human doses quoted verbatim (decision 10); side effects moved to side_effects. | common_vial_sizes: Vendor sells 10 mg (5/5 mg). | clinical_studies: Old bullets uncited. PubMed searched for CJC-1295 or Mod GRF with GHRP-6: none. | amino_acid_sequence: Null for blends. | half_life: Old GHRP-6 '15-60 min' contradicted by the human PK study. | bioavailability: Old 'high' unsupported. | side_effects: Added FDA status; old 'gynecomastia over time' unsourced. | stacks_with: Old value was a string ('Ipamorelin'). No published combination (decision 14). | alternative_names: Added vendor names that state the no-DAC form.","sources":[{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"},{"url":"https://api.fda.gov/drug/drugsfda.json","note":"openFDA Drugs@FDA sweep (decision 61): no application found for the blend name or its alternative names"},{"url":"https://www.corepeptides.com/peptides/cjc-1295-ghrp-6-10mg-blend/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/2108187/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9661645/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/7962295/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6714155/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16989643/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15817669/","note":"evidence_level"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23099431/","note":"bioavailability"}],"data_version":2,"slug":"cjc-1295-ghrp-6-blend","url":"https://peptidelabs.app/peptides/cjc-1295-ghrp-6-blend/"},{"id":94,"name":"CJC-1295 + Ipamorelin Blend","description":"Vial blend of CJC-1295 without DAC (Mod GRF 1-29) and ipamorelin, sold as 10 mg (5 mg each); the two act on separate GH-releasing receptors, and no study has tested the pair.","benefits":"GH pulse after IV ipamorelin (human PK study); GH release by Mod GRF 1-29 inferred from related GHRH analogs; body-composition, sleep and recovery claims untested for the blend or either component","categories":["growth hormone","muscle growth","blend"],"recommended_dose":"200 to 500 mcg of blend per injection (100 to 250 mcg of each at the 5 mg/5 mg ratio), 1 to 3x daily: vendor/community range, no published human dose of the blend or of Mod GRF 1-29","detailed_description":"Both catalog vendors sell this as CJC-1295 without DAC, also called Mod GRF 1-29, mixed 5 mg/5 mg with ipamorelin. That is a different molecule from CJC-1295 with DAC, which lasts days; Mod GRF 1-29 has no published study of its own, and its D-Ala2 substitution only extends the half-time of GHRH(1-29) to about 7 min in men (Soule 1994). Ipamorelin released GH without raising cortisol in swine (Raun 1998) and has one human PK study and one negative phase 2 trial in postoperative ileus (Beck 2014). GHRH and GHRP-class peptides act synergistically on GH release in men (Bowers 1990), the rationale for pairing them, but no study has tested this blend. FDA lists ipamorelin in category 2 for 503B outsourcing and CJC-1295 in the withdrawn-nomination table of its compounding safety-risk page.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":[],"dose_min_mcg":200,"dose_max_mcg":500,"dose_unit":"mcg","dose_frequency":"1-3x daily","recon_volume_ml":2,"common_vial_sizes":[10],"dosing_notes":"Subcutaneous in community use, usually fasted or at bedtime; neither timing has been compared in a study of this blend. Human ipamorelin doses were IV and weight-based: 4 to 140 nmol/kg over 15 min (about 3 to 100 mcg/kg) in the PK study and 0.03 mg/kg twice daily in the ileus trial. No human dose of Mod GRF 1-29 has been published. The 5 days on, 2 days off pattern is community convention.","mechanism_of_action":"Proposed, from component and class studies. Mod GRF 1-29 is a tetrasubstituted GHRH(1-29) analog that binds the GHRH receptor on pituitary somatotrophs; its D-Ala2 change blocks cleavage between residues 2 and 3 in plasma, but its activity has not been measured directly. Ipamorelin is a pentapeptide agonist of the ghrelin receptor (GHS-R1a); in swine it released GH with GHRP-6-like potency without raising ACTH or cortisol (Raun 1998). In men, GHRH(1-44) given with GHRP-6 produced a GH response larger than either alone (Bowers 1990), which is the basis for pairing the two receptor pathways. The older claims of 2 to 5 times greater GH release and of a 'cleanest' stack have no published source for this blend.","clinical_studies":["D-Ala2 substitution, one of Mod GRF 1-29's four changes, raised the plasma half-time of GHRH(1-29) from 4.3 to 6.7 min in 10 normal men (Soule et al., 1994)","Ipamorelin released GH with GHRP-6-like potency but without ACTH or cortisol rise in swine (Raun et al., 1998)","IV ipamorelin in 40 healthy men: dose-proportional PK, 2 h terminal half-life, single GH peak at 40 min (Gobburu et al., 1999)","Phase 2 RCT of IV ipamorelin in postoperative ileus (n=114): well tolerated, no efficacy difference from placebo (Beck et al., 2014)","Human-trial status: no study has tested the blend as sold, and none has tested Mod GRF 1-29 itself. GHRH(1-44) plus GHRP-6 was synergistic for GH release in men (Bowers et al., 1990); CJC-1295 with DAC, a different molecule, raised GH and IGF-1 for days in phase 1/2 trials (Teichman et al., 2006)"],"evidence_level":"preclinical","references":[{"title":"Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men","authors":"Soule S, King JA, Millar RP","journal":"Journal of Clinical Endocrinology & Metabolism","year":1994,"doi":"10.1210/jcem.79.4.7962295","pmid":"7962295"},{"title":"In vitro stability of growth hormone releasing factor (GRF) analogs in porcine plasma","authors":"Su CM, Jensen LR, Heimer EP, Felix AM, Pan YC, Mowles TF","journal":"Hormone and Metabolic Research","year":1991,"doi":"10.1055/s-2007-1003601","pmid":"1826667"},{"title":"Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog","authors":"Jette L, Leger R, Thibaudeau K, et al.","journal":"Endocrinology","year":2005,"doi":"10.1210/en.2004-1286","pmid":"15817669"},{"title":"Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults","authors":"Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA","journal":"Journal of Clinical Endocrinology & Metabolism","year":2006,"doi":"10.1210/jc.2005-1536","pmid":"16352683"},{"title":"Ipamorelin, the first selective growth hormone secretagogue","authors":"Raun K, Hansen BS, Johansen NL, et al.","journal":"European Journal of Endocrinology","year":1998,"doi":"10.1530/eje.0.1390552","pmid":"9849822"},{"title":"Pharmacokinetic-pharmacodynamic modeling of ipamorelin, a growth hormone releasing peptide, in human volunteers","authors":"Gobburu JV, Agerso H, Jusko WJ, Ynddal L","journal":"Pharmaceutical Research","year":1999,"doi":"10.1023/a:1018955126402","pmid":"10496658"},{"title":"Prospective, randomized, controlled, proof-of-concept study of the Ghrelin mimetic ipamorelin for the management of postoperative ileus in bowel resection patients","authors":"Beck DE, Sweeney WB, McCarter MD; Ipamorelin 201 Study Group","journal":"International Journal of Colorectal Disease","year":2014,"doi":"10.1007/s00384-014-2030-8","pmid":"25331030","url":"https://clinicaltrials.gov/study/NCT00672074"},{"title":"Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone","authors":"Bowers CY, Reynolds GA, Durham D, Barrera CM, Pezzoli SS, Thorner MO","journal":"Journal of Clinical Endocrinology & Metabolism","year":1990,"doi":"10.1210/jcem-70-4-975","pmid":"2108187"}],"molecular_weight":null,"amino_acid_sequence":null,"alternative_names":["CJC/Ipa","GH Stack","Gold Standard GH Blend","Mod GRF 1-29 + Ipamorelin","CJC-1295 no DAC + Ipamorelin"],"half_life":"Mod GRF 1-29 not measured; D-Ala2-GHRH(1-29) ~6.7 min (human, IV). Ipamorelin ~2 h terminal (human, IV). The ~30 min figure for Mod GRF is community lore","bioavailability":"Not measured for either component by subcutaneous injection; human ipamorelin data are IV. No data for the blend","side_effects":"No human safety study of the blend or of Mod GRF 1-29 has been published. IV ipamorelin was well tolerated in a 114-patient phase 2 trial (Beck 2014). Commonly reported by users (anecdotal): injection-site reactions, flushing, head rush, water retention and joint aches; reduced insulin sensitivity and carpal tunnel symptoms are reported with sustained GH elevation. Ipamorelin is in category 2 of FDA's 503B interim policy (added 2023-09-29), and ipamorelin and CJC-1295 are in the withdrawn-nomination table for 503A, as of 2026-04-22: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks. FDA cites serious adverse events with CJC-1295, including increased heart rate and a systemic vasodilatory reaction.","last_reviewed_at":"2026-10-06T08:17:46.265Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Blend: molecular_weight and amino_acid_sequence null by design. Dose numbers are vendor/community per decision 11; no human dose of the blend exists. recon_volume_ml is the vendor/community value, not checked. CJC-1295 form is no DAC per both vendor product descriptions. | description: Vendors specify the no-DAC form; old text did not say which CJC-1295. | benefits: Old 'muscle growth, fat loss' had no source for either component. | detailed_description: Old text called it the 'gold standard' and claimed improved body composition and sleep with no source. | mechanism_of_action: Old text claimed 2 to 5x GH release with no source. | evidence_level: Blend takes the minimum across components. Vendors sell the no-DAC form (Mod GRF 1-29), which is preclinical with no literature of its own (decision 5, batch 01). | recommended_dose: Decision 11; per-component amounts from the 1:1 vial. | dosing_notes: Decisions 10 and 53: human doses quoted verbatim, molar dose with mass equivalent (ipamorelin 711.9 Da). Side-effect text moved to side_effects. | common_vial_sizes: Both vendors sell 10 mg (5/5 mg); no 5 mg blend found. | clinical_studies: Old bullets uncited and called ipamorelin 'cleanest'. PubMed searched for CJC-1295 or Mod GRF with ipamorelin: reviews and doping-analysis papers only. | amino_acid_sequence: Null for blends. | half_life: Old text also gave the DAC half-life; vendors sell no-DAC. Values per batch 01. | bioavailability: Old 'high for both' unsupported. | side_effects: Added FDA 503A/503B status (decision 32); removed 'periodic glucose monitoring is sensible' (advice). | stacks_with: Old value was a string ('GHRP-2, GHRP-6'). No published combination or documented protocol adds a second GHRP to this blend (decision 14). | alternative_names: Added the vendor names that state the no-DAC form.","sources":[{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"},{"url":"https://api.fda.gov/drug/drugsfda.json","note":"openFDA Drugs@FDA sweep (decision 61): no application found for the blend name or its alternative names"},{"url":"https://www.corepeptides.com/peptides/cjc-1295-ipamorelin-10mg-blend/","note":"alternative_names"},{"url":"https://ameanopeptides.com/product/cjc-no-dac-ipamorelin-blend-5mg-5mg/","note":"common_vial_sizes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/10496658/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/7962295/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9849822/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/25331030/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/2108187/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1826667/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15817669/","note":"evidence_level"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16352683/","note":"clinical_studies"}],"data_version":2,"slug":"cjc-1295-ipamorelin-blend","url":"https://peptidelabs.app/peptides/cjc-1295-ipamorelin-blend/"},{"id":154,"name":"CJC-1295 no DAC (Mod GRF 1-29)","description":"Tetrasubstituted GHRH(1-29) analog ([D-Ala2, Gln8, Ala15, Leu27]), the peptide part of CJC-1295 without its albumin-binding linker; no published study of this exact peptide, each substitution characterized separately.","benefits":"GH release expected from GHRH(1-29) pharmacology (no study of the exact peptide), DPP-IV resistance from D-Ala2 (porcine plasma; human PK of D-Ala2-GHRH(1-29)), higher receptor affinity from Ala15 (in vitro), reduced Asn8 deamidation from Gln8 (in vitro)","categories":["growth hormone","muscle growth"],"recommended_dose":"No human data for this peptide; research-community range 100-300 mcg SC per injection, 1-3x daily","detailed_description":"'Mod GRF 1-29' is a community name for [D-Ala2, Gln8, Ala15, Leu27]-GHRH(1-29)-NH2, the GHRH portion of CJC-1295 without its C-terminal maleimide-lysine linker (Jette 2005). 'CJC-1295 no DAC' is a vendor coinage. No peer-reviewed study of this exact peptide was found. The substitutions are each characterized separately: D-Ala2 blocks dipeptidyl peptidase IV cleavage between residues 2 and 3 (Su 1991, porcine plasma) and raised the plasma half-time of GHRH(1-29) from 4.3 to 6.7 min in men (Soule 1994); Ala15 raises GHRH-receptor affinity 4-5 fold in vitro (Campbell 1991); replacing Asn8 removes the main deamidation site that degrades GHRH analogs in solution (Friedman 1991); Leu27 replaces oxidation-prone Met27. Human data on the related peptide come only from the DAC conjugate (Teichman 2006). Evidence level is preclinical.","storage_temp":"Refrigerated (2-8°C)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"24+ months at room temperature","stacks_with":["Ipamorelin","GHRP-6","GHRP-2"],"dose_min_mcg":100,"dose_max_mcg":300,"dose_unit":"mcg","dose_frequency":"1-3x daily","recon_volume_ml":2,"common_vial_sizes":[2,5],"dosing_notes":"Subcutaneous in research use. The D-Ala2 substitution extends the plasma half-time of GHRH(1-29) only to about 7 min in men (Soule 1994), so each injection produces a single short GH pulse. GHRH plus GHRP synergy is documented in men for GHRH(1-44) with GHRP-6 (Bowers 1990), not for this peptide specifically.","mechanism_of_action":"Acts at the pituitary GHRH receptor like the parent GHRH(1-29). The four substitutions address GHRH's instability: D-Ala2 prevents dipeptidyl peptidase IV from removing the N-terminal dipeptide, the step that inactivates GHRH within minutes (Su 1991); Gln8 removes the asparagine whose deamidation degrades GHRH analogs in neutral solution (Friedman 1991); Ala15 increases receptor affinity by stabilizing the amphiphilic helix (Campbell 1991); Leu27 replaces an oxidizable methionine. In CJC-1295 this same peptide, with a linker added, activates the GHRH receptor while albumin-bound (Jette 2005). Synergy with GHRPs, which act through GHS-R1a, is documented for GHRH itself (Bowers 1990); the '2-3x' figure in the old record had no source.","clinical_studies":["No peer-reviewed study of this exact peptide was located (PubMed and Crossref searched October 2026)","D-Ala2 substitution reduced metabolic clearance of GHRH(1-29) and raised its plasma half-time from 4.3 to 6.7 min in 10 normal men (Soule et al., 1994)","D-Ala2 completely prevented cleavage between residues 2 and 3 in porcine plasma; Ala15 alone gave a small gain (Su et al., 1991)","Ala15-substituted GHRH(1-29) analogs bound the GHRH receptor 4-5x more tightly in vitro (Campbell et al., 1991)","The same tetrasubstituted peptide plus a maleimide-lysine linker is CJC-1295, which raised GH and IGF-1 for days in humans (Jette et al., 2005; Teichman et al., 2006)","Human-trial status: none for this peptide; evidence is in vitro and animal work on the individual substitutions"],"evidence_level":"preclinical","references":[{"title":"Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog","authors":"Jette L, Leger R, Thibaudeau K, et al.","journal":"Endocrinology","year":2005,"doi":"10.1210/en.2004-1286","pmid":"15817669"},{"title":"Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men","authors":"Soule S, King JA, Millar RP","journal":"Journal of Clinical Endocrinology & Metabolism","year":1994,"doi":"10.1210/jcem.79.4.7962295","pmid":"7962295"},{"title":"GRF analogs and fragments: correlation between receptor binding, activity and structure","authors":"Campbell RM, Lee Y, Rivier J, Heimer EP, Felix AM, Mowles TF","journal":"Peptides","year":1991,"doi":"10.1016/0196-9781(91)90103-v","pmid":"1656403"},{"title":"In vitro stability of growth hormone releasing factor (GRF) analogs in porcine plasma","authors":"Su CM, Jensen LR, Heimer EP, Felix AM, Pan YC, Mowles TF","journal":"Hormone and Metabolic Research","year":1991,"doi":"10.1055/s-2007-1003601","pmid":"1826667"},{"title":"Degradation of growth hormone releasing factor analogs in neutral aqueous solution is related to deamidation of asparagine residues. Replacement of asparagine residues by serine stabilizes","authors":"Friedman AR, Ichhpurani AK, Brown DM, et al.","journal":"International Journal of Peptide and Protein Research","year":1991,"doi":"10.1111/j.1399-3011.1991.tb00727.x","pmid":"1904406"},{"title":"Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults","authors":"Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA","journal":"Journal of Clinical Endocrinology & Metabolism","year":2006,"doi":"10.1210/jc.2005-1536","pmid":"16352683"},{"title":"Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone","authors":"Bowers CY, Reynolds GA, Durham D, Barrera CM, Pezzoli SS, Thorner MO","journal":"Journal of Clinical Endocrinology & Metabolism","year":1990,"doi":"10.1210/jcem-70-4-975","pmid":"2108187"},{"title":"Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency","authors":"Prakash A, Goa KL","journal":"BioDrugs","year":1999,"doi":"10.2165/00063030-199912020-00007","pmid":"18031173"}],"molecular_weight":3367.9,"amino_acid_sequence":"Y[D-A]DAIFTQSYRKVLAQLSARKLLQDILSR[NH2]","alternative_names":["Mod GRF 1-29","Modified GRF","CJC-1295 without DAC","tetrasubstituted GRF(1-29)"],"half_life":"Not reported for this exact peptide; D-Ala2-GHRH(1-29) ~6.7 min (human, IV infusion; Soule 1994). The ~30 min figure is community lore","bioavailability":null,"side_effects":"No safety data exist for this exact peptide. For GHRH(1-29) itself, transient facial flushing and injection-site pain were the common trial adverse events (Prakash 1999). Head rush, water retention, joint aches and reduced insulin sensitivity are commonly reported (anecdotal).","last_reviewed_at":"2026-10-06T08:17:26.138Z","reviewed_by":"audit-2026-10","review_notes":"description: The ~30 min half-life has no source; no PK of this peptide exists. | benefits: Anti-aging, fat loss, sleep and recovery have no source. | detailed_description: States what is and is not known about the exact compound. | recommended_dose: Marks the range as community per style guide. | dosing_notes: Removes advice phrasing. | mechanism_of_action: Removes the ~30 min half-life and 'maintains GH axis sensitivity' claims. Old value omitted for length. | clinical_studies: Old bullets were community lore ('extensive community data'). | half_life: Closest primary measurement. | bioavailability: No data for this peptide. | side_effects: Anecdote labeled. | amino_acid_sequence: One-letter format; substitutions per the CJC-1295 literature.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/16132413","note":"sermorelin MW 3357.9 used as the base for the substitution arithmetic"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3093533/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18031173/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15817669/","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/7962295/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1656403/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1904406/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1826667/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16352683/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/2108187/","note":"mechanism_of_action"}],"data_version":2,"slug":"cjc-1295-no-dac-mod-grf-1-29","url":"https://peptidelabs.app/peptides/cjc-1295-no-dac-mod-grf-1-29/"},{"id":77,"name":"Cortagen","description":"Khavinson-series synthetic tetrapeptide (AEDP) designed from the brain extract Cortexin; studied in rats for sciatic nerve regeneration and in rodent brain for antioxidant effects.","benefits":"Faster sciatic nerve fiber regrowth and conduction (rat), lower lipid peroxidation in brain and serum (rat), gene expression changes in heart (mouse)","categories":["bioregulator","cognitive","neuroprotection"],"recommended_dose":"200 to 1000 mcg daily in 10 to 20 day courses: vendor/community range, no published human dose. Rats received 10 mcg/kg intramuscularly","detailed_description":"Cortagen (also spelled Korthagen) is a synthetic tetrapeptide (AEDP, Ala-Glu-Asp-Pro) made by the St. Petersburg Institute of Bioregulation and Gerontology from the amino acid make-up of Cortexin, a brain cortex peptide drug (Anisimov 2004). In rats with a cut and sutured sciatic nerve, 10 mcg/kg intramuscularly for 10 days raised regrowth rate by 27% and conduction velocity by 40% (Turchaninova 2000). It lowered lipid peroxidation in rat brain and serum (Kozina 2007) and sped recovery of behavior in rats with chronic brain ischemia (Zarubina 2011). One paper says it aided human nerve recovery, but no human study is indexed.","storage_temp":"Room temperature","shelf_life_reconstituted":null,"shelf_life_powder":"24+ months","stacks_with":[],"dose_min_mcg":200,"dose_max_mcg":1000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Sold as oral capsules and as lyophilized powder for injection. The nerve study gave 10 mcg/kg intramuscularly daily for 10 days in rats (Turchaninova 2000). Community protocols run 10 to 20 day courses two or three times a year; no study compared schedules.","mechanism_of_action":"Proposed. In mouse heart, five daily injections changed expression of 110 known genes out of 15,247 transcripts screened (up to 5.4 fold up, 2.9 fold down) (Anisimov 2004). In rats it lowered lipid peroxidation products and oxidative protein modification in serum and cortex (Kozina 2007). Blood-brain barrier passage has not been measured; the old claim that it enters neurons and regulates synaptic genes has no published source.","clinical_studies":["At 10 mcg/kg intramuscularly for 10 days after sciatic nerve transection, nerve fiber growth rate rose 27% and conduction velocity 40% in rats (Turchaninova et al., 2000)","Five daily injections changed expression of 110 known genes in mouse heart by cDNA microarray (Anisimov et al., 2004)","Lowered lipid peroxidation products and oxidative protein modification in rat serum and cerebral cortex (Kozina et al., 2007)","Sped recovery of behavior and limited lipid peroxidation in rats with chronic brain ischemia (Zarubina et al., 2011)","Human-trial status: no indexed human study; a 2004 paper states it aided human peripheral nerve recovery without giving data"],"evidence_level":"preclinical","references":[{"title":"Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers","authors":"Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, et al.","journal":"International Journal of Molecular Sciences","year":2022,"doi":"10.3390/ijms23147733","pmid":"35887081"},{"title":"Elucidation of the effect of brain cortex tetrapeptide Cortagen on gene expression in mouse heart by microarray","authors":"Anisimov SV, Khavinson VKh, Anisimov VN","journal":"Neuro Endocrinology Letters","year":2004,"pmid":"15159690"},{"title":"Effect of tetrapeptide cortagen on regeneration of sciatic nerve","authors":"Turchaninova LN, Kolosova LI, Malinin VV, Moiseeva AB, et al.","journal":"Bulletin of Experimental Biology and Medicine","year":2000,"pmid":"11276314"},{"title":"Effects of bioactive tetrapeptides on free-radical processes","authors":"Kozina LS","journal":"Bulletin of Experimental Biology and Medicine","year":2007,"doi":"10.1007/s10517-007-0230-8","pmid":"18239817"},{"title":"Cortexin and cortagen as correcting agents in functional and metabolic disorders in the brain in chronic ischemia (in Russian)","authors":"Zarubina IV, Shabanov PD","journal":"Eksperimental'naia i Klinicheskaia Farmakologiia","year":2011,"pmid":"21476278"}],"molecular_weight":430.41,"amino_acid_sequence":"AEDP (Ala-Glu-Asp-Pro)","alternative_names":["Korthagen","AEDP","Ala-Glu-Asp-Pro"],"half_life":"No published pharmacokinetic data in any species","bioavailability":"Not measured in any species; brain penetration not tested","side_effects":"No controlled safety study has been published in any species, and the animal and cell studies, almost all from the developing institute, were not designed to detect harm. Commonly reported (anecdotal): injection-site irritation with injectable forms; oral capsules draw few complaints.","last_reviewed_at":"2026-10-06T08:17:39.536Z","reviewed_by":"audit-2026-10","review_notes":"storage: not verified against a CoA. Molecular weight 430.41 matches PubChem CID 18439621 (name 'Cortagen', 430.4). Dose range is vendor/community. | description: Old text named cognitive decline, which no paper found supports. | benefits: Tiers added; cognitive claim removed. | detailed_description: Old text claimed cognitive enhancement with no source. | mechanism_of_action: Old text asserted BBB penetration and synaptic gene regulation with no source. | clinical_studies: Old bullets described human cognitive outcomes with no source. | amino_acid_sequence: Format only. | alternative_names: Korthagen is the spelling in Khavinson 2022. 'Cortex-4' appears in no paper found. | recommended_dose: Decision 11: no published human dose exists, so the numeric range is labelled vendor/community and the change is low confidence. | dosing_notes: Adds the one published dose verbatim. | half_life: No measurement exists. | bioavailability: Old text claimed CNS activity after oral use without a source. | side_effects: Removes advice phrasing and the unsourced 'minimal adverse effects' claim. | stacks_with: Decisions 14 and 30: no published combination and no established community protocol found for the old entries.","sources":[{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC9323678/","note":"identity: Khavinson 2022 Table 2 maps product names to sequences and lists the patents behind several tissue claims"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/18439621/property/MolecularFormula,MolecularWeight/JSON","note":"molecular weight 430.4, C17H26N4O9"},{"url":"https://pubmed.ncbi.nlm.nih.gov/12134478/","note":"Kolosova 2002, delayed effect on nerve function (no abstract)"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15159690/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11276314/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18239817/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/21476278/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/35887081/","note":"stacks_with"}],"data_version":2,"slug":"cortagen","url":"https://peptidelabs.app/peptides/cortagen/"},{"id":103,"name":"Decapeptide-12","description":"Synthetic decapeptide (YRSRKYSSWY, Lumixyl) that competitively inhibits tyrosinase in vitro; a 5-person split-face placebo-controlled pilot and open-label studies report lighter melasma.","benefits":"Melasma lightening (split-face RCT, n=5; open-label, n=33), photodamage pigment clearance (open-label, n=13), tyrosinase inhibition and lower melanocyte melanin (in vitro)","categories":["cosmetic","skin health"],"recommended_dose":"Topical, 0.01% (w/w) cream in all published human studies. No oral or injectable dose exists.","detailed_description":"Decapeptide-12 came from an oligopeptide library screened by Hantash's group for tyrosinase inhibitors that are not toxic to melanocytes; the 10-residue hit inhibited mushroom tyrosinase with an IC50 of 40 microM (hydroquinone 680 microM) and cut melanocyte melanin 43% over 7 days (Abu Ubeid et al., 2009). It is sold as Lumixyl. Human data: a split-face, double-blind, placebo-controlled pilot in five women with melasma at 0.01% twice daily for 16 weeks (Hantash and Jimenez, 2009), then open-label studies of a regimen pairing it with 20% glycolic acid and sunscreen (Kassim et al., 2012; Ramírez et al., 2013). Most studies come from the developer.","storage_temp":"Room temperature, away from light","shelf_life_reconstituted":"N/A (ready to use)","shelf_life_powder":"2 years at room temp","stacks_with":[],"dose_min_mcg":null,"dose_max_mcg":null,"dose_unit":null,"dose_frequency":"2x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Topical cream applied to pigmented areas. Studies ran 16 to 24 weeks; most paired it with glycolic acid and sunscreen, so effects of the peptide alone come only from the five-person pilot.","mechanism_of_action":"Competitive inhibition of tyrosinase. In kinetic studies the decapeptide competitively inhibited mushroom tyrosinase (IC50 40 microM) and at 100 microM inhibited human tyrosinase by 25 to 35%, with substrate-dependent results suggesting two catalytic sites. Melanin in cultured human melanocytes fell 43% after 7 days without effects on proliferation or viability (Abu Ubeid et al., 2009). Claims of action at multiple steps of melanogenesis or superiority to hydroquinone in people have no published head-to-head data.","clinical_studies":["Inhibited mushroom tyrosinase (IC50 40 microM vs 680 microM for hydroquinone) and lowered melanocyte melanin 43% without cytotoxicity (Abu Ubeid et al., 2009)","Split-face, double-blind, placebo-controlled pilot: 0.01% twice daily for 16 weeks in five women with recalcitrant melasma, all improved, no irritation (Hantash and Jimenez, 2009)","Open-label, 33 Hispanic women: a 0.01% cream plus 20% glycolic acid and sunscreen lowered MASI scores 60% by week 16 (Ramírez et al., 2013)","Open-label, 13 women with photodamage pigment: 38.5% reached complete clearance at 24 weeks on the same regimen (Kassim et al., 2012)","Human-trial status: one randomized placebo-controlled pilot (n=5); other studies are open-label multi-product regimens, mostly from the developer's group"],"evidence_level":"clinical","references":[{"title":"Short-sequence oligopeptides with inhibitory activity against mushroom and human tyrosinase","authors":"Abu Ubeid A, Zhao L, Wang Y, Hantash BM","journal":"The Journal of investigative dermatology","year":2009,"doi":"10.1038/jid.2009.124","pmid":"19440221"},{"title":"A split-face, double-blind, randomized and placebo-controlled pilot evaluation of a novel oligopeptide for the treatment of recalcitrant melasma","authors":"Hantash BM, Jimenez F","journal":"Journal of drugs in dermatology : JDD","year":2009,"pmid":"19663110"},{"title":"Treatment of mild to moderate facial melasma with the Lumixyl topical brightening system","authors":"Hantash BM, Jimenez F","journal":"Journal of drugs in dermatology : JDD","year":2012,"pmid":"22527440"},{"title":"Open-label evaluation of the skin-brightening efficacy of a skin-brightening system using decapeptide-12","authors":"Kassim AT, Hussain M, Goldberg DJ","journal":"Journal of cosmetic and laser therapy : official publication of the European Society for Laser Dermatology","year":2012,"doi":"10.3109/14764172.2012.672745","pmid":"22401652"},{"title":"Open-label evaluation of a novel skin brightening system containing 0.01% decapeptide-12 in combination with 20% buffered glycolic acid for the treatment of mild to moderate facial melasma","authors":"Ramírez SP, Carvajal AC, Salazar JC, Arroyave G, et al.","journal":"Journal of drugs in dermatology : JDD","year":2013,"pmid":"23839199"},{"title":"Combined topical delivery and dermalinfusion of decapeptide-12 accelerates resolution of post-inflammatory hyperpigmentation in skin of color","authors":"Bhatia A, Hsu JTs, Hantash BM","journal":"Journal of drugs in dermatology : JDD","year":2014,"pmid":"24385124"}],"molecular_weight":1395.54,"amino_acid_sequence":"YRSRKYSSWY (Tyr-Arg-Ser-Arg-Lys-Tyr-Ser-Ser-Trp-Tyr)","alternative_names":["Lumixyl","Lumixyl peptide","YRSRKYSSWY"],"half_life":"No published pharmacokinetic data in any species","bioavailability":"Not measured in any species; skin penetration of decapeptide-12 has not been published","side_effects":"No irritation or allergy in the five-person RCT (Hantash and Jimenez, 2009) and no adverse events in the 33-person open-label study (Ramírez et al., 2013). No cytotoxicity to cultured melanocytes at 100 microM (Abu Ubeid et al., 2009). Commonly reported (anecdotal): dryness or redness, mostly attributed to the glycolic acid in combined regimens.","last_reviewed_at":"2026-10-06T08:17:42.883Z","reviewed_by":"audit-2026-10","review_notes":"N/A-by-design: topical. dose_min_mcg/dose_max_mcg stay null because a concentration in a formulation cannot be written as mcg per dose (decision 2). storage: not verified against a CoA. | description: Adds sequence and trial sizes. | benefits: Each item now carries its tier. | detailed_description: Old text was generic and called the sequence proprietary. Old value omitted for length. | mechanism_of_action: Old text claimed high-affinity active-site binding and superiority to hydroquinone and kojic acid without sources. | clinical_studies: Old bullets included an unsourced Stanford patent claim and comparisons to hydroquinone. | recommended_dose: Published concentration. | dose_frequency: Twice daily in the RCT. | dosing_notes: Field was empty. | half_life: Nothing measured. | bioavailability: Old claim had no source. | side_effects: Removes advice phrasing; adds sourced tolerability. | molecular_weight: PubChem CID 25087629 (synonyms Decapeptide-12, Lumixyl, CAS 137665-91-9): C65H90N18O17, 1395.5. Residue arithmetic for YRSRKYSSWY reproduces the formula: 1395.54. | amino_acid_sequence: Decision 31: read from the PubChem systematic name for CID 25087629 and confirmed by reproducing its formula. The 2009 paper abstract does not print the sequence. | alternative_names: 'Tyrosinase inhibitor peptide' is a description, not a name. | stacks_with: Decisions 14 and 30: the published combinations are with glycolic acid and sunscreen, not catalog peptides.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/25087629","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/30666274/","note":"Jiang 2018 multi-ingredient night cream RCT; decapeptide-12 content not stated in abstract, not cited"},{"url":"https://pubmed.ncbi.nlm.nih.gov/19440221/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/19663110/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23839199/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22401652/","note":"dosing_notes"}],"data_version":2,"slug":"decapeptide-12","url":"https://peptidelabs.app/peptides/decapeptide-12/"},{"id":27,"name":"Dihexa","description":"Angiotensin IV-derived peptide analog; rodent studies report memory rescue in some models, but the founding papers for its HGF/c-Met mechanism were retracted in 2025.","benefits":"Memory rescue in some rodent models (mixed results; one rat model showed no protection)","categories":["cognitive","neuroprotection"],"recommended_dose":"10-30 mcg daily (oral) - no established human dose","detailed_description":"Dihexa is a small modified peptide derived from angiotensin IV, developed as a procognitive agent. Two of the developer group's foundational papers, which proposed HGF/c-Met activation and synaptogenesis, were retracted in April 2025, and a third (McCoy 2013) has carried an expression of concern since 2021. Independent rodent studies are mixed: memory rescue in APP/PS1 mice and after repeated mild brain injury, no protection in a rat Huntington-like model. There are no human trials. Its clinical successor, fosgonimeton, failed a phase 2/3 Alzheimer's trial.","storage_temp":"Room temperature, away from light","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"12+ months","stacks_with":["Semax","Selank"],"dose_min_mcg":10,"dose_max_mcg":30,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[10,20],"dosing_notes":"No published human dose. Earlier potency claims trace to papers retracted in 2025.","mechanism_of_action":"Proposed. The HGF/c-Met mechanism and the claim of potency about 10 million times that of BDNF come from papers retracted in April 2025 (notices PMID 40312092 and 40312093) and are not treated as established. McCoy et al., 2013 described dihexa as a metabolically stabilized angiotensin IV analog; that paper has an expression of concern. Independent work reported memory rescue in APP/PS1 mice with PI3K/AKT pathway changes (Sun et al., 2021) and rescue of working memory after repeated mild traumatic brain injury in rodents (Martino et al., 2025).","clinical_studies":["Metabolically stabilized angiotensin IV analogs including dihexa were procognitive in rodent dementia models (McCoy et al., 2013); the paper has carried an expression of concern since 2021","Dihexa rescued cognitive impairment in APP/PS1 mice, with PI3K/AKT signalling changes (Sun et al., 2021)","Dihexa did not protect against 3-nitropropionic acid-induced Huntington-like symptoms in rats (Wells et al., 2024)","An HGF/MET activator rescued working memory deficits after repeated mild traumatic brain injury in rodents (Martino et al., 2025)","Two foundational papers from the developer group were retracted in April 2025 (notices PMID 40312092 and 40312093)","Human-trial status: none for dihexa. Its successor compound fosgonimeton failed the LIFT-AD phase 2/3 trial in mild-to-moderate Alzheimer's disease, NCT04488419 (Porsteinsson et al., 2025)"],"evidence_level":"preclinical","references":[{"title":"Evaluation of metabolically stabilized angiotensin IV analogs as procognitive/antidementia agents","authors":"McCoy AT, Benoist CC, Wright JW, et al.","journal":"The Journal of Pharmacology and Experimental Therapeutics","year":2013,"doi":"10.1124/jpet.112.199497","pmid":"23055539"},{"title":"AngIV-Analog Dihexa Rescues Cognitive Impairment and Recovers Memory in the APP/PS1 Mouse via the PI3K/AKT Signaling Pathway","authors":"Sun X, Deng Y, Fu X, et al.","journal":"Brain Sciences","year":2021,"doi":"10.3390/brainsci11111487","pmid":"34827486"},{"title":"Effects of an Angiotensin IV Analog on 3-Nitropropionic Acid-Induced Huntington's Disease-Like Symptoms in Rats","authors":"Wells RG, Azzam AF, Hiller AL, et al.","journal":"Journal of Huntington's Disease","year":2024,"doi":"10.3233/JHD-231507","pmid":"38489193"},{"title":"Hepatocyte Growth Factor/MET Activator Rescues Working Memory Deficits after Repeated Mild Traumatic Brain Injury","authors":"Martino KA, Nakhre A, Demarest RM, et al.","journal":"Neurotrauma Reports","year":2025,"doi":"10.1177/2689288X251392851","pmid":"42825082"},{"title":"Fosgonimeton in mild-to-moderate Alzheimer's disease","authors":"Porsteinsson AP, Sabbagh M, Tariot PN, et al.","journal":"Journal of Alzheimer's Disease Reports","year":2025,"doi":"10.1177/25424823251405817","pmid":"41393340"},{"title":"Retraction notice to \"Development of Angiotensin IV Analogs as Hepatocyte Growth Factor/Met Modifiers\" [J Pharmacol Exp Ther 340 (2012) 539-548","authors":"Kawas LH, McCoy AT, Yamamoto BJ, et al.","journal":"The Journal of Pharmacology and Experimental Therapeutics","year":2025,"doi":"10.1016/j.jpet.2025.103566","pmid":"40312092"},{"title":"Retraction notice to \"The Procognitive and Synaptogenic Effects of Angiotensin IV-Derived Peptides Are Dependent on Activation of the Hepatocyte Growth Factor/c-Met System\" [J Pharmacol Exp Ther 351 (2014) 390-402","authors":"Benoist CC, Kawas LH, Zhu M, et al.","journal":"The Journal of Pharmacology and Experimental Therapeutics","year":2025,"doi":"10.1016/j.jpet.2025.103567","pmid":"40312093"}],"molecular_weight":504.7,"amino_acid_sequence":"N-hexanoyl-Tyr-Ile-(6)-aminohexanoic amide (modified dipeptide)","alternative_names":["PNB-0408"],"half_life":"Not established in humans; no half-life verified from non-retracted sources","bioavailability":"Not measured in humans. Oral and subcutaneous activity claims come from the original developer group, whose foundational papers were retracted","side_effects":"No human safety data. The proposed mechanism is HGF/c-Met activation, a pathway linked to tumor growth, so a theoretical concern about existing tumors has been raised; the papers that established that mechanism are retracted. Commonly reported (anecdotal): headache, irritability.","last_reviewed_at":"2026-10-06T08:26:26.454Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Retraction documented per decision 22. | description: Decision 22: the headline claim (HGF/c-Met activator driving synaptogenesis) rests on Kawas 2012 and Benoist 2014, both retracted April 2025. | benefits: Synaptogenesis came from the retracted papers. Independent work is mixed (Wells 2024 did not protect). | detailed_description: Old text claimed potency \"billions of times\" that of BDNF, which traces to the retracted lineage (decision 22). | mechanism_of_action: Old text stated the retracted mechanism and the 10-million-fold figure as fact, plus unsourced BBB and oral bioavailability claims. | clinical_studies: Old bullets were unsourced and included \"Extremely potent, microdose ranges used\", which rests on retracted work. | molecular_weight: PubChem CID 129010512 gives 504.7 Da (C27H44N4O5). | half_life: Old value had no species or source. | bioavailability: \"Oral: Good\" had no verified source. | side_effects: Old text stated HGF/c-Met activation as fact. | dosing_notes: \"Very potent\" is the retracted potency claim. Removed; no dose content added. | alternative_names: \"HGF activator\" is a mechanism description resting on retracted work, not a name.","sources":[{"url":"https://doi.org/10.1124/jpet.111.188136","note":"Kawas 2012, retracted (Crossref update: retraction; notice 10.1016/j.jpet.2025.103566)"},{"url":"https://doi.org/10.1124/jpet.114.218735","note":"Benoist 2014, retracted (notice 10.1016/j.jpet.2025.103567)"},{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/129010512","note":"molecular_weight"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40312092/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40312093/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/34827486/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42825082/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/38489193/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23055539/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/41393340/","note":"clinical_studies"},{"url":"https://clinicaltrials.gov/study/NCT04488419","note":"clinical_studies"}],"data_version":2,"slug":"dihexa","url":"https://peptidelabs.app/peptides/dihexa/"},{"id":22,"name":"DSIP","description":"Endogenous nonapeptide first isolated from rabbit brain; older, small human studies looked at sleep onset, stress-axis normalization and chronic pain.","benefits":"Improved sleep quality, stress reduction, recovery","categories":["sleep"],"recommended_dose":"100 to 200 mcg before sleep (community range; human trials used 25 to 30 nmol/kg intravenously, about 1.5 to 2 mg for a 70 kg adult)","detailed_description":"DSIP is a nonapeptide isolated in 1977 from rabbit cerebral venous blood, named for the delta electroencephalogram enhancement it produced on intraventricular infusion (Schoenenberger and Monnier, 1977). Human work is small, intravenous and four decades old: double-blind studies in chronic insomniacs reported sleep normalisation and better daytime performance (Schneider-Helmert, 1986), while a controlled parallel-group trial found the effects weak and concluded short-term treatment was unlikely to help much (Bes et al., 1992). An open pilot reported lower pain scores in 7 patients with chronic pain (Larbig et al., 1984). No DSIP gene, precursor or receptor has been identified, and a review by researchers in the field treats the sleep hypothesis as unresolved (Kovalzon and Strekalova, 2006). Measured half-life is minutes.","storage_temp":"Refrigerated (2-8°C)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"24+ months at room temperature","stacks_with":["Epithalon"],"dose_min_mcg":100,"dose_max_mcg":200,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[5],"dosing_notes":"Human studies used intravenous dosing only: 25 nmol/kg before three nights (Bes et al., 1992) and 30 nmol/kg for 6 doses over a week (Schneider-Helmert, 1986), with slow injection described as necessary (Schneider-Helmert and Schoenenberger, 1983). Those doses are about 1.5 to 2 mg for a 70 kg adult, roughly ten times the 100 to 200 mcg subcutaneous range used in the research community, which no study has tested. Measured half-life is minutes in dog, monkey and rat, and the peptide is degraded in blood (Kato et al., 1984). One small study used the intranasal route (PMID 11763019).","mechanism_of_action":"DSIP is the nonapeptide Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu, isolated in 1977 from cerebral venous blood of rabbits whose electroencephalogram showed delta enhancement after intraventricular infusion (Schoenenberger and Monnier, 1977). No DSIP gene, precursor protein or receptor has ever been identified, which is why its own reviewers call the sleep-factor hypothesis poorly documented and propose that the activity belongs to an unidentified DSIP-like peptide (Kovalzon and Strekalova, 2006). Reported actions in rodents include effects on glutamate and GABA receptor currents in cortex, hippocampus and cerebellum, and anticonvulsant activity. Blood-brain barrier passage has been measured in guinea pig and dog preparations. The peptide is degraded rapidly in blood, with tryptophan-containing fragments appearing within minutes.","clinical_studies":["Isolated from rabbit cerebral venous blood; intraventricular infusion enhanced delta and spindle electroencephalogram patterns in 58 rabbits, and five fragments and two analogs did not (Schoenenberger and Monnier, 1977)","Five double-blind human studies with single and repeated intravenous dosing reported sleep normalisation in insomniacs plus higher daytime alertness; slow injection was described as essential (Schneider-Helmert and Schoenenberger, 1983)","One week of intravenous dosing in 18 chronic insomniacs (6 doses at 30 nmol/kg) improved sleep toward normal values, with the effect tracking baseline severity (Schneider-Helmert, 1986)","A double-blind parallel-group trial in 16 chronic insomniacs (25 nmol/kg intravenously before three nights) found higher sleep efficiency and shorter latency, but the authors judged the effects weak and partly attributable to a shift in the placebo group (Bes et al., 1992)","An open pilot in 7 patients with chronic pain episodes reported lower pain scores after intravenous dosing on 5 consecutive days then every 48 to 72 hours (Larbig et al., 1984)","Human-trial status: the human work is small, 1980s and intravenous, with one controlled trial reporting little therapeutic benefit. No modern trial, no approval anywhere, and the field's own review calls the link between DSIP and sleep unresolved (Kovalzon and Strekalova, 2006)"],"evidence_level":"clinical","references":[{"title":"Characterization of a delta-electroencephalogram (-sleep)-inducing peptide","authors":"Schoenenberger GA, Monnier M","journal":"Proceedings of the National Academy of Sciences","year":1977,"doi":"10.1073/pnas.74.3.1282","pmid":"265572"},{"title":"Delta-sleep-inducing peptide (DSIP): a review","authors":"Graf MV, Kastin AJ","journal":"Neuroscience and Biobehavioral Reviews","year":1984,"doi":"10.1016/0149-7634(84)90022-8","pmid":"6145137"},{"title":"Effects of DSIP in man. Multifunctional psychophysiological properties besides induction of natural sleep","authors":"Schneider-Helmert D, Schoenenberger GA","journal":"Neuropsychobiology","year":1983,"doi":"10.1159/000117964","pmid":"6689058"},{"title":"Efficacy of DSIP to normalize sleep in middle-aged and elderly chronic insomniacs","authors":"Schneider-Helmert D","journal":"European Neurology","year":1986,"doi":"10.1159/000116050","pmid":"3792404"},{"title":"Effects of delta sleep-inducing peptide on sleep of chronic insomniac patients. A double-blind study","authors":"Bes F, Hofman W, Schuur J, Van Boxtel C","journal":"Neuropsychobiology","year":1992,"doi":"10.1159/000118919","pmid":"1299794"},{"title":"Development of an enzyme immunoassay for delta sleep-inducing peptide (DSIP) and its use in the determination of the metabolic clearance rate of DSIP administered to dogs","authors":"Kato N, Honda Y, Ebihara S, Naruse H, Takahashi Y","journal":"Neuroendocrinology","year":1984,"doi":"10.1159/000123952","pmid":"6379493"},{"title":"Delta sleep-inducing peptide (DSIP): a still unresolved riddle","authors":"Kovalzon VM, Strekalova TV","journal":"Journal of Neurochemistry","year":2006,"doi":"10.1111/j.1471-4159.2006.03693.x","pmid":"16539679"},{"title":"Therapeutic effects of delta-sleep-inducing peptide (DSIP) in patients with chronic, pronounced pain episodes. A clinical pilot study","authors":"Larbig W, Gerber WD, Kluck M, Schoenenberger GA","journal":"European Neurology","year":1984,"doi":"10.1159/000115716","pmid":"6548970"}],"molecular_weight":848.81,"amino_acid_sequence":"Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu","alternative_names":["Delta sleep-inducing peptide","Deltaran (Russian preparation)"],"half_life":"~4.0 min (dog, IV; clearance 30.7 mL/kg/min), 2.9 min in a monkey and ~2.0 min in rats (Kato et al., 1984); no human figure published","bioavailability":"No bioavailability figure published for any route. Blood-brain barrier passage was measured in perfused guinea pig brain and in dog cerebrospinal fluid; intravenous peptide is degraded in blood within minutes (Kato et al., 1984).","side_effects":"Reported effects are limited to injection-site irritation, headache, and next-day grogginess. Human data comes from a handful of small studies, so the safety profile is not well characterized.","last_reviewed_at":"2026-10-06T08:17:36.165Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Reference DOI corrected (the cited Graf and Kastin review has a different DOI and title). Half-life replaced with the measured animal values. Dose range left at the community figure with the trial dose in dosing_notes per decision 10. Contested sleep-factor status named per decision 19. | half_life: The only measured half-lives are in dogs, a monkey and rats, and they are about five times shorter than the record's figure. Degradation in blood is what clears it (Graf et al., 1987). | mechanism_of_action: Old text asserted delta-sleep promotion by cortical synchronisation, circadian and HPA normalisation, blood pressure and temperature regulation and antioxidant properties as established mechanism, for a peptide with no known receptor. Decision 19: the dispute is now named. Old value omitted for length. | clinical_studies: Old bullets claimed increased delta activity in human studies, cortisol reduction, opioid and alcohol withdrawal benefit and minimal next-day sedation, none cited. The cortisol claim is contradicted: DSIP did not affect CRH-stimulated or meal-stimulated ACTH and cortisol in healthy men (PMID 7777652). | detailed_description: Old text stated sleep architecture, stress reduction and cortisol normalisation as demonstrated. Old value omitted for length. | recommended_dose: Decision 10: the published human dose is weight-based and roughly tenfold above the community figure, so it is stated rather than converted into the numeric fields. | dosing_notes: Replaces a restatement of the name with the published routes, doses and the gap against community practice. | bioavailability: 'Intranasal also effective' rested on one small P300 study, and no route has a measured bioavailability. | evidence_level: Kept: double-blind placebo-controlled human trials in insomnia exist, which meets decision 4. But they are small, from the 1980s, intravenous, and the best-controlled one was close to null, so this is the weakest 'clinical' in the batc","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/68816","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/7777652/","note":"DSIP did not affect CRH-stimulated or meal-induced ACTH and cortisol in healthy men"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11763019/","note":"intranasal DSIP increased P300 in a small study"},{"url":"https://pubmed.ncbi.nlm.nih.gov/2547200/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3628078/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6379493/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/265572/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16539679/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6689058/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3792404/","note":"dose_frequency"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1299794/","note":"evidence_level"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6548970/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18975104/","note":"alternative_names"}],"data_version":2,"slug":"dsip","url":"https://peptidelabs.app/peptides/dsip/"},{"id":14,"name":"Epithalon","description":"Synthetic tetrapeptide Ala-Glu-Asp-Gly (PubChem CID 219042); human cell cultures show telomerase induction, and in mice it raised maximum but not mean lifespan.","benefits":"Telomerase induction and telomere elongation (human fibroblasts in vitro), extra population doublings in senescing human cells (in vitro), raised maximum lifespan and 6-fold fewer leukemias (mouse), melatonin rhythm normalization (reported for the bovine pineal extract, not the peptide)","categories":["anti-aging","sleep"],"recommended_dose":"5 to 10 mg daily for 10 to 20 days: research-community range, no published human dose-finding study","detailed_description":"Epitalon (AEDG) is a synthetic tetrapeptide designed from the amino acid composition of Epithalamin, a bovine pineal gland extract, and later reported in pineal polypeptide complex. The headline findings are in cell culture: added to telomerase-negative human fetal fibroblasts it induced hTERT expression, telomerase activity and telomere elongation (Khavinson 2003), and senescing fibroblasts made about 10 extra passages past the Hayflick limit (Khavinson 2004). An independent 2025 group reproduced dose-dependent telomere lengthening in normal human cells and found ALT activation in cancer lines (Al-Dulaimi 2025). In mice given 1 mcg per animal on 5 days a month for life, mean lifespan did not change (Anisimov 2003). No controlled trial of the synthetic peptide has been published; the long-term human studies used the bovine extract.","storage_temp":"Refrigerated (2-8°C)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"24+ months at room temperature","stacks_with":["DSIP"],"dose_min_mcg":5000,"dose_max_mcg":10000,"dose_unit":"mcg","dose_frequency":"Daily (10-20 day cycle)","recon_volume_ml":2,"common_vial_sizes":[10,50],"dosing_notes":"Subcutaneous or intramuscular in research use; intranasal and intramuscular routes were both used in rodent studies. Cycling of 10 to 20 days, 2 to 3 times a year, is community convention with no published basis. Mouse geroprotection studies used 1 mcg per animal, roughly 30 to 40 mcg/kg, on 5 consecutive days each month for life (Anisimov 2003), which is a different schedule from any human protocol.","mechanism_of_action":"Proposed mechanisms, all from cell culture and rodent work. In telomerase-negative human fibroblasts AEDG induced expression of the telomerase catalytic subunit and measurable telomerase activity, with telomere elongation (Khavinson 2003); a 2025 independent replication found the same in normal cells through hTERT upregulation, and separately ALT activation in breast cancer lines (Al-Dulaimi 2025). Molecular modelling and binding work from the same group proposes direct interaction of short peptides with DNA promoter regions and with LAT and PEPT family transporters for cell entry; neither is established. Effects on melatonin are not settled: perifused rat pineal glands showed no change in melatonin secretion at 10 to the minus 4 through 10 to the minus 6 M (Djeridane 2003), while the extract studies in elderly subjects report rhythm normalization.","clinical_studies":["Induced telomerase catalytic subunit expression, telomerase activity and telomere elongation in telomerase-negative human fetal fibroblasts (Khavinson et al., 2003)","Senescing human fetal lung fibroblasts treated at passage 34 elongated their telomeres and completed about 10 further passages, past the Hayflick limit (Khavinson et al., 2004)","Independent replication in 2025: dose-dependent telomere lengthening through hTERT and telomerase upregulation in normal human cells, and ALT activation in breast cancer lines (Al-Dulaimi et al., 2025)","In female SHR mice dosed for life, mean lifespan and total tumor incidence did not change; the last decile of survivors gained 13.3%, maximum lifespan 12.3%, bone marrow chromosome aberrations fell 17.1% and leukemia incidence was 6-fold lower (Anisimov et al., 2003)","Perifused pineal glands from young and old rats showed no change in melatonin secretion at any tested concentration, with or without isoproterenol (Djeridane et al., 2003)","Human-trial status: no controlled trial of the synthetic tetrapeptide has been published and none is registered on ClinicalTrials.gov. Human exposure data are limited to in vitro work on donor lymphocytes; the 12-year randomized geroprotection study in elderly coronary patients used Epithalamin, the bovine pineal extract, not AEDG (Korkushko et al., 2006)"],"evidence_level":"preclinical","references":[{"title":"Epithalon peptide induces telomerase activity and telomere elongation in human somatic cells","authors":"Khavinson VKh, Bondarev IE, Butyugov AA","journal":"Bulletin of Experimental Biology and Medicine","year":2003,"doi":"10.1023/a:1025493705728","pmid":"12937682"},{"title":"Peptide promotes overcoming of the division limit in human somatic cell","authors":"Khavinson VKh, Bondarev IE, Butyugov AA, Smirnova TD","journal":"Bulletin of Experimental Biology and Medicine","year":2004,"doi":"10.1023/b:bebm.0000038164.49947.8c","pmid":"15455129"},{"title":"Epitalon increases telomere length in human cell lines through telomerase upregulation or ALT activity","authors":"Al-Dulaimi S, Thomas R, Matta S, Roberts T","journal":"Biogerontology","year":2025,"doi":"10.1007/s10522-025-10315-x","pmid":"40908429"},{"title":"Effect of Epitalon on biomarkers of aging, life span and spontaneous tumor incidence in female Swiss-derived SHR mice","authors":"Anisimov VN, Khavinson VKh, Popovich IG, Zabezhinski MA, et al.","journal":"Biogerontology","year":2003,"doi":"10.1023/a:1025114230714","pmid":"14501183"},{"title":"Inhibitory effect of the peptide epitalon on the development of spontaneous mammary tumors in HER-2/neu transgenic mice","authors":"Anisimov VN, Khavinson VK, Provinciali M, Alimova IN, et al.","journal":"International Journal of Cancer","year":2002,"doi":"10.1002/ijc.10570","pmid":"12209581"},{"title":"Effect of a synthetic pineal tetrapeptide (Ala-Glu-Asp-Gly) on melatonin secretion by the pineal gland of young and old rats","authors":"Djeridane Y, Khavinson VKh, Anisimov VN, Touitou Y","journal":"Journal of Endocrinological Investigation","year":2003,"doi":"10.1007/BF03345159","pmid":"12809170"},{"title":"Overview of Epitalon: Highly Bioactive Pineal Tetrapeptide with Promising Properties","authors":"Araj SK, Brzezik J, Madra-Gackowska K, Szeleszczuk L","journal":"International Journal of Molecular Sciences","year":2025,"doi":"10.3390/ijms26062691","pmid":"40141333"},{"title":"Geroprotective effect of epithalamine (pineal gland peptide preparation) in elderly subjects with accelerated aging","authors":"Korkushko OV, Khavinson VKh, Shatilo VB, Antonyuk-Shcheglova IA","journal":"Bulletin of Experimental Biology and Medicine","year":2006,"doi":"10.1007/s10517-006-0365-z","pmid":"17426848"}],"molecular_weight":390.35,"amino_acid_sequence":"AEDG","alternative_names":["Epitalon","Epithalone","AEDG peptide","Ala-Glu-Asp-Gly"],"half_life":"No pharmacokinetic study in any species has been published; the 2025 review of 25 years of Epitalon research reports no absorption, distribution or elimination data","bioavailability":"Not measured in any species. Rodent studies dosed intramuscularly and intranasally and reported central effects by both routes, with onset at 24 h intramuscularly and 1.5 h intranasally","side_effects":"No controlled safety study of the synthetic peptide exists in any species at human-relevant doses. Lifelong dosing in mice produced no change in food consumption, body weight or total tumor incidence, and the authors described long-term administration as well tolerated in that model (Anisimov 2003). The randomized human studies reporting no adverse effects used Epithalamin, the bovine pineal extract. Commonly reported by users: injection-site irritation. One 2015 regulatory analysis identified AEDG in two illegal pharmaceutical preparations, so product identity and purity are a practical risk.","last_reviewed_at":"2026-10-06T08:17:37.850Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Dose range is community convention, no published human dose. Molecular weight and sequence confirmed against PubChem CID 219042 by formula arithmetic. Epithalamin extract evidence is separated from AEDG evidence throughout. | description: The old wording implied a lifespan effect in general. Anisimov 2003 found no change in mean lifespan; only the last decile (+13.3%) and maximum lifespan (+12.3%) moved. | benefits: Each item now carries its model system. Sleep and immune claims had no compound-specific source; the melatonin work is on Epithalamin, a bovine pineal extract, which is a different substance. | detailed_description: Old text asserted improvements in sleep quality and neuroendocrine function with no model system and no source. Rewritten from the primary papers. Old value omitted for length. | mechanism_of_action: Old text asserted melatonin stimulation, HPG axis modulation, antioxidant enzyme induction and epigenetic gene regulation as settled. The direct rat pineal experiment was negative, and that is now stated. Old value omitted for length. | recommended_dose: Decision 11. No published human dose of the synthetic peptide exists, so the field now says the range is community convention. | dosing_notes: Decision 10: the published animal dose is weight-based and stays in text. The cycling schedule is labelled as convention. | clinical_studies: Old bullets cited a 13% mouse lifespan gain that the paper does not support, an Anisimov 2002 human study that does not exist, and Korkushko 2006 as if it tested the peptide. The negative rat melatonin result was missing entirely. | half_life: The 2 to 4 hour figure has no source. A full-text read of the 2025 review found no PK section for this peptide. | bioavailability: \"High\" subcutaneous availability has no source. Replaced with what the literature actually shows. | side_effects: Old text attributed safety to \"the small Russian clinical series\", which tested the extract, not the peptide","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/219042/property/MolecularFormula,MolecularWeight,IUPACName/JSON","note":"identity and molecular weight 390.35, C14H22N4O9, for AEDG"},{"url":"https://clinicaltrials.gov/api/v2/studies?query.term=Epitalon","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/25535022/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/31761987/","note":"Khavinson 2019, AEDG on telomere length in donor lymphocytes in vitro, n=11"},{"url":"https://pubmed.ncbi.nlm.nih.gov/41240216/","note":"correction notice for Al-Dulaimi 2025"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/219042/property/MolecularFormula,MolecularWeight/JSON","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/12937682/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/14501183/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15455129/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17426848/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40908429/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40141333/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/12809170/","note":"clinical_studies"}],"data_version":2,"slug":"epithalon","url":"https://peptidelabs.app/peptides/epithalon/"},{"id":38,"name":"FGL-S","description":"Peptide mimetic of neural cell adhesion molecule (NCAM) defined in patent filings; one published study tested it in rats and monkeys, and the memory literature belongs to its parent FGL.","benefits":"Cognitive support, nerve regeneration","categories":["cognitive","neuroprotection"],"recommended_dose":"Vendor/community range 500 to 2000 mcg daily; no published human dose for FGL-S.","detailed_description":"FGL-S is a peptide mimetic of NCAM whose structure is defined in a patent family from ENKAM rather than in a peer-reviewed paper. It appears in one published study, which measured pharmacokinetics and emotional behavior for several NCAM mimetics in rats and non-human primates. The memory, FGFR1 and neuroprotection literature in circulation is for FGL, the parent 15-residue peptide, and the human phase 1 study was of FGL-L, a different peptide. No human data exist for FGL-S.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["Semax","Selank"],"dose_min_mcg":500,"dose_max_mcg":2000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[10],"dosing_notes":"Subcutaneous per vendors. The only human dosing data belong to the related FGL-L: single intranasal doses of 25, 100 and 200 mg in 24 healthy men (Anand 2007). They do not establish a dose for FGL-S.","mechanism_of_action":"Proposed by analogy: the parent FGL peptide mimics the NCAM fibronectin type III module that binds fibroblast growth factor receptor 1, and FGL-S is assumed to share that action. No mechanism study of FGL-S itself is published. The only FGL-S paper measured pharmacokinetics and emotional behavior in rats and non-human primates (Turner et al., 2019).","clinical_studies":["FGL-S was tested with other NCAM peptide mimetics for pharmacokinetics and emotional behavior in rats and non-human primates (Turner et al., 2019)","The structure of FGL-S is defined in ENKAM patent filings, not in a peer-reviewed paper","Rodent memory, LTP and neuroprotection findings in circulation used the parent FGL peptide, not FGL-S","Human-trial status: none for FGL-S. A different NCAM mimetic, FGL-L (FGLL), was given intranasally at 25 to 200 mg to healthy volunteers in a phase 1 tolerability and pharmacokinetic study (Anand et al., 2007)"],"evidence_level":"anecdotal","references":[{"title":"Neural cell adhesion molecule peptide mimetics modulate emotionality: pharmacokinetic and behavioral studies in rats and non-human primates","authors":"Turner CA, Lyons DM, Buckmaster CL, et al.","journal":"Neuropsychopharmacology","year":2019,"doi":"10.1038/s41386-018-0052-6","pmid":"29703997"},{"title":"Tolerability, safety and pharmacokinetics of the FGLL peptide, a novel mimetic of neural cell adhesion molecule, following intranasal administration in healthy volunteers","authors":"Anand R, Seiberling M, Kamtchoua T, et al.","journal":"Clinical Pharmacokinetics","year":2007,"doi":"10.2165/00003088-200746040-00007","pmid":"17375985"}],"molecular_weight":null,"amino_acid_sequence":null,"alternative_names":null,"half_life":"No human data. Rat and primate pharmacokinetics were reported for NCAM mimetics (Turner et al., 2019); an FGL-S value was not extracted in this audit","bioavailability":"Not established in humans; no published bioavailability figure for FGL-S","side_effects":"No human safety data; effects unknown beyond animal studies, where FGL peptides were tolerated in rodents at the doses tested. The exact identity of material sold under this name is unclear in the literature, which adds product risk.","last_reviewed_at":"2026-10-06T08:27:09.211Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Identity from patent only (decision 27). | description: Old text attributed the parent FGL's FGFR1 and rodent memory findings to FGL-S. | detailed_description: Decisions 26 and 27: identity from a patent; analog data stated as analog data. | mechanism_of_action: Decision 56: analog data named in the first sentence. Old text called FGL-S a shorter variant designed for stability and CNS penetration, which no source supports. | clinical_studies: The old \"Phase 1 studies completed showing safety\" bullet belongs to FGL-L (decision 26). | evidence_level: Decision 27: identity from a patent only caps the exact compound at anecdotal, even with the one animal paper. | amino_acid_sequence: This is the parent FGL 15-mer, not FGL-S. FGL-S has no published sequence (decision 27). | molecular_weight: 1780.9 matches neither compound. PubChem gives 1649.8 for the parent FGL (CID 16200289); FGL-S has no published structure. | half_life: Old value had no source or species. | bioavailability: Neither claim had a source. | alternative_names: \"FG Loop peptide\" is the parent FGL's name and \"NCAM mimetic\" is a class. | Dose-field follow-up for batch 07 (decisions 11, 24, 25, 26). | recommended_dose: Decision 11. | dosing_notes: Decision 26: analog trial named as the analog.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/16200289","note":"molecular_weight"},{"url":"https://pubmed.ncbi.nlm.nih.gov/29703997/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17375985/","note":"dosing_notes"}],"data_version":3,"slug":"fgl-s","url":"https://peptidelabs.app/peptides/fgl-s/"},{"id":39,"name":"Follistatin-315","description":"Mature circulating form of follistatin (315 residues), a glycoprotein that binds activin strongly and myostatin weakly; muscle-mass gains come from transgenic and gene-transfer animals, not injected protein.","benefits":"Muscle mass and strength in transgenic mice and after AAV gene transfer (rodent, >2 years of effect); activin and myostatin neutralisation in vitro. No study of injected follistatin protein in any species and no human data.","categories":["muscle growth"],"recommended_dose":"No dosing data in any species; research-community range 100 to 300 mcg daily in 10 to 30 day cycles","detailed_description":"Follistatin is an activin-binding glycoprotein. The FST gene makes two precursors by alternative splicing, 344 and 317 residues (Shimasaki 1988); after the signal peptide is removed these give the mature proteins FS315 and FS288. FS315 is the circulating form, with low affinity for cell-surface heparan sulfate, while the shorter FS288 sticks to cell surfaces (Sugino 1993). Follistatin binds activin A with high affinity and myostatin and GDF-11 considerably more weakly (Schneyer 2008). Transgenic mice over-expressing follistatin in muscle gained mass comparable to myostatin-knockout mice (Lee and McPherron 2001), and one AAV injection of follistatin raised muscle mass and strength in normal and dystrophic mice for over two years (Haidet 2008). No study has injected follistatin protein as a drug, in animals or humans.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["IGF-1 LR3","MGF (IGF-1 Ec)"],"dose_min_mcg":100,"dose_max_mcg":300,"dose_unit":"mcg","dose_frequency":"1x daily for 10-30 days","recon_volume_ml":1,"common_vial_sizes":[1],"dosing_notes":"Short cycles. Very expensive. No human dosing data exists. Systemic activin blockade also suppresses FSH and affects reproductive signalling; research-grade material is frequently mislabeled or biologically inactive.","mechanism_of_action":"Follistatin binds TGF-beta superfamily ligands and blocks them from reaching activin type II receptors. Affinity is not uniform: it binds activin A tightly and myostatin (GDF-8) and GDF-11 much less so, which is why follistatin-based muscle effects come with activin-pathway effects such as FSH suppression (Schneyer 2008; Sugino 1993). FS315 is the mature secreted form with four EGF-like domains and little heparan-sulfate affinity, so it circulates rather than concentrating on cell surfaces (Shimasaki 1988; Sugino 1993). Blocking myostatin signaling through ActRIIB removes a brake on muscle growth: transgenic muscle-specific follistatin expression produced dramatic muscle-mass increases in mice, matching myostatin knockouts (Lee and McPherron 2001).","clinical_studies":["Transgenic mice expressing follistatin under a skeletal-muscle promoter showed muscle-mass increases comparable to myostatin-knockout mice (Lee and McPherron, 2001)","A single AAV administration of follistatin or other myostatin inhibitors increased muscle mass and strength in normal and dystrophic mice for more than two years, including in aged animals (Haidet et al., 2008)","Follistatin binds activin A with much higher affinity than myostatin or GDF-11, so activin-pathway effects are inseparable from the muscle effect (Schneyer et al., 2008)","The FST gene yields 344- and 317-residue precursors by alternative splicing, giving the mature FS315 and FS288 proteins (Shimasaki et al., 1988)","FS288, the carboxy-terminal truncated form, binds granulosa-cell heparan sulfate proteoglycans far more tightly than FS315, which is why FS315 is the circulating species (Sugino et al., 1993)","Human-trial status: none for injected follistatin protein. The only human data are AAV1-FS344 gene-therapy trials (see Follistatin-344)"],"evidence_level":"preclinical","references":[{"title":"Primary structure of the human follistatin precursor and its genomic organization","authors":"Shimasaki S, Koga M, Esch F, et al.","journal":"Proceedings of the National Academy of Sciences","year":1988,"doi":"10.1073/pnas.85.12.4218","pmid":"3380788"},{"title":"Molecular heterogeneity of follistatin, an activin-binding protein. Higher affinity of the carboxyl-terminal truncated forms for heparan sulfate proteoglycans on the ovarian granulosa cell","authors":"Sugino K, Kurosawa N, Nakamura T, et al.","journal":"Journal of Biological Chemistry","year":1993,"doi":"10.1016/s0021-9258(18)82296-7","pmid":"8340384"},{"title":"Differential antagonism of activin, myostatin and growth and differentiation factor 11 by wild-type and mutant follistatin","authors":"Schneyer AL, Sidis Y, Gulati A, et al.","journal":"Endocrinology","year":2008,"doi":"10.1210/en.2008-0259","pmid":"18535106"},{"title":"Regulation of myostatin activity and muscle growth","authors":"Lee SJ, McPherron AC","journal":"Proceedings of the National Academy of Sciences","year":2001,"doi":"10.1073/pnas.151270098","pmid":"11459935"},{"title":"Long-term enhancement of skeletal muscle mass and strength by single gene administration of myostatin inhibitors","authors":"Haidet AM, Rizo L, Handy C, et al.","journal":"Proceedings of the National Academy of Sciences","year":2008,"doi":"10.1073/pnas.0709144105","pmid":"18334646"},{"title":"Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: Results of a randomized, placebo-controlled clinical trial","authors":"Campbell C, McMillan HJ, Mah JK, et al.","journal":"Muscle & Nerve","year":2017,"doi":"10.1002/mus.25268","pmid":"27462804"}],"molecular_weight":34754.3,"amino_acid_sequence":null,"alternative_names":["FS315","Follistatin short form","Circulating follistatin"],"half_life":"Not measured for injected follistatin in any species","bioavailability":null,"side_effects":"No human or animal safety data exist for injected follistatin protein. Follistatin binds activin A much more tightly than myostatin (Schneyer 2008), and activin blockade affects FSH secretion and, in other drugs of this pathway, vascular integrity: ACE-031, a different activin-receptor blocker, was stopped in trials for nosebleeds and telangiectasia (Campbell 2017). Most research-grade material is E. coli-derived and may be inactive or endotoxin-bearing, which is the more immediate practical risk.","last_reviewed_at":"2026-10-06T08:17:34.498Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. No study of injected follistatin protein exists in any species; all evidence is transgenic, gene-transfer or in vitro. | description: Follistatin's affinity for activin is far higher than for myostatin or GDF-11 (Schneyer 2008), and the muscle data are genetic, not injection. | benefits: Separates what the gene-therapy evidence shows from what an injected peptide product can claim. | detailed_description: Old text was the same generic paragraph used for Follistatin-344 with no model systems. Old value omitted for length. | recommended_dose: Marks the range as community per the style guide. No injected-protein study exists to compare it with. | mechanism_of_action: Old text implied equal neutralisation of activin and myostatin. Old value omitted for length. | clinical_studies: Old bullets included 'research compound - used in bodybuilding community' and 'very expensive and limited availability', which are not studies. | molecular_weight: Average mass of UniProt P19883 residues 30-344 (the 315-residue mature chain), unglycosylated. Native follistatin is glycosylated and runs higher on a gel, which is where the 36 kDa figure comes from. | amino_acid_sequence: A 315-residue chain does not fit a sequence field; the description is not a sequence. UniProt P19883 residues 30-344 is the authoritative source. | half_life: 'Hours to days (glycoprotein)' is a guess from the molecule class, not a measurement. | bioavailability: No study of injected follistatin protein exists, so there is no bioavailability to report. | side_effects: Gives the pathway-level safety concern a resolvable citation instead of leaving it as 'theoretical'.","sources":[{"url":"https://rest.uniprot.org/uniprotkb/P19883.fasta","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3380788/","note":"molecular_weight"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18535106/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11459935/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18334646/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/8340384/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/27462804/","note":"side_effects"}],"data_version":2,"slug":"follistatin-315","url":"https://peptidelabs.app/peptides/follistatin-315/"},{"id":40,"name":"Follistatin-344","description":"The 344-residue follistatin precursor, which yields mature circulating follistatin (FS315) after its signal peptide is cut; the human evidence is AAV1-FS344 gene therapy delivering the gene, not an injected protein.","benefits":"Improved 6-minute walk distance after AAV1-FS344 gene therapy in small open-label trials (Becker muscular dystrophy n=6, sporadic inclusion body myositis n=6, both contested); muscle mass and strength after AAV follistatin in mice. No injected-protein data.","categories":["muscle growth"],"recommended_dose":"No dosing data for follistatin protein in any species; research-community range 100 to 300 mcg daily in 10 to 30 day cycles. The human trials dosed an AAV vector (3 to 6 x 10^11 vg/kg per leg), not a peptide","detailed_description":"FS344 is one of two follistatin precursors produced by alternative splicing of the FST gene (344 and 317 residues); removing the 29-residue signal peptide gives mature FS315 and FS288 (Shimasaki 1988). The FS344 transcript is what gene-therapy programmes deliver: AAV1.CMV.FS344 was injected into the quadriceps of six Becker muscular dystrophy patients at 3 or 6 x 10^11 vg/kg per leg, where four of six improved 6-minute walk distance by 29 to 125 m with no adverse events (Mendell 2015; Al-Zaidy 2015), and the same vector in six sporadic inclusion body myositis patients gave a reported +56.0 m/year against -25.8 m/year in matched untreated subjects (Mendell 2017). That result was publicly disputed on grounds of control selection and open-label design (Greenberg 2017). Nothing has been injected as follistatin protein in a human study.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["IGF-1 LR3","MGF (IGF-1 Ec)"],"dose_min_mcg":100,"dose_max_mcg":300,"dose_unit":"mcg","dose_frequency":"1x daily for 10-30 days","recon_volume_ml":1,"common_vial_sizes":[1],"dosing_notes":"No human dosing data for injected follistatin protein; community protocols use short cycles. FS344 is the precursor of circulating FS315, not a tissue-retained variant. Follistatin binds activin A more tightly than myostatin, so activin-pathway effects including FSH suppression come with it (Schneyer 2008). Research-grade material is frequently mislabeled or biologically inactive.","mechanism_of_action":"FS344 is a precursor: its 29-residue signal peptide is removed to give mature 315-residue follistatin, the circulating form with low heparan-sulfate affinity (Shimasaki 1988). The shorter FS288, not FS344, is the heparin-binding form that concentrates on cell surfaces, so the idea that FS344 provides tissue-specific retention is backwards. Mature follistatin binds activin A tightly and myostatin and GDF-11 more weakly, blocking them from activin type II receptors (Schneyer 2008). Gene-therapy programmes chose the FS344 splice form specifically to reduce off-target cell-surface binding (Mendell 2015). Removing the myostatin brake on muscle growth is what produced large muscle gains in follistatin-transgenic mice (Lee and McPherron 2001).","clinical_studies":["AAV1.CMV.FS344 injected into both quadriceps of six Becker muscular dystrophy patients (3 or 6 x 10^11 vg/kg per leg): four improved 6-minute walk distance by 29 to 125 m, two did not, with reduced endomysial fibrosis on biopsy and no adverse events (Mendell et al., 2015)","Follow-up of the same cohort reported sustained ambulation gains (Al-Zaidy et al., 2015)","The same vector in six sporadic inclusion body myositis patients gave a reported +56.0 m/year on the 6-minute walk against -25.8 m/year in eight matched untreated subjects (Mendell et al., 2017)","That inclusion-body-myositis result was publicly contested over control selection and the open-label design (Greenberg, 2017)","One AAV administration of follistatin increased muscle mass and strength in normal and dystrophic mice for over two years (Haidet et al., 2008)","Human-trial status: two small open-label AAV1-FS344 gene-therapy trials, one disputed. No trial of injected follistatin protein, and no regulatory approval"],"evidence_level":"preclinical","references":[{"title":"A phase 1/2a follistatin gene therapy trial for becker muscular dystrophy","authors":"Mendell JR, Sahenk Z, Malik V, et al.","journal":"Molecular Therapy","year":2015,"doi":"10.1038/mt.2014.200","pmid":"25322757"},{"title":"Follistatin Gene Therapy Improves Ambulation in Becker Muscular Dystrophy","authors":"Al-Zaidy SA, Sahenk Z, Rodino-Klapac LR, et al.","journal":"Journal of Neuromuscular Diseases","year":2015,"doi":"10.3233/JND-150083","pmid":"27858738"},{"title":"Follistatin Gene Therapy for Sporadic Inclusion Body Myositis Improves Functional Outcomes","authors":"Mendell JR, Sahenk Z, Al-Zaidy S, et al.","journal":"Molecular Therapy","year":2017,"doi":"10.1016/j.ymthe.2017.02.015","pmid":"28279643"},{"title":"Unfounded Claims of Improved Functional Outcomes Attributed to Follistatin Gene Therapy in Inclusion Body Myositis","authors":"Greenberg SA","journal":"Molecular Therapy","year":2017,"doi":"10.1016/j.ymthe.2017.09.002","pmid":"28927986"},{"title":"Primary structure of the human follistatin precursor and its genomic organization","authors":"Shimasaki S, Koga M, Esch F, et al.","journal":"Proceedings of the National Academy of Sciences","year":1988,"doi":"10.1073/pnas.85.12.4218","pmid":"3380788"},{"title":"Long-term enhancement of skeletal muscle mass and strength by single gene administration of myostatin inhibitors","authors":"Haidet AM, Rizo L, Handy C, et al.","journal":"Proceedings of the National Academy of Sciences","year":2008,"doi":"10.1073/pnas.0709144105","pmid":"18334646"},{"title":"Differential antagonism of activin, myostatin and growth and differentiation factor 11 by wild-type and mutant follistatin","authors":"Schneyer AL, Sidis Y, Gulati A, et al.","journal":"Endocrinology","year":2008,"doi":"10.1210/en.2008-0259","pmid":"18535106"},{"title":"Regulation of myostatin activity and muscle growth","authors":"Lee SJ, McPherron AC","journal":"Proceedings of the National Academy of Sciences of the United States of America","year":2001,"doi":"10.1073/pnas.151270098","pmid":"11459935"}],"molecular_weight":38007.2,"amino_acid_sequence":null,"alternative_names":["FS344","Full-length follistatin"],"half_life":"Not measured for injected follistatin protein; the AAV gene-therapy construct produces protein for months to years (mouse, >2 years)","bioavailability":null,"side_effects":"No safety data exist for injected follistatin protein. In the AAV1-FS344 gene-therapy trials no adverse effects were reported in six Becker muscular dystrophy patients (Mendell 2015). Follistatin binds activin A much more tightly than myostatin (Schneyer 2008), and blocking this pathway with ACE-031 caused nosebleeds and telangiectasia severe enough to stop a trial in boys with Duchenne muscular dystrophy. Research-grade material is frequently inactive or mislabeled, adding contamination risk.","last_reviewed_at":"2026-10-06T08:17:34.498Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Human evidence is AAV1-FS344 gene therapy, not injected protein; evidence_level stays preclinical for the product. | description: Names what FS344 actually is and what was administered in the trials. | benefits: Ties each claim to the intervention that produced it and notes the published dispute. | detailed_description: Old text was the same generic paragraph as Follistatin-315. Old value omitted for length. | recommended_dose: Marks the range as community and makes the gene-therapy dose non-transferable. | mechanism_of_action: The old text claimed FS344 has higher heparin-binding affinity than FS315 and provides local retention. That is FS288's property, and Mendell 2015 chose FS344 for the opposite reason. Old value omitted for length. | clinical_studies: Old bullets claimed 'local intramuscular injection provides sustained myostatin inhibition' and that gene therapy was 'being developed by several companies', neither sourced. | molecular_weight: Average mass of the full 344-residue precursor (UniProt P19883), unglycosylated. If a vendor ships the mature processed protein, the correct mass is 34754.3 (same as Follistatin-315). | amino_acid_sequence: Not a sequence, and the heparin-binding claim is wrong: that is FS288. | half_life: Removes the tissue-binding claim and separates vector durability from peptide PK. | bioavailability: No injected-protein study exists, and the stated mechanism belongs to FS288. | dosing_notes: Corrects 'systemic variant' framing and sources the activin point. | side_effects: Replaces 'theoretical off-target risk' with the trial evidence that exists on both sides.","sources":[{"url":"https://rest.uniprot.org/uniprotkb/P19883.fasta","note":"amino_acid_sequence"},{"url":"https://doi.org/10.1002/mus.25268","note":"Campbell 2017: ACE-031 trial stopped for epistaxis and telangiectasias"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3380788/","note":"molecular_weight"},{"url":"https://pubmed.ncbi.nlm.nih.gov/25322757/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/28279643/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/28927986/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18334646/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/27858738/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/8340384/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18535106/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11459935/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/27462804/","note":"side_effects"}],"data_version":2,"slug":"follistatin-344","url":"https://peptidelabs.app/peptides/follistatin-344/"},{"id":41,"name":"FOXO4-DRI","description":"Cell-penetrating D-retro-inverso peptide that blocks the FOXO4-p53 interaction, shown in aged mice to selectively kill senescent cells and restore renal function and fitness.","benefits":"Selective apoptosis of senescent cells (human cells in vitro), restored fitness, fur density and renal function in fast-aging and naturally aged mice, improved testosterone output and spermatogenesis in aged mice. No human data by any route","categories":["anti-aging"],"recommended_dose":"5 to 10 mg: vendor and community range, no published human dose. Mouse studies used 5 mg/kg intravenously or intraperitoneally on alternate days","detailed_description":"FOXO4-DRI is a 46-residue all-D retro-inverso peptide, built from a FOXO4 segment plus a cationic cell-penetrating carrier, designed to block the FOXO4 interaction with p53 (Baar 2017). In that paper it killed senescent but not control IMR90 human fibroblasts, and in mice given 5 mg/kg intravenously or intraperitoneally on 3 alternate days it neutralized doxorubicin liver toxicity and restored fitness, fur density and renal markers in fast-aging XpdTTD/TTD and naturally aged animals. Later work extended it to aged mouse Leydig cells, spermatogenesis and keloid fibroblasts. One result cuts the other way: in mice and rats, clearing senescent pulmonary endothelial cells with FOXO4-DRI or ABT263 worsened pulmonary hemodynamics (Born 2023). No human study exists and none is registered.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":[],"dose_min_mcg":5000,"dose_max_mcg":10000,"dose_unit":"mcg","dose_frequency":"1x daily (short cycles)","recon_volume_ml":2,"common_vial_sizes":[5,10],"dosing_notes":"No human data by any route. The published mouse regimen was 3 doses of 5 mg/kg, intravenous or intraperitoneal, on days 1, 3 and 5, from a 5 mg/mL solution in PBS (Baar 2017), not daily subcutaneous dosing. The 5 to 10 mg figure sold to researchers is a scaled guess with no safety validation. Senolysis is not uniformly beneficial: clearing senescent pulmonary endothelial cells with this peptide worsened pulmonary hemodynamics in mice and rats (Born 2023).","mechanism_of_action":"Senescent cells keep p53 in the nucleus through an interaction with FOXO4, which blocks apoptosis. FOXO4-DRI competes for that interaction, p53 is excluded from the nucleus and cell-intrinsic apoptosis follows, selectively in senescent cells (Baar 2017). Solution NMR has since mapped the binding: FOXO4-DRI, itself disordered, binds the disordered second transactivation domain of p53 and forms a transiently folded complex, with the cationic cell-penetrating segment contributing to the interaction rather than only carrying the peptide across the membrane, and p53 phosphorylation increasing affinity for both FOXO4 and the peptide (Bourgeois 2025). The retro-inverso all-D design was chosen for protease resistance; no measurement of its stability or exposure in an animal has been published.","clinical_studies":["Killed senescent human IMR90 fibroblasts while sparing control cells, with potency increasing over consecutive rounds of treatment; in mice, 3 doses of 5 mg/kg on alternate days neutralized doxorubicin liver toxicity and restored fitness, fur density and renal markers in fast-aging and naturally aged animals (Baar et al., 2017)","In naturally aged mice, FOXO4-DRI induced apoptosis in senescent Leydig cells, reduced senescence-associated secretion and raised testosterone output (Zhang et al., 2020)","In aged mice it improved sperm quality and spermatogenesis, with reduced senescence-associated secretion from Leydig cells (Li et al., 2024)","In human chondrocytes expanded to population doubling level 9 it removed over half the cells and lowered the senescence level, but did not improve chondrogenic potential (Huang et al., 2021)","Contrary result: in SM22-5-HTT+ mice and monocrotaline rats, senolytic clearance of pulmonary endothelial cells with FOXO4-DRI or ABT263 raised right ventricular systolic pressure and worsened vessel remodeling (Born et al., 2023)","Human-trial status: no human study of FOXO4-DRI has been published and no trial is registered on ClinicalTrials.gov. The mechanism has an active commercial program (Cleara Biotech) and patents, but no clinical candidate has entered trials"],"evidence_level":"preclinical","references":[{"title":"Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging","authors":"Baar MP, Brandt RMC, Putavet DA, Klein JDD, et al.","journal":"Cell","year":2017,"doi":"10.1016/j.cell.2017.02.031","pmid":"28340339"},{"title":"The disordered p53 transactivation domain is the target of FOXO4 and the senolytic compound FOXO4-DRI","authors":"Bourgeois B, Spreitzer E, Platero-Rochart D, Paar M, et al.","journal":"Nature Communications","year":2025,"doi":"10.1038/s41467-025-60844-9","pmid":"40593617"},{"title":"FOXO4-DRI alleviates age-related testosterone secretion insufficiency by targeting senescent Leydig cells in aged mice","authors":"Zhang C, Xie Y, Chen H, Lv L, et al.","journal":"Aging (Albany NY)","year":2020,"doi":"10.18632/aging.102682","pmid":"31959736"},{"title":"FOXO4-DRI improves spermatogenesis in aged mice through reducing senescence-associated secretory phenotype secretion from Leydig cells","authors":"Li Y, Zhang C, Cheng H, Lv L, et al.","journal":"Experimental Gerontology","year":2024,"doi":"10.1016/j.exger.2024.112522","pmid":"39025385"},{"title":"Senolytic Peptide FOXO4-DRI Selectively Removes Senescent Cells From in vitro Expanded Human Chondrocytes","authors":"Huang Y, He Y, Makarcyzk MJ, Lin H","journal":"Frontiers in Bioengineering and Biotechnology","year":2021,"doi":"10.3389/fbioe.2021.677576","pmid":"33996787"},{"title":"FOXO4-DRI induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53-serine 15 phosphorylation","authors":"Kong YX, Li ZS, Liu YB, Pan B, et al.","journal":"Communications Biology","year":2025,"doi":"10.1038/s42003-025-07738-0","pmid":"39994346"},{"title":"Eliminating Senescent Cells Can Promote Pulmonary Hypertension Development and Progression","authors":"Born E, Lipskaia L, Breau M, Houssaini A, et al.","journal":"Circulation","year":2023,"doi":"10.1161/CIRCULATIONAHA.122.058794","pmid":"36515093"},{"title":"FOXO4-D-Retro-Inverso targets extracellular matrix production in fibroblasts and ameliorates bleomycin-induced pulmonary fibrosis in mice","authors":"Liu Y, Hou Q, Wang R, Liu Y, et al.","journal":"Naunyn-Schmiedeberg's Archives of Pharmacology","year":2023,"doi":"10.1007/s00210-023-02452-2","pmid":"37074394"}],"molecular_weight":5358.2,"amino_acid_sequence":"ltlrkepaseiaqsileaysqngwanrrsggkrppprrrqrrkkrg (46 residues, all D-configuration, retro-inverso; lower case denotes D-amino acids. The C-terminal krppprrrqrrkkrg segment is the cell-penetrating carrier)","alternative_names":["FOXO4-p53 interfering peptide","Senolytic peptide"],"half_life":"Not measured in any species. The all-D retro-inverso backbone was chosen to resist proteolysis, and the paper reports no pharmacokinetic data; dosing on alternate days was an empirical schedule","bioavailability":"Not measured. Published animal dosing was intravenous or intraperitoneal; no subcutaneous or oral study exists. Cell entry in vitro is carried by the cationic C-terminal segment, which also contributes to p53 binding","side_effects":"No human safety data exist. In mice the published doses were described as well tolerated, with no weight loss over the dosing window (Baar 2017). The principal published risk is not off-target apoptosis but the senolysis itself: eliminating senescent pulmonary endothelial cells worsened pulmonary hemodynamics and vessel remodeling in two rodent models (Born 2023). FDA lists several research peptides sold through the same channels on its compounding safety-risk page; FOXO4-DRI itself is not named there.","last_reviewed_at":"2026-10-06T08:17:37.850Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Sequence and molecular weight taken from the Baar 2017 methods and confirmed against PubChem CID 167312269 by formula arithmetic. Dose range is vendor convention; published dosing is weight-based mouse IV and IP. No human data by any route. | molecular_weight: The defining paper prints the sequence and MW 5358.2 in its methods. PubChem CID 167312269 (CAS 2460055-10-9) gives C228H388N86O64 at 5358, and residue arithmetic on the printed 46-residue sequence reproduces C228H388N86O64 at 5358.15. The stored 4881.5 matches no form of this peptide. | amino_acid_sequence: Printed verbatim in the Baar 2017 methods section (\"H-ltlrkepaseiaqsileaysqngwanrrsggkrppprrrqrrkkrg-OH, MW: 5358.2\"), read from the PMC full text. The field previously held a description, not a sequence. | benefits: Each item now carries its model system, and the absence of human data is stated in the field itself. | detailed_description: Old text had no doses, no species detail and no counter-evidence. Decision 19 applied to the pulmonary hypertension result. Old value omitted for length. | mechanism_of_action: Old text asserted p53 translocation to mitochondria, which the primary paper describes as nuclear exclusion, and asserted that D-amino acids confer cell penetration, which the carrier segment does. Old value omitted for length. | recommended_dose: Decisions 10 and 11. The published dose is weight-based animal dosing and must not be converted; the numeric range stays as community convention and now says so. | dosing_notes: Adds the exact published regimen and replaces the theoretical risk sentence with a published one. | clinical_studies: Old bullets attributed the kidney and in vitro results to no source and said \"proof-of-concept\", which is not a finding. The chondrocyte and pulmonary hypertension results are both relevant and were missing. | half_life: \"Extended\" was an inference from the chemistry, not a measurement. | bioavailability: Corrects the attribution of cell","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/167312269/synonyms/JSON","note":"FOXO4-DRI, CAS 2460055-10-9, C228H388N86O64, MW 5358"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5556182/","note":"Baar 2017 full text: printed sequence, MW 5358.2, 5 mg/kg on days 1, 3 and 5"},{"url":"https://clinicaltrials.gov/api/v2/studies?query.term=FOXO4-DRI","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/28340339/","note":"side_effects"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/167312269/property/MolecularFormula,MolecularWeight/JSON","note":"molecular_weight"},{"url":"https://pubmed.ncbi.nlm.nih.gov/31959736/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/39025385/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/39994346/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/36515093/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40593617/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/33996787/","note":"clinical_studies"},{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"}],"data_version":2,"slug":"foxo4-dri","url":"https://peptidelabs.app/peptides/foxo4-dri/"},{"id":97,"name":"Fragment 176-191 + Mod GRF + Ipamorelin","description":"Vial blend of a GH fragment sold as 176-191, Mod GRF 1-29 and ipamorelin (12 mg: 6/3/3 mg); fat-loss claims rest on rodent data, and no study has tested the mix.","benefits":"Reduced fat gain (rodent, related hGH fragments); GH release (human, ipamorelin IV; inferred for Mod GRF 1-29); human trials of the analog AOD9604 published only safety. No data for the blend","categories":["growth hormone","fat loss","blend"],"recommended_dose":"350 to 700 mcg of blend per injection (about 175 to 350 mcg fragment and 90 to 175 mcg each of Mod GRF 1-29 and ipamorelin at the 6/3/3 mg ratio), 1 to 2x daily: vendor/community range, no published human dose of the blend, hGH 176-191 or Mod GRF 1-29","detailed_description":"Sold as a 12 mg vial: 6 mg GH fragment, 3 mg Mod GRF 1-29 (CJC-1295 without DAC) and 3 mg ipamorelin. True hGH 176-191 starts with Phe; vendor 'Fragment 176-191' often lists the AOD9604 sequence, which starts with Tyr, so the exact fragment in a vial is uncertain. The one study of hGH 176-191 itself found a brief rise in blood glucose in rats (Ng 1978); related fragments cut fat gain in obese rodents, and six human AOD9604 trials published safety but no efficacy. Mod GRF 1-29 has no study of its own, and ipamorelin has one human PK study and a negative phase 2 ileus trial (Beck 2014). No study has tested any two of these together. FDA lists ipamorelin in category 2 for 503B outsourcing, and CJC-1295 and AOD-9604 in the withdrawn-nomination table of its compounding safety-risk page.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":null,"dose_min_mcg":350,"dose_max_mcg":700,"dose_unit":"mcg","dose_frequency":"1-2x daily","recon_volume_ml":2,"common_vial_sizes":[12],"dosing_notes":"Subcutaneous in community use, often fasted in the morning or at bedtime. The earlier statement that AOD9604 failed against placebo in 12-week trials is not supported by published data: only safety results of the AOD9604 obesity trials were published (Stier 2013). Human ipamorelin doses were IV (0.03 mg/kg twice daily in the ileus trial); no human dose of hGH 176-191 or Mod GRF 1-29 exists.","mechanism_of_action":"Proposed, from component studies. The hGH fragment is the C-terminal end of growth hormone; related fragments raised fat oxidation in obese mice without binding the hGH receptor (Heffernan 2001), while hGH 176-191 itself raised blood glucose and insulin briefly in rats (Ng 1978). Mod GRF 1-29 is a tetrasubstituted GHRH(1-29) analog acting on the pituitary GHRH receptor; its activity has not been measured directly. Ipamorelin is a ghrelin-receptor agonist that released GH without raising ACTH or cortisol in swine (Raun 1998). The idea that the fragment adds direct lipolysis to a GH pulse from the other two has not been tested.","clinical_studies":["hGH 176-191 caused a short-lived rise in blood glucose and a more sustained rise in insulin in rats (Ng and Bornstein, 1978)","Chronic treatment with the tyrosine analog AOD9604 raised fat oxidation and reduced weight in obese mice without hyperglycaemia (Heffernan et al., 2001)","Six placebo-controlled human AOD9604 trials (about 900 adults, oral or IV) found no change in IGF-1 or glucose tolerance; only safety results were published (Stier et al., 2013)","IV ipamorelin in 40 healthy men gave a single GH peak at 40 min with a 2 h terminal half-life (Gobburu et al., 1999)","D-Ala2 substitution in Mod GRF 1-29 raised the plasma half-time of GHRH(1-29) only from 4.3 to 6.7 min in men (Soule et al., 1994)","Human-trial status: no study has tested the blend as sold or any pair within it. Ipamorelin's only RCT, in postoperative ileus, was negative (Beck et al., 2014); AOD9604 human data are for that analog, not hGH 176-191"],"evidence_level":"preclinical","references":[{"title":"Hyperglycemic action of synthetic C-terminal fragments of human growth hormone","authors":"Ng FM, Bornstein J","journal":"American Journal of Physiology","year":1978,"doi":"10.1152/ajpendo.1978.234.5.E521","pmid":"645904"},{"title":"Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone or a modified C-terminal fragment","authors":"Heffernan MA, Thorburn AW, Fam B, et al.","journal":"International Journal of Obesity and Related Metabolic Disorders","year":2001,"doi":"10.1038/sj.ijo.0801740","pmid":"11673763"},{"title":"Safety and Tolerability of the Hexadecapeptide AOD9604 in Humans","authors":"Stier H, Vos E, Kenley D","journal":"Journal of Endocrinology and Metabolism","year":2013,"doi":"10.4021/jem157w"},{"title":"Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men","authors":"Soule S, King JA, Millar RP","journal":"Journal of Clinical Endocrinology & Metabolism","year":1994,"doi":"10.1210/jcem.79.4.7962295","pmid":"7962295"},{"title":"Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog","authors":"Jette L, Leger R, Thibaudeau K, et al.","journal":"Endocrinology","year":2005,"doi":"10.1210/en.2004-1286","pmid":"15817669"},{"title":"Ipamorelin, the first selective growth hormone secretagogue","authors":"Raun K, Hansen BS, Johansen NL, et al.","journal":"European Journal of Endocrinology","year":1998,"doi":"10.1530/eje.0.1390552","pmid":"9849822"},{"title":"Pharmacokinetic-pharmacodynamic modeling of ipamorelin, a growth hormone releasing peptide, in human volunteers","authors":"Gobburu JV, Agerso H, Jusko WJ, Ynddal L","journal":"Pharmaceutical Research","year":1999,"doi":"10.1023/a:1018955126402","pmid":"10496658"},{"title":"Prospective, randomized, controlled, proof-of-concept study of the Ghrelin mimetic ipamorelin for the management of postoperative ileus in bowel resection patients","authors":"Beck DE, Sweeney WB, McCarter MD; Ipamorelin 201 Study Group","journal":"International Journal of Colorectal Disease","year":2014,"doi":"10.1007/s00384-014-2030-8","pmid":"25331030","url":"https://clinicaltrials.gov/study/NCT00672074"}],"molecular_weight":null,"amino_acid_sequence":null,"alternative_names":["Fat Loss Stack","Recomp Blend","Frag/Mod/Ipa","Fragment 176-191 + CJC-1295 + Ipamorelin"],"half_life":"hGH fragment: not published. Mod GRF 1-29 not measured; D-Ala2-GHRH(1-29) ~6.7 min (human, IV). Ipamorelin ~2 h terminal (human, IV)","bioavailability":"Not measured by subcutaneous injection for any component; human ipamorelin data are IV and AOD9604 trials used oral or IV dosing","side_effects":"No human safety study of the blend, of hGH 176-191 or of Mod GRF 1-29 has been published. In rats hGH 176-191 briefly raised blood glucose and insulin (Ng 1978). In AOD9604 trials headache and GI effects occurred at placebo-like rates (Stier 2013), and IV ipamorelin was well tolerated in a phase 2 trial (Beck 2014). Commonly reported by users (anecdotal): injection-site irritation, water retention, joint aches, head rush. Ipamorelin is in category 2 of FDA's 503B interim policy (added 2023-09-29), and ipamorelin, CJC-1295 and AOD-9604 are in the withdrawn-nomination table for 503A, as of 2026-04-22: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks. FDA cites serious adverse events with CJC-1295, including increased heart rate and a systemic vasodilatory reaction.","last_reviewed_at":"2026-10-06T08:17:46.265Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Blend: molecular_weight and amino_acid_sequence null by design. Dose numbers are vendor/community per decision 11; no human dose of the blend exists. recon_volume_ml is the vendor/community value, not checked. Per-component split 6/3/3 mg from vendor page; order assumed to follow the product name. | description: Composition from vendor page; evidence framing per batches 01 and 03. | benefits: Tiers added. | detailed_description: Old text claimed enhanced fat burning with lean tissue preservation, with no source. | mechanism_of_action: Old text said the fragment acts 'without affecting glucose', which Ng 1978 contradicts (batch 03). | evidence_level: Blend takes the minimum across components. Vendors sell the no-DAC form (Mod GRF 1-29), which is preclinical with no literature of its own (decision 5, batch 01). | recommended_dose: Decision 11; per-component amounts from the 6/3/3 mg vial. | dosing_notes: Corrected an unsupported efficacy claim per batch 03. | common_vial_sizes: Vendor sells 12 mg (6/3/3 mg); no 10 mg product found. | clinical_studies: Old bullets uncited. PubMed searched for 176-191 or AOD9604 with ipamorelin, GHRH or CJC: reviews only. | amino_acid_sequence: Null for blends. | half_life: Old fragment '15-30 min' unsourced (batch 03). | bioavailability: Old 'high' unsupported. | side_effects: Added the rat glucose finding and FDA status. | alternative_names: Added the vendor's alternate product name.","sources":[{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"},{"url":"https://api.fda.gov/drug/drugsfda.json","note":"openFDA Drugs@FDA sweep (decision 61): no application found for the blend name or its alternative names"},{"url":"https://www.corepeptides.com/peptides/fragment-176-191-mod-grf-1-29-ipamorelin-blend-12mg/","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11673763/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/10496658/","note":"bioavailability"},{"url":"https://doi.org/10.4021/jem157w","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/645904/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/25331030/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9849822/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/7962295/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15817669/","note":"evidence_level"}],"data_version":2,"slug":"fragment-176-191-mod-grf-ipamorelin","url":"https://peptidelabs.app/peptides/fragment-176-191-mod-grf-ipamorelin/"},{"id":42,"name":"GH Fragment 176-191","description":"Synthetic C-terminal fragment of human growth hormone (residues 176-191). Related fragments cut fat gain in obese rodents; the one study of 176-191 itself found a brief rise in blood glucose in rats.","benefits":"Antilipogenic activity (rat fat tissue, hGH 177-191), reduced weight gain and fat mass (obese mice, hGH 177-191), raised fat oxidation (obese mice, AOD9604 analog); no human data for this fragment","categories":["fat loss","metabolic"],"recommended_dose":"250 to 500 mcg 2 to 3 times daily (vendor/community range, no published human dose)","detailed_description":"GH Fragment 176-191 is the last 16 residues of human growth hormone, FLRIVQCRSVEGSCGF. Monash University work from the 1970s on found that C-terminal hGH fragments affect fat and glucose metabolism. In rats, hGH 176-191 and related fragments caused a short-lived rise in blood glucose and insulin, and fragments containing 178-191 reduced insulin sensitivity (Ng 1978). The shorter hGH 177-191 had antilipogenic activity in rat fat (Wu 1993) and reduced weight gain and fat mass in obese mice (Natera 1994). The tyrosine analog AOD9604 was the version taken forward; it did not alter glucose in rodents or humans (Heffernan 2001). No human study of hGH 176-191 itself exists. Products sold under this name often list the AOD9604 sequence.","storage_temp":"Refrigerate 2-8°C (36-46°F); general lyophilised-peptide guidance, no compound-specific CoA located","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["Ipamorelin","CJC-1295"],"dose_min_mcg":250,"dose_max_mcg":500,"dose_unit":"mcg","dose_frequency":"2x daily","recon_volume_ml":2,"common_vial_sizes":[5],"dosing_notes":"Community protocols inject subcutaneously, often fasted. No human dose of hGH 176-191 has been published; rodent work dosed by weight (5 nmol/kg IV in rats, Ng 1978). Human trials used the AOD9604 analog, orally or IV (Stier 2013).","mechanism_of_action":"The C-terminal region of hGH carries its lipolytic and antilipogenic activity. hGH 177-191 inhibited lipogenesis in rat adipose tissue without measurable lipolysis (Wu 1993); a 177-191 analog stimulated hormone-sensitive lipase and inhibited acetyl-CoA carboxylase in rat fat (Ng 2000, J Mol Endocrinol). The related AOD9604 does not bind the GH receptor (Heffernan 2001). For hGH 176-191 specifically, the only data show acute hyperglycaemic and insulin-raising effects in rats (Ng 1978), so a glucose-neutral profile is not established for this fragment. Beta-3-adrenergic involvement is not supported; AOD9604 acted independently of that receptor (Heffernan 2001).","clinical_studies":["hGH 176-191 and related C-terminal fragments caused a short-lived rise in blood glucose and a more sustained rise in insulin in rats; fragments with residues 178-191 reduced insulin sensitivity (Ng and Bornstein, 1978)","hGH 177-191 matched the antilipogenic activity of intact hGH in rat fat pads (Wu and Ng, 1993)","Chronic hGH 177-191 reduced weight gain and fat mass in obese ob/ob mice (Natera et al., 1994)","Contested: the tyrosine analog AOD9604 did not raise glucose in obese mice (Heffernan et al., 2001) or in human trials (Stier et al., 2013), unlike the 1978 result for 176-191","Human-trial status: none for hGH 176-191; human trials were run only with AOD9604"],"evidence_level":"preclinical","references":[{"title":"Hyperglycemic action of synthetic C-terminal fragments of human growth hormone","authors":"Ng FM, Bornstein J","journal":"American Journal of Physiology","year":1978,"doi":"10.1152/ajpendo.1978.234.5.E521","pmid":"645904"},{"title":"Antilipogenic action of synthetic C-terminal sequence 177-191 of human growth hormone","authors":"Wu Z, Ng FM","journal":"Biochemistry and Molecular Biology International","year":1993,"pmid":"8358331"},{"title":"Reduction of cumulative body weight gain and adipose tissue mass in obese mice: response to chronic treatment with synthetic hGH 177-191 peptide","authors":"Natera SH, Jiang WJ, Ng FM","journal":"Biochemistry and Molecular Biology International","year":1994,"pmid":"7987248"},{"title":"Effects of oral administration of a synthetic fragment of human growth hormone on lipid metabolism","authors":"Heffernan MA, Jiang WJ, Thorburn AW, Ng FM","journal":"American Journal of Physiology - Endocrinology and Metabolism","year":2000,"doi":"10.1152/ajpendo.2000.279.3.E501","pmid":"10950816"},{"title":"Molecular and cellular actions of a structural domain of human growth hormone (AOD9401) on lipid metabolism in Zucker fatty rats","authors":"Ng FM, Jiang WJ, Gianello R, et al.","journal":"Journal of Molecular Endocrinology","year":2000,"doi":"10.1677/jme.0.0250287","pmid":"11116208"},{"title":"Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone or a modified C-terminal fragment","authors":"Heffernan MA, Thorburn AW, Fam B, et al.","journal":"International Journal of Obesity and Related Metabolic Disorders","year":2001,"doi":"10.1038/sj.ijo.0801740","pmid":"11673763"},{"title":"Safety and Tolerability of the Hexadecapeptide AOD9604 in Humans","authors":"Stier H, Vos E, Kenley D","journal":"Journal of Endocrinology and Metabolism","year":2013,"doi":"10.4021/jem157w"}],"molecular_weight":1799.1,"amino_acid_sequence":"FLRIVQCRSVEGSCGF [disulfide Cys7-Cys14]","alternative_names":["HGH Frag 176-191","HGH Fragment 176-191","hGH(176-191)"],"half_life":"Not published in any species","bioavailability":"Not reported. A related oral fragment (AOD9401) was active in obese mice (Heffernan 2000); no subcutaneous data","side_effects":"No human safety data for hGH 176-191. In rats it produced a short-lived rise in blood glucose and insulin (Ng 1978). The related AOD9604 showed headache and GI effects at placebo-like rates in human trials (Stier 2013). Injection-site irritation and headache are commonly reported (anecdotal).","last_reviewed_at":"2026-10-06T08:17:29.477Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. No human data for this fragment; the old sequence and molecular weight were AOD9604's. | description: The old claim of no glucose effect is contradicted by the only paper on this exact fragment (Ng and Bornstein 1978); the no-glucose-effect data belong to AOD9604. | benefits: Separates which fragment produced which finding. | detailed_description: Old text said 'Studies demonstrate fat reduction without effects on glucose metabolism or insulin sensitivity', which the 1978 paper contradicts for this fragment. Old value omitted for length. | mechanism_of_action: Old text claimed 'beta3-adrenergic receptor-like pathways' and no IGF-1 or glucose effect without sources. Old value omitted for length. | clinical_studies: Old bullets cited 'Ng & Borstein' for a result their paper does not report, claimed lipolysis in human tissue explants (that was AOD9401, Heffernan 2000) and used 'Popular in bodybuilding' as a finding. | side_effects: Old text said it 'does not appear to affect glucose tolerance', which the only fragment-specific study contradicts. | recommended_dose: Decision 11. | dosing_notes: Old note said AOD9604 'failed to produce significant fat loss over placebo in a 12-week obesity study'; that result is unpublished. | half_life: No PK study of hGH 176-191 located (PubMed search for the fragment returns no PK work); the only fragment-specific paper reports acute effects, not kinetics. The old figure had no source. | bioavailability: 'High' was unsourced. | molecular_weight: Calculated for FLRIVQCRSVEGSCGF with one disulfide (decision 16): residue masses plus water minus 2H = 1799.08. 1817.12 is the reduced mass of the Tyr sequence (AOD9604). PubChem CID 172966176 'HGH Fragment 176-191' lists C80H127N23O24S2, 1859.1, which fits neither sequence, so it was not used. | amino_acid_sequence: UniProt P01241: mature hGH residues 176-191 (precursor 202-217) are FLRIVQCRSVEGSCGF; residue 176 is Phe. The old Tyr sequence is AOD9604. hGH has a nat","sources":[{"url":"https://rest.uniprot.org/uniprotkb/P01241.fasta","note":"amino_acid_sequence"},{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/172966176","note":"alternative_names"},{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/71300630","note":"AOD9604 1815.1, for comparison with the old record value"},{"url":"https://pubmed.ncbi.nlm.nih.gov/645904/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/7987248/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11673763/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/8358331/","note":"clinical_studies"},{"url":"https://doi.org/10.4021/jem157w","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11116208/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11713213/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/?term=%22176-191%22+growth+hormone","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/10950816/","note":"bioavailability"}],"data_version":2,"slug":"gh-fragment-176-191","url":"https://peptidelabs.app/peptides/gh-fragment-176-191/"},{"id":43,"name":"GHK Basic","description":"Copper-free form of the human tripeptide GHK (Gly-His-Lys), studied for collagen synthesis and wound repair, though nearly all published data use the copper complex.","benefits":"Collagen synthesis in fibroblast culture, from 10 to the minus 12 M, peaking at 10 to the minus 9 M (in vitro, copper complex), wound repair in rodent and in vitro models, reversal of myofibroblast senescence markers (mouse and human cells). Copper-free GHK has no study of its own in any species","categories":["skin health","anti-aging","healing & recovery"],"recommended_dose":"1 to 5 mg daily: vendor and community range, no published human dose for GHK by any route","detailed_description":"GHK is a tripeptide first isolated from human plasma as a growth-modulating factor and synthesized in 1973 (Pickart 1973; Schlesinger 1977). The sequence occurs in the alpha-2 chain of type I collagen, which is where the wound-healing hypothesis comes from (Maquart 1988). GHK Basic is the apo form, sold without the copper ion. Nearly every published result uses the copper complex: GHK-Cu stimulated fibroblast collagen synthesis from 10 to the minus 12 M (Maquart 1988), and the proposed physiological role of the free peptide is to carry copper into cells (Pickart 1980). One 2024 commentary reports GHK alone reversing senescence markers and inducing apoptosis in myofibroblasts. The catalog also lists GHK-Cu (id 44), the copper complex, which is the molecule most of these references describe.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["BPC-157","TB-500"],"dose_min_mcg":1000,"dose_max_mcg":5000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[50],"dosing_notes":"Copper-free apo form, sold for subcutaneous or topical research use. Published work is in cell culture at molar concentrations (collagen stimulation from 10 to the minus 12 to 10 to the minus 9 M) or in topical formulations, not at a systemic dose. No study has dosed GHK in a human by injection. Copper availability matters for activity, so results obtained with the complex do not transfer to the apo form without that caveat.","mechanism_of_action":"The proposed mechanism for the free peptide is copper transport: GHK binds copper(II) with high affinity and the 1980 Nature paper concluded that its growth-modulating activity works by facilitating copper uptake into cells (Pickart 1980), with the solution structure of the complex solved two years later (Freedman 1982). Downstream effects are reported for the complex, not the apo form: GHK-Cu raised collagen synthesis in human fibroblast cultures in a concentration range starting at 10 to the minus 12 M and independent of cell number (Maquart 1988), and the gene-expression work describing broad resets of matrix and antioxidant programs used GHK-Cu or GHK in serum-containing media where copper is available (Pickart 2015). Copper-independent activity of the apo peptide has not been demonstrated.","clinical_studies":["GHK was isolated from human plasma as a growth-modulating factor, identified as glycyl-histidyl-lysine and reproduced synthetically (Pickart et al., 1973; Schlesinger et al., 1977)","The free tripeptide's activity was attributed to facilitating copper uptake into cells, with the structure of the copper complex solved in 1982 (Pickart et al., 1980; Freedman et al., 1982)","GHK-Cu stimulated collagen synthesis in human fibroblast cultures from 10 to the minus 12 M, maximal at 10 to the minus 9 M, with no change in cell number (Maquart et al., 1988)","GHK reversed senescence markers and induced apoptosis in myofibroblasts and improved fibroblast migration and collagen contraction in aged mouse and human cells, reported in a 2024 commentary rather than a primary trial (He et al., 2024)","Peptide-copper complexes stimulated hair follicles in C3H mice; the hair-growth literature is on complexes, not the apo peptide (Trachy et al., 1991)","Human-trial status: no clinical trial of copper-free GHK exists in any indication. The human evidence for this sequence is cosmetic and formulation work on GHK-Cu, and FDA lists GHK-Cu for injectable routes in the withdrawn-nomination table of its compounding safety-risk page as of 2026-04-22"],"evidence_level":"preclinical","references":[{"title":"A synthetic tripeptide which increases survival of normal liver cells, and stimulates growth in hepatoma cells","authors":"Pickart L, Thayer L, Thaler MM","journal":"Biochemical and Biophysical Research Communications","year":1973,"doi":"10.1016/0006-291x(73)91459-9","pmid":"4356974"},{"title":"Growth-modulating serum tripeptide is glycyl-histidyl-lysine","authors":"Schlesinger DH, Pickart L, Thaler MM","journal":"Experientia","year":1977,"doi":"10.1007/BF02002806","pmid":"858356"},{"title":"Growth-modulating plasma tripeptide may function by facilitating copper uptake into cells","authors":"Pickart L, Freedman JH, Loker WJ, Peisach J","journal":"Nature","year":1980,"doi":"10.1038/288715a0","pmid":"7453802"},{"title":"Structure of the glycyl-L-histidyl-L-lysine-copper(II) complex in solution","authors":"Freedman JH, Pickart L, Weinstein B, Mims WB","journal":"Biochemistry","year":1982,"doi":"10.1021/bi00262a004","pmid":"6291585"},{"title":"Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+","authors":"Maquart FX, Pickart L, Laurent M, Gillery P, et al.","journal":"FEBS Letters","year":1988,"doi":"10.1016/0014-5793(88)80509-x","pmid":"3169264"},{"title":"GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration","authors":"Pickart L, Vasquez-Soltero JM, Margolina A","journal":"BioMed Research International","year":2015,"doi":"10.1155/2015/648108","pmid":"26236730"},{"title":"The naturally occurring peptide GHK reverses age-related fibrosis by modulating myofibroblast function","authors":"He Q, Mazzola J, Ladiges W","journal":"Aging Pathobiology and Therapeutics","year":2024,"doi":"10.31491/apt.2024.12.158","pmid":"40823151"},{"title":"The hair follicle-stimulating properties of peptide copper complexes. Results in C3H mice","authors":"Trachy RE, Fors TD, Pickart L, Uno H","journal":"Annals of the New York Academy of Sciences","year":1991,"doi":"10.1111/j.1749-6632.1991.tb24420.x","pmid":"1809108"}],"molecular_weight":340.38,"amino_acid_sequence":"GHK (apo form, no copper ion)","alternative_names":["Copper-free GHK","GHK tripeptide","Apo-GHK"],"half_life":"No pharmacokinetic study of GHK or GHK-Cu has been published in any species. GHK is present in human plasma and its concentration is reported to decline with age (Pickart 2015)","bioavailability":"Not measured by any route in any species. Topical delivery of this sequence is studied as a formulation problem, and the apo peptide's activity depends on binding copper once in contact with tissue","side_effects":"No systemic safety data exist for GHK by any route, and no human trial has recorded adverse events for the copper-free form. Topical cosmetic use of this sequence is reported as well tolerated in formulation studies, with irritation, redness and stinging the commonly reported complaints (anecdotal). For the copper complex by injection, FDA states it may pose a risk of immunogenicity for certain routes and that no human safety data were identified; GHK-Cu sits in the withdrawn-nomination table of that page as of 2026-04-22.","last_reviewed_at":"2026-10-06T08:17:37.850Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Dose range is vendor convention, no published human dose by any route. Molecular weight confirmed against PubChem CID 73587. Almost all cited evidence describes the copper complex and says so; GHK-Cu regulatory status sourced from fda.gov (withdrawn-nomination table). | categories: The hair-growth evidence is a 1991 C3H mouse study of peptide-copper complexes, not of copper-free GHK. Replaced with healing and recovery, which the wound-healing literature supports. | benefits: Each item now carries its model system, and the field states that the copper-free form itself is unstudied. | detailed_description: Old text claimed research shows tissue repair and collagen stimulation for this form, which is the one thing the literature does not show. Decision 18 cross-reference to id 44 added. Old value omitted for length. | mechanism_of_action: Old text stated that the primary mechanisms are copper-independent and that the peptide directly activates fibroblasts and keratinocytes through integrins and growth factor receptors. No source supports either; the Nature paper argues the opposite. Old value omitted for length. | recommended_dose: Decision 11. No human dosing study of GHK or GHK-Cu exists; cosmetic studies use concentrations in a formulation, not a dose. | dosing_notes: Adds what the literature actually dosed and flags the copper dependency that the whole record turns on. | clinical_studies: Every old bullet was an unsourced generality (\"shows wound healing activity in some models\", \"may be preferred when copper status is already adequate\"). Replaced with named studies and their model systems. | half_life: \"Minutes\" has no source. The plasma-decline statement comes from the review rather than a primary measurement, hence medium confidence. | bioavailability: \"Good\" has no source. | side_effects: Old text was advice in the second person (\"patch test a small area\", \"avoid application\"), which the style guide forbids. Decision 32 sentence added","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/73587/property/MolecularFormula,MolecularWeight,IUPACName/JSON","note":"molecular weight 340.38, C14H24N6O4, for Gly-His-Lys, CID 73587"},{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/29986520/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1809108/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3169264/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40823151/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/26236730/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/4356974/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/858356/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/7453802/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6291585/","note":"clinical_studies"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/73587/property/MolecularFormula,MolecularWeight/JSON","note":"amino_acid_sequence"}],"data_version":2,"slug":"ghk-basic","url":"https://peptidelabs.app/peptides/ghk-basic/"},{"id":44,"name":"GHK-Cu","description":"Copper complex of the tripeptide Gly-His-Lys, isolated from human plasma in 1973; raises collagen synthesis in cell and rat studies, with mixed results in small topical human trials.","benefits":"Wound healing (topical; 1 positive RCT in diabetic foot ulcers, 1 negative in venous ulcers), collagen synthesis (cell culture, rat wounds), hair follicle growth (mouse), skin appearance (topical, no objective benefit in 1 small RCT)","categories":["skin health","hair growth","healing & recovery"],"recommended_dose":"1 to 2 mg daily SC: vendor/community range, no published human injected dose. Topical trial products included a 0.4% cream","detailed_description":"GHK was isolated from human plasma in 1973 and binds copper(II) tightly. Cell and rat studies show raised collagen and glycosaminoglycan synthesis and faster wound closure. Human data are topical only: a gel helped diabetic foot ulcers close in one RCT, a 0.4% cream did no better than placebo in venous ulcers, and a 13-person post-laser study found no objective skin benefit. No injected or oral human study has been published, and a 2026 independent review calls the clinical evidence sparse. Much of the review literature comes from the discoverer's group. Same molecule as the GHK-Cu Capsule entry (id 28). Listed on FDA's 503A category 2 (safety concerns) page as GHK-Cu for injectable routes, withdrawn-nomination table, as of 2026-04-22: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["BPC-157","TB-500"],"dose_min_mcg":1000,"dose_max_mcg":2000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[50,100],"dosing_notes":"Subcutaneous injection is community practice; no injected human study has been published. Human data are topical: daily gel after debridement in diabetic foot ulcers, 0.4% cream in venous ulcers. GHK-Cu is about 16% copper by mass, so 2 mg carries about 0.3 mg copper, against a US adult upper intake level of 10 mg/day for oral copper. No parenteral limit is set for this compound.","mechanism_of_action":"Proposed. GHK binds Cu2+ with high affinity. In fibroblast culture GHK-Cu raised collagen synthesis starting at 10^-12 to 10^-11 M, maximal at 10^-9 M, independent of cell number (Maquart et al., 1988). Injected into rat wound chambers it increased collagen, glycosaminoglycans, DNA and type I and III collagen mRNA in a concentration-dependent way, without raising TGF-beta mRNA (Maquart et al., 1993). Topical gel lowered TNF-alpha, MMP-2 and MMP-9 in ischemic rat wounds (Canapp et al., 2003). Claims that GHK resets thousands of human genes come from cell-line expression database analyses in reviews by the discovering group and have not been tested in tissue.","clinical_studies":["Collagen synthesis in fibroblast culture rose from 10^-12 M GHK-Cu and peaked at 10^-9 M, independent of cell number (Maquart et al., 1988)","In rat wound chambers GHK-Cu raised collagen, glycosaminoglycan and DNA content in a concentration-dependent way (Maquart et al., 1993)","Topical gel on ischemic rat wounds: 64.5% area reduction by day 13 vs 45.6% with vehicle and 28.2% untreated (Canapp et al., 2003)","Multicenter evaluator-blinded RCT of a GHK-Cu gel in diabetic neuropathic plantar ulcers: median closure 98.5% vs 60.8% with vehicle, infections 7% vs 34% (Mulder et al., 1994)","Evaluator-blinded RCT in venous stasis ulcers (n=86): 0.4% GHK-Cu cream was no better than placebo, while silver sulfadiazine was (Bishop et al., 1992)","Human-trial status: topical only, with mixed results; a 13-person post-laser trial found no objective benefit (Mateescu et al., 2026). No injected or oral human study. Hair claims rest on mouse data (Trachy et al., 1991). Most reviews come from the discovering group"],"evidence_level":"preclinical","references":[{"title":"Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+","authors":"Maquart FX, Pickart L, Laurent M, et al.","journal":"FEBS Letters","year":1988,"doi":"10.1016/0014-5793(88)80509-x","pmid":"3169264"},{"title":"In vivo stimulation of connective tissue accumulation by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+ in rat experimental wounds","authors":"Maquart FX, Bellon G, Chaqour B, et al.","journal":"The Journal of Clinical Investigation","year":1993,"doi":"10.1172/JCI116842","pmid":"8227353"},{"title":"The effect of topical tripeptide-copper complex on healing of ischemic open wounds","authors":"Canapp SO Jr, Farese JP, Schultz GS, et al.","journal":"Veterinary Surgery","year":2003,"doi":"10.1111/j.1532-950x.2003.00515.x","pmid":"14648529"},{"title":"The hair follicle-stimulating properties of peptide copper complexes. Results in C3H mice","authors":"Trachy RE, Fors TD, Pickart L, et al.","journal":"Annals of the New York Academy of Sciences","year":1991,"doi":"10.1111/j.1749-6632.1991.tb24420.x","pmid":"1809108"},{"title":"Enhanced healing of ulcers in patients with diabetes by topical treatment with glycyl-l-histidyl-l-lysine copper","authors":"Mulder GD, Patt LM, Sanders L, et al.","journal":"Wound Repair and Regeneration","year":1994,"doi":"10.1046/j.1524-475X.1994.20406.x","pmid":"17147644"},{"title":"A prospective randomized evaluator-blinded trial of two potential wound healing agents for the treatment of venous stasis ulcers","authors":"Bishop JB, Phillips LG, Mustoe TA, et al.","journal":"Journal of Vascular Surgery","year":1992,"doi":"10.1067/mva.1992.37086","pmid":"1495150"},{"title":"Human skin penetration of a copper tripeptide in vitro as a function of skin layer","authors":"Hostynek JJ, Dreher F, Maibach HI","journal":"Inflammation Research","year":2011,"doi":"10.1007/s00011-010-0238-9","pmid":"20721598"},{"title":"GHK-Cu as a Bioactive Metallopeptide and Drug-Delivery Cargo: Coordination Chemistry, Formulation Science, Therapeutic Evidence, and a Translational Roadmap","authors":"Mateescu DM, Gavrilescu DM, Mincioaga RI, et al.","journal":"Pharmaceutics","year":2026,"doi":"10.3390/pharmaceutics18091077","pmid":"42797253"}],"molecular_weight":402.92,"amino_acid_sequence":"GHK [Cu2+ complex]","alternative_names":["Copper Peptide","GHK-Copper","Glycyl-L-histidyl-L-lysine:copper(II)","Prezatide copper","Copper tripeptide-1"],"half_life":"Not measured: no published pharmacokinetic study by any route or species","bioavailability":"Topical: in human skin in vitro, copper from GHK-Cu permeated dermatomed skin at 2.43 x 10^-4 cm/h, 136 mcg/cm2 over 48 h (Hostynek et al., 2011). Injected: not measured","side_effects":"No controlled safety data exist for injected GHK-Cu. Topical RCTs in diabetic and venous ulcers and post-laser skin reported no specific safety signal in their abstracts, and the diabetic ulcer trial found fewer infections (7% vs 34%) (Mulder et al., 1994). FDA's category 2 entry for injectable GHK-Cu cites possible immunogenicity from aggregation and peptide-related impurities and limited human data; the nomination was later withdrawn. Copper load is a theoretical concern in disorders of copper excretion such as Wilson's disease. Commonly reported (anecdotal): injection-site stinging, redness and lumps; topical irritation.","last_reviewed_at":"2026-10-06T08:17:41.213Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance (not verified). recon_volume_ml and common_vial_sizes are vendor values not checked in this pass. Dose numbers are vendor/community per decision 11. | description: Old text stated wound repair as established; human results are split (one positive, two negative topical trials). | benefits: Tiers added; 'anti-aging' has no direct study and is dropped. | detailed_description: Old text called the effects 'potent' with no model system. Decisions 18, 32, 45. | mechanism_of_action: Old text claimed TGF-beta modulation (Maquart 1993 found TGF-beta mRNA unchanged), proteasome activation and cytokine suppression without sources. | clinical_studies: Old bullet 2 (Canapp 2003) said diabetic mice; it was rats with ischemic wounds. Old bullet 3 (Pyo 2007) said mice; it studied a different peptide, AHK-Cu, on human follicles ex vivo. The '31% of genes' bullet is a review claim. Decision 45 in the last bullet. | evidence_level: Decision 17: the product sold is an injectable vial and every human study is topical. One topical RCT is positive and one negative. If topical use counts as the same product, clinical stands under decision 4; Josh decides. | recommended_dose: Decision 11. The 0.1 to 1% topical range has no source beyond the 0.4% venous ulcer cream. | dosing_notes: Copper fraction is arithmetic: 63.55 / 402.92 = 15.8%. The old 'copper-overload risk' wording overstated what 1 to 2 mg delivers. | half_life: Old values had no source; a PubMed search for GHK-Cu pharmacokinetics found only an assay method paper. | bioavailability: Replaces unsourced text with the measured in vitro value; the study measured copper, not intact peptide. | side_effects: Old text gave advice (patch test first, avoid) and asserted significant injection-site reactions without a source. | molecular_weight: PubChem maps the INN prezatide copper and INCI copper tripeptide-1 to CID 71587328, C14H23CuN6O4+, 402.92. The old 403.93 is GHK (340.38) plus Cu (63.55) with no proton loss, w","sources":[{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/71587328/property/MolecularFormula,MolecularWeight/JSON","note":"alternative_names"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/139035031/property/MolecularFormula,MolecularWeight/JSON","note":"alternative GHK-Cu representation, 400.90"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/73587/property/MolecularFormula,MolecularWeight/JSON","note":"amino_acid_sequence"},{"url":"https://ods.od.nih.gov/factsheets/Copper-HealthProfessional/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/4349963/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16847171/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17703734/","note":"Pyo 2007 studied AHK-Cu, not GHK-Cu; cited wrongly in the old record"},{"url":"https://pubmed.ncbi.nlm.nih.gov/29986520/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22666519/","note":"Pickart 2012 review, the paper the old PMID 22577490 was meant to cite"},{"url":"https://clinicaltrials.gov/api/v2/studies/NCT07437586","note":"Hudson Biotech registration, recruiting, no results; same sponsor as a self-described example record"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3169264/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/8227353/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17147644/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1495150/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1809108/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42797253/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/14648529/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/20721598/","note":"bioavailability"}],"data_version":2,"slug":"ghk-cu","url":"https://peptidelabs.app/peptides/ghk-cu/"},{"id":28,"name":"GHK-Cu Capsule","description":"Oral capsule formulation of the copper tripeptide GHK-Cu; oral absorption and systemic efficacy are unestablished, with human evidence limited to topical GHK-Cu.","benefits":"Reported skin, hair and anti-aging support; oral efficacy unproven","categories":["skin health","hair growth","anti-aging"],"recommended_dose":"1 to 10 mg daily orally: vendor/community range, no published oral dose in any species","detailed_description":"GHK-Cu Capsule is an oral formulation of the copper-binding tripeptide GHK. The published human evidence for GHK-Cu is topical and mixed; no study in any species has shown that oral GHK-Cu survives digestion intact or reaches skin, hair follicles or connective tissue at active concentrations. Reported benefits are extrapolated from topical, rodent and cell-culture work. Same molecule as the GHK-Cu entry (id 44), which covers the injectable and topical literature.","storage_temp":"Room temperature","shelf_life_reconstituted":null,"shelf_life_powder":"12+ months","stacks_with":[],"dose_min_mcg":1000,"dose_max_mcg":10000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Oral capsule. No oral study of GHK-Cu exists in any species; topical is the researched route. GHK-Cu is about 16% copper by mass, so 1 to 10 mg carries about 0.16 to 1.6 mg copper, against a US adult upper intake level of 10 mg/day for copper from food and supplements.","mechanism_of_action":"Same molecule as injectable and topical GHK-Cu. GHK binds Cu2+ with high affinity, and GHK-Cu raised collagen synthesis in fibroblast culture at 10^-12 to 10^-9 M (Maquart et al., 1988). Whether any intact GHK-Cu is absorbed after oral dosing is unknown; no oral absorption study of GHK-Cu exists in any species.","clinical_studies":["Collagen synthesis in fibroblast culture rose from 10^-12 M GHK-Cu and peaked at 10^-9 M (Maquart et al., 1988)","Topical GHK-Cu gel improved closure of diabetic neuropathic plantar ulcers vs vehicle (median 98.5% vs 60.8%) in a multicenter RCT (Mulder et al., 1994)","Topical 0.4% GHK-Cu cream was no better than placebo in venous stasis ulcers (n=86) (Bishop et al., 1992)","Copper from topical GHK-Cu permeated human skin in vitro at 2.43 x 10^-4 cm/h (Hostynek et al., 2011)","Human-trial status: no oral study of GHK-Cu in any species; all human data are topical, and a 2026 independent review rates the clinical evidence as sparse (Mateescu et al., 2026)"],"evidence_level":"anecdotal","references":[{"title":"Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+","authors":"Maquart FX, Pickart L, Laurent M, et al.","journal":"FEBS Letters","year":1988,"doi":"10.1016/0014-5793(88)80509-x","pmid":"3169264"},{"title":"Enhanced healing of ulcers in patients with diabetes by topical treatment with glycyl-l-histidyl-l-lysine copper","authors":"Mulder GD, Patt LM, Sanders L, et al.","journal":"Wound Repair and Regeneration","year":1994,"doi":"10.1046/j.1524-475X.1994.20406.x","pmid":"17147644"},{"title":"A prospective randomized evaluator-blinded trial of two potential wound healing agents for the treatment of venous stasis ulcers","authors":"Bishop JB, Phillips LG, Mustoe TA, et al.","journal":"Journal of Vascular Surgery","year":1992,"doi":"10.1067/mva.1992.37086","pmid":"1495150"},{"title":"Human skin penetration of a copper tripeptide in vitro as a function of skin layer","authors":"Hostynek JJ, Dreher F, Maibach HI","journal":"Inflammation Research","year":2011,"doi":"10.1007/s00011-010-0238-9","pmid":"20721598"},{"title":"GHK-Cu as a Bioactive Metallopeptide and Drug-Delivery Cargo: Coordination Chemistry, Formulation Science, Therapeutic Evidence, and a Translational Roadmap","authors":"Mateescu DM, Gavrilescu DM, Mincioaga RI, et al.","journal":"Pharmaceutics","year":2026,"doi":"10.3390/pharmaceutics18091077","pmid":"42797253"}],"molecular_weight":402.92,"amino_acid_sequence":"GHK [Cu2+ complex]","alternative_names":["Copper tripeptide oral","GHK oral"],"half_life":"Not measured: no pharmacokinetic study of oral GHK-Cu in any species","bioavailability":"Oral: not measured; no oral absorption study of GHK-Cu in any species","side_effects":"No human safety data exist for oral GHK-Cu. At 1 to 10 mg the copper content (about 0.16 to 1.6 mg) is below the US adult upper intake level of 10 mg/day, which is set from liver damage seen with long-term excess intake; disorders of copper excretion such as Wilson's disease are a theoretical concern. Commonly reported (anecdotal): nausea, stomach upset.","last_reviewed_at":"2026-10-06T08:17:41.213Z","reviewed_by":"audit-2026-10","review_notes":"N/A-by-design: oral capsule, so recon_volume_ml and common_vial_sizes are null. storage: general guidance. | detailed_description: Decision 18 sentence added; 'mixed' reflects one positive and one negative topical RCT. | mechanism_of_action: Old text claimed 4,000 affected genes, DNA repair and 'systemic distribution' after oral dosing without sources. | clinical_studies: Old bullets had no citations; 'hair growth in clinical cosmetic studies' has no published human trial behind it. | recommended_dose: Decision 11. | dosing_notes: Copper fraction is arithmetic (63.55 / 402.92). The old copper-accumulation wording overstated the copper these doses contain. | half_life: Decision 33. | bioavailability: Decision 33: the old text claimed systemic effects with no source. | side_effects: Old text gave advice ('should avoid') and implied copper accumulation at catalog doses. | stacks_with: Decisions 14 and 41: no published oral combination or documented oral protocol. | molecular_weight: Same basis as id 44: PubChem CID 71587328 (prezatide copper), 402.92. | amino_acid_sequence: One-letter codes.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/71587328/property/MolecularFormula,MolecularWeight/JSON","note":"molecular_weight"},{"url":"https://ods.od.nih.gov/factsheets/Copper-HealthProfessional/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/29986520/","note":"Pickart and Margolina 2018, the paper the bad DOI was meant to cite"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17147644/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1495150/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42797253/","note":"stacks_with"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3169264/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/20721598/","note":"clinical_studies"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/73587/property/MolecularFormula,MolecularWeight/JSON","note":"amino_acid_sequence"}],"data_version":2,"slug":"ghk-cu-capsule","url":"https://peptidelabs.app/peptides/ghk-cu-capsule/"},{"id":156,"name":"Ghrelin","description":"28-amino-acid stomach hormone and the endogenous GHS-R1a ligand; drives hunger, GH release and gastric motility in human infusion studies.","benefits":"Food intake +28% (human RCT crossover, n=9), GH release (human, dose-dependent), gastric emptying in idiopathic gastroparesis (human, n=6), LV function, exercise capacity and lean mass in chronic heart failure (human, n=10, open label)","categories":["growth hormone","appetite","metabolic"],"recommended_dose":"~1 mcg/kg IV bolus for GH release (about 70 mcg; Takaya 2000); 3.6 nmol/kg SC (about 12 mcg/kg, ~850 mcg) for appetite (Druce 2006); 2 mcg/kg IV 2x daily in heart failure (Nagaya 2004); no established research range","detailed_description":"Ghrelin is a 28-amino acid peptide hormone produced primarily in the stomach. It is the endogenous ligand for the growth hormone secretagogue receptor (GHS-R). Research demonstrates roles in appetite regulation, GH secretion, gastric motility, and energy homeostasis. Studied for applications in cachexia, gastroparesis, and growth hormone deficiency.","storage_temp":"Refrigerated (2-8°C)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"24+ months at room temperature","stacks_with":["GHRP-6","MK-677"],"dose_min_mcg":70,"dose_max_mcg":850,"dose_unit":"mcg","dose_frequency":"1-2x daily","recon_volume_ml":2,"common_vial_sizes":[2,5],"dosing_notes":"Only Ser3-octanoylated ghrelin activates GHS-R1a; des-acyl ghrelin is inactive at this receptor (Kojima 1999). Human studies used IV bolus or infusion; one RCT showed a single SC injection of 3.6 nmol/kg raised energy intake 27% (Druce 2006). Acyl ghrelin disappears from plasma in about 10 min (Akamizu 2004). An IV dose raised glucose and lowered insulin for about 2 h in healthy men (Broglio 2001).","mechanism_of_action":"Ghrelin is a 28 amino acid orexigenic peptide primarily produced by gastric oxyntic cells. Requires octanoylation (fatty acid attachment) at Ser3 by GOAT enzyme for biological activity. Binds to GHS-R1a (growth hormone secretagogue receptor type 1a), a GPCR that couples to Gq and G12/13. In hypothalamus, stimulates appetite through NPY/AgRP neurons while inhibiting POMC neurons. In pituitary, stimulates GH release synergistically with GHRH. Also regulates gastric motility, reward pathways, and glucose homeostasis. Levels rise pre-meal and fall post-prandially.","clinical_studies":["Identified as the endogenous GHS-R ligand; a 28-residue stomach peptide whose Ser3 octanoyl group is required for activity (Kojima et al., 1999)","IV 0.2-5 mcg/kg released GH dose-dependently (peak 107 ng/mL at 5 mcg/kg) and raised ACTH, cortisol and prolactin in 4 men (Takaya et al., 2000)","IV infusion increased buffet energy intake 28% in every subject in a randomized double-blind crossover, n=9 (Wren et al., 2001)","Acyl ghrelin half-life 9-13 min, total ghrelin 27-31 min after IV bolus; adverse effects transient (Akamizu et al., 2004)","3 weeks of 2 mcg/kg IV twice daily improved LV ejection fraction, peak VO2 and lean mass in 10 chronic heart failure patients (Nagaya et al., 2004)","Human-trial status: ghrelin itself is not approved anywhere; the ghrelin-receptor agonist anamorelin was approved in Japan (Adlumiz, 22 Jan 2021) for cancer cachexia after the ROMANA phase 3 trials, and is not FDA-approved"],"evidence_level":"clinical","references":[{"title":"Ghrelin is a growth-hormone-releasing acylated peptide from stomach","authors":"Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K","journal":"Nature","year":1999,"doi":"10.1038/45230","pmid":"10604470"},{"title":"Ghrelin strongly stimulates growth hormone release in humans","authors":"Takaya K, Ariyasu H, Kanamoto N, et al.","journal":"Journal of Clinical Endocrinology & Metabolism","year":2000,"doi":"10.1210/jcem.85.12.7167","pmid":"11134161"},{"title":"Ghrelin enhances appetite and increases food intake in humans","authors":"Wren AM, Seal LJ, Cohen MA, et al.","journal":"Journal of Clinical Endocrinology & Metabolism","year":2001,"doi":"10.1210/jcem.86.12.8111","pmid":"11739476"},{"title":"Ghrelin, a natural GH secretagogue produced by the stomach, induces hyperglycemia and reduces insulin secretion in humans","authors":"Broglio F, Arvat E, Benso A, et al.","journal":"Journal of Clinical Endocrinology & Metabolism","year":2001,"doi":"10.1210/jcem.86.10.8098","pmid":"11600590"},{"title":"Pharmacokinetics, safety, and endocrine and appetite effects of ghrelin administration in young healthy subjects","authors":"Akamizu T, Takaya K, Irako T, et al.","journal":"European Journal of Endocrinology","year":2004,"doi":"10.1530/eje.0.1500447","pmid":"15080773"},{"title":"Effects of ghrelin administration on left ventricular function, exercise capacity, and muscle wasting in patients with chronic heart failure","authors":"Nagaya N, Moriya J, Yasumura Y, et al.","journal":"Circulation","year":2004,"doi":"10.1161/01.CIR.0000149746.62908.BB","pmid":"15569841"},{"title":"Influence of ghrelin on gastric emptying and meal-related symptoms in idiopathic gastroparesis","authors":"Tack J, Depoortere I, Bisschops R, Verbeke K, Janssens J, Peeters T","journal":"Alimentary Pharmacology & Therapeutics","year":2005,"doi":"10.1111/j.1365-2036.2005.02658.x","pmid":"16225494"},{"title":"Subcutaneous administration of ghrelin stimulates energy intake in healthy lean human volunteers","authors":"Druce MR, Neary NM, Small CJ, et al.","journal":"International Journal of Obesity (London)","year":2006,"doi":"10.1038/sj.ijo.0803158","pmid":"16247504"}],"molecular_weight":3370.9,"amino_acid_sequence":"GS[S(n-octanoyl)]FLSPEHQRVQQRKESKKPPAKLQPR","alternative_names":["Lenomorelin","Acyl ghrelin","Hunger hormone"],"half_life":"9-13 min acyl ghrelin, 27-31 min total ghrelin (human, IV bolus; Akamizu 2004)","bioavailability":"SC injection of 3.6 nmol/kg was active on energy intake (human; Druce 2006); no absolute bioavailability figure located","side_effects":"In a placebo-controlled study of 1-5 mcg/kg IV, adverse effects were transient and no more frequent than placebo (Akamizu 2004). Documented acute effects in humans: increased hunger and food intake (Wren 2001), a rise in blood glucose with a fall in insulin lasting about 2 h (Broglio 2001), and rises in ACTH, cortisol and prolactin (Takaya 2000). Flushing, sweating and a mild drop in blood pressure are commonly reported (anecdotal).","last_reviewed_at":"2026-10-06T08:17:26.138Z","reviewed_by":"audit-2026-10","review_notes":"benefits: Tiers and sizes. | recommended_dose: Human doses are weight-based and higher than the record's 50-100 mcg, which had no source. | dose_min_mcg: 1 mcg/kg at 70 kg. | dose_max_mcg: 3.6 nmol/kg x 3.37 kDa x 70 kg. | dosing_notes: Removes the unsourced claim about vendor material; sources the rest. | clinical_studies: Old bullets said anamorelin was 'FDA-approved ... in Japan'; it was approved by Japan's regulator, not the FDA. | half_life: The record's ~30 min was the total-ghrelin figure; the active acyl form clears in about 10 min. | bioavailability: Old text was not a bioavailability figure. | side_effects: Removes the unsourced vendor-material claim; labels anecdote. | amino_acid_sequence: One-letter format. | alternative_names: 'Growth hormone secretagogue' is a drug class, not a name.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/16133832","note":"amino_acid_sequence"},{"url":"https://www.ono-pharma.com/en/news/20210122.html","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/26906526/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15917842/","note":"Druce 2005: IV ghrelin raises intake in obese and lean subjects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11739476/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11134161/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16225494/","note":"benefits"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15569841/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16247504/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/10604470/","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15080773/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11600590/","note":"side_effects"},{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/91668172","note":"alternative_names"}],"data_version":2,"slug":"ghrelin","url":"https://peptidelabs.app/peptides/ghrelin/"},{"id":151,"name":"GHRH","description":"Native hypothalamic hormone (somatorelin, GHRH 1-44) that triggers GH release from pituitary somatotrophs; used clinically as a diagnostic GH-stimulation agent.","benefits":"GH release and pituitary reserve testing (human, GHRH-arginine test validated in hundreds of patients), growth acceleration in GH-deficient children with pulsatile dosing (human, n=5, open label), reference ligand for GH-axis research","categories":["growth hormone","hormonal"],"recommended_dose":"1 mcg/kg IV (diagnostic GHRH-arginine test, about 70-100 mcg); 1-2 mcg/kg per SC pulse in a pediatric treatment study; research-community range 100-200 mcg SC nightly","detailed_description":"Growth hormone-releasing hormone (somatorelin, GRF) is the 44-residue hypothalamic peptide that drives pituitary GH secretion. It was isolated in 1982 from pancreatic tumors causing acromegaly (Guillemin 1982; Rivier 1982). Plasma dipeptidyl peptidase cleaves the N-terminal Tyr-Ala within minutes, leaving an inactive GHRH(3-44) (Frohman 1986). Its main clinical role is diagnostic: GHRH 1 mcg/kg IV plus arginine is a validated test for adult GH deficiency, with BMI-specific cut-offs (Aimaretti 1998; Corneli 2005). Nocturnal pulsatile SC GHRH(1-40) accelerated growth in 3 of 5 GH-deficient children (Smith 1986). The approved drugs built on it are the 1-29 fragment sermorelin and the stabilized 1-44 analog tesamorelin.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["Ipamorelin","CJC-1295"],"dose_min_mcg":100,"dose_max_mcg":200,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":2,"common_vial_sizes":[2,5],"dosing_notes":"Native GHRH(1-44). IV bolus in diagnostic testing; SC in the pediatric pulsatile study. Intact peptide disappears from plasma with a half-life of about 7 min, so each injection gives one brief GH pulse (Frohman 1986). Facial flushing lasting 1-3 min occurred in 16 of 18 men given 1 mcg/kg IV (Bowers 1990).","mechanism_of_action":"GHRH (Growth Hormone Releasing Hormone, also called GRF or somatoliberin) is a 44 amino acid peptide from the hypothalamus that stimulates GH secretion from pituitary somatotrophs. Binds to GHRH-R, a G-protein coupled receptor, activating adenylyl cyclase and cAMP production. This triggers calcium influx and GH granule exocytosis. Native GHRH has a very short half-life (~7-10 minutes) due to DPP-IV cleavage, necessitating development of more stable analogs like CJC-1295 and tesamorelin.","clinical_studies":["Isolated and sequenced from pancreatic tumors causing acromegaly (Guillemin et al., 1982; Rivier et al., 1982)","Plasma clearance 194 L/m2/day; elimination-phase half-life of immunoreactive GRF 52 min after IV injection in men (Frohman et al., 1984)","Intact GHRH(1-44) half-life 6.8 min in vivo; cleaved to inactive GHRH(3-44) by a plasma dipeptidylaminopeptidase (Frohman et al., 1986)","Nocturnal pulsatile SC GHRH(1-40) raised growth velocity from 3.7 to 7.2 cm/year in 3 of 5 GH-deficient children (Smith et al., 1986)","GHRH + arginine test is as sensitive as insulin hypoglycemia for adult GH deficiency, with BMI-specific cut-offs from 640 subjects (Aimaretti et al., 1998; Corneli et al., 2005)","Human-trial status: used clinically as a diagnostic stimulus; the approved therapeutics are its analogs sermorelin (1997) and tesamorelin (2010)"],"evidence_level":"clinical","references":[{"title":"Growth hormone-releasing factor from a human pancreatic tumor that caused acromegaly","authors":"Guillemin R, Brazeau P, Bohlen P, Esch F, Ling N, Wehrenberg WB","journal":"Science","year":1982,"doi":"10.1126/science.6812220","pmid":"6812220"},{"title":"Characterization of a growth hormone-releasing factor from a human pancreatic islet tumour","authors":"Rivier J, Spiess J, Thorner M, Vale W","journal":"Nature","year":1982,"doi":"10.1038/300276a0","pmid":"6292724"},{"title":"Metabolic clearance and plasma disappearance rates of human pancreatic tumor growth hormone releasing factor in man","authors":"Frohman LA, Thominet JL, Webb CB, et al.","journal":"Journal of Clinical Investigation","year":1984,"doi":"10.1172/JCI111333","pmid":"6425363"},{"title":"Rapid enzymatic degradation of growth hormone-releasing hormone by plasma in vitro and in vivo to a biologically inactive product cleaved at the NH2 terminus","authors":"Frohman LA, Downs TR, Williams TC, Heimer EP, Pan YC, Felix AM","journal":"Journal of Clinical Investigation","year":1986,"doi":"10.1172/JCI112679","pmid":"3093533"},{"title":"Nocturnal pulsatile growth hormone releasing hormone treatment in growth hormone deficiency","authors":"Smith PJ, Brook CG, Rivier J, Vale W, Thorner MO","journal":"Clinical Endocrinology (Oxford)","year":1986,"doi":"10.1111/j.1365-2265.1986.tb03593.x","pmid":"3098459"},{"title":"Comparison between insulin-induced hypoglycemia and growth hormone (GH)-releasing hormone + arginine as provocative tests for the diagnosis of GH deficiency in adults","authors":"Aimaretti G, Corneli G, Razzore P, et al.","journal":"Journal of Clinical Endocrinology & Metabolism","year":1998,"doi":"10.1210/jcem.83.5.4837","pmid":"9589665"},{"title":"The cut-off limits of the GH response to GH-releasing hormone-arginine test related to body mass index","authors":"Corneli G, Di Somma C, Baldelli R, et al.","journal":"European Journal of Endocrinology","year":2005,"doi":"10.1530/eje.1.01967","pmid":"16061832"},{"title":"Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone","authors":"Bowers CY, Reynolds GA, Durham D, Barrera CM, Pezzoli SS, Thorner MO","journal":"Journal of Clinical Endocrinology & Metabolism","year":1990,"doi":"10.1210/jcem-70-4-975","pmid":"2108187"}],"molecular_weight":5040.4,"amino_acid_sequence":"YADAIFTNSYRKVLGQLSARKLLQDIMSRQQGESNQERGARARL[NH2]","alternative_names":["GRF","Somatoliberin","GHRH(1-44)"],"half_life":"~7 min for intact GHRH(1-44) (human, IV; HPLC, Frohman 1986); immunoreactive elimination phase ~52 min (human, IV; Frohman 1984)","bioavailability":null,"side_effects":"Transient facial flushing (1-3 min) in 16 of 18 men after 1 mcg/kg IV (Bowers 1990). No adverse effects reported in the pediatric pulsatile study (Smith 1986). Injection-site redness, headache, water retention, joint aches and reduced insulin sensitivity are commonly reported (anecdotal) with sustained GH elevation.","last_reviewed_at":"2026-10-06T08:17:26.138Z","reviewed_by":"audit-2026-10","review_notes":"benefits: Tiers and sizes. | detailed_description: Expands a stub. | recommended_dose: Literature doses added; numeric minimum lowered to the 70 mcg diagnostic dose. | dose_frequency: Mono-friendly format. | dosing_notes: Sourced version. | clinical_studies: Old bullets were generic statements with no citations. | half_life: Adds route, species and the two measurement methods. | bioavailability: No SC bioavailability study located; old text was not a bioavailability figure. | side_effects: Removes 'glucose monitoring is sensible' advice. | amino_acid_sequence: One-letter format.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/16132353","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/2108187/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9589665/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16061832/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3098459/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6812220/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6292724/","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3093533/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6425363/","note":"half_life"}],"data_version":2,"slug":"ghrh","url":"https://peptidelabs.app/peptides/ghrh/"},{"id":45,"name":"GHRP-2","description":"Synthetic hexapeptide ghrelin-receptor agonist (pralmorelin, KP-102) that raised GH and food intake 36% in healthy men (n=7); approved in Japan as a single-dose GH-deficiency diagnostic (GHRP Kaken 100).","benefits":"Sustained GH and IGF-1 elevation over 30 days of SC infusion (human, older adults, n=17), increased food intake (human, n=7), validated GH-deficiency diagnostic (human, approved in Japan), growth velocity in GH-deficient children (human, n=6, open label)","categories":["growth hormone","muscle growth","appetite"],"recommended_dose":"1 mcg/kg IV or 100 mcg IV fixed dose (diagnostic); 1 mcg/kg/h SC infusion (30-day study); 0.3-3 mcg/kg/day SC in children; research-community range 100-300 mcg SC 1-3x daily","detailed_description":"GHRP-2 (pralmorelin, KP-102) is a second-generation GHRP from the Bowers series. In children, 1 mcg/kg IV gave a predictable GH rise with a 33 min plasma half-life (Pihoker 1998), and intranasal 5-20 mcg/kg was active (Pihoker 1995). Six GH-deficient children treated SC for 8 months grew faster, though IGF-1 did not rise and the effect of each injection was brief (Mericq 1998). In older adults, 30 days of continuous SC infusion at 1 mcg/kg/h sustained GH secretion at 1.8-fold and raised IGF-1 to a stable plateau (Bowers 2004). A 270 min SC infusion increased ad libitum food intake 36% in healthy men (Laferrere 2005). In Japan a 100 mcg IV test with a 15 mcg/L GH cut-off diagnoses severe adult GH deficiency (Chihara 2007) and it is approved there as a diagnostic. US development was discontinued. No body-composition or sleep trial exists.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["CJC-1295","Ipamorelin"],"dose_min_mcg":100,"dose_max_mcg":300,"dose_unit":"mcg","dose_frequency":"2-3x daily","recon_volume_ml":2,"common_vial_sizes":[5,10],"dosing_notes":"IV bolus in diagnostic use, SC injection or infusion in research. GH peaks within 60 min and the GH effect of a single SC dose is brief (Chihara 2007; Mericq 1998). GHRP-2 raised ACTH and cortisol in swine where ipamorelin did not (Raun 1998). Continuous 30-day SC infusion in older adults kept safety screening tests normal (Bowers 2004).","mechanism_of_action":"GHRP-2 is an agonist at the ghrelin receptor GHS-R1a on pituitary somatotrophs and in the hypothalamus. It releases GH through a pathway distinct from GHRH, and the two synergize in children and adults (Pihoker 1995; Bowers 2004). Like ghrelin it increases food intake in humans (Laferrere 2005). It also stimulates ACTH and cortisol release (Raun 1998, swine), which ipamorelin does not. GH responses are lower in GH-deficient patients than in healthy subjects regardless of age or adiposity, the basis of its diagnostic use (Chihara 2007).","clinical_studies":["1 mcg/kg IV: predictable GH rise, plasma half-life 33 min, in 10 children (Pihoker et al., 1998)","Intranasal 5-20 mcg/kg released GH in children; IV GHRP-2 + GHRH was synergistic (Pihoker et al., 1995)","8 months of SC 0.3-3 mcg/kg/day raised growth velocity in 6 GH-deficient children without raising IGF-1 (Mericq et al., 1998)","30-day continuous SC infusion at 1 mcg/kg/h sustained GH secretion and IGF-1 in 17 older adults (Bowers et al., 2004)","SC infusion increased ad libitum food intake 36% in 7 healthy men (Laferrere et al., 2005)","Human-trial status: approved in Japan as a GH-deficiency diagnostic (100 mcg IV, 15 mcg/L cut-off; Chihara et al., 2007); US development discontinued; no approved therapeutic use"],"evidence_level":"clinical","references":[{"title":"Growth hormone releasing peptide-2 (GHRP-2), like ghrelin, increases food intake in healthy men","authors":"Laferrere B, Abraham C, Russell CD, Bowers CY","journal":"Journal of Clinical Endocrinology & Metabolism","year":2005,"doi":"10.1210/jc.2004-1719","pmid":"15699539"},{"title":"Sustained elevation of pulsatile growth hormone (GH) secretion and insulin-like growth factor I (IGF-I), IGF-binding protein-3 (IGFBP-3), and IGFBP-5 concentrations during 30-day continuous subcutaneous infusion of GH-releasing peptide-2 in older men and women","authors":"Bowers CY, Granda R, Mohan S, Kuipers J, Baylink D, Veldhuis JD","journal":"Journal of Clinical Endocrinology & Metabolism","year":2004,"doi":"10.1210/jc.2003-031799","pmid":"15126555"},{"title":"A simple diagnostic test using GH-releasing peptide-2 in adult GH deficiency","authors":"Chihara K, Shimatsu A, Hizuka N, Tanaka T, Seino Y, Kato Y; KP-102 Study Group","journal":"European Journal of Endocrinology","year":2007,"doi":"10.1530/EJE-07-0066","pmid":"17609397"},{"title":"Pharmacokinetics and pharmacodynamics of growth hormone-releasing peptide-2: a phase I study in children","authors":"Pihoker C, Kearns GL, French D, Bowers CY","journal":"Journal of Clinical Endocrinology & Metabolism","year":1998,"doi":"10.1210/jcem.83.4.4744","pmid":"9543135"},{"title":"Diagnostic studies with intravenous and intranasal growth hormone-releasing peptide-2 in children of short stature","authors":"Pihoker C, Middleton R, Reynolds GA, Bowers CY, Badger TM","journal":"Journal of Clinical Endocrinology & Metabolism","year":1995,"doi":"10.1210/jcem.80.10.7559885","pmid":"7559885"},{"title":"Effects of eight months treatment with graded doses of a growth hormone (GH)-releasing peptide in GH-deficient children","authors":"Mericq V, Cassorla F, Bowers CY, Avila A, Gonen B, Merriam GR","journal":"Journal of Clinical Endocrinology & Metabolism","year":1998,"doi":"10.1210/jcem.83.7.4969","pmid":"9661608"},{"title":"Pralmorelin: GHRP 2, GPA 748, growth hormone-releasing peptide 2, KP-102 D, KP-102 LN, KP-102D, KP-102LN","authors":"Adis R&D Profile","journal":"Drugs in R&D","year":2004,"doi":null,"pmid":"15230633"},{"title":"Ipamorelin, the first selective growth hormone secretagogue","authors":"Raun K, Hansen BS, Johansen NL, et al.","journal":"European Journal of Endocrinology","year":1998,"doi":"10.1530/eje.0.1390552","pmid":"9849822"}],"molecular_weight":817.96,"amino_acid_sequence":"[D-A][D-2-Nal]AW[D-F]K[NH2]","alternative_names":["Growth Hormone Releasing Peptide 2","GHRP2","Pralmorelin","KP-102","GPA-748","GHRP Kaken 100"],"half_life":"~33 min (t1/2 beta; children, IV bolus; Pihoker 1998)","bioavailability":"Intranasal: GH response at 5-20 mcg/kg in children (Pihoker 1995); no absolute bioavailability figure located","side_effects":"No side effects or toxicities were observed over 8 months in GH-deficient children (Mericq 1998) and safety tests stayed normal over a 30-day infusion in older adults (Bowers 2004). Increased food intake is a documented human effect (Laferrere 2005). ACTH and cortisol rise acutely (Raun 1998, swine). Water retention, tingling in the hands, joint aches and reduced insulin sensitivity are commonly reported (anecdotal). Regulatory: GHRP-2 (injectable and nasal) is on FDA's 503B category 2 (significant safety risks) table, added 2023-09-29, page content as of 2026-04-22: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","last_reviewed_at":"2026-10-06T08:18:03.656Z","reviewed_by":"audit-2026-10","review_notes":"description: The 'less hunger than GHRP-6' claim has no human source; Laferrere 2005 shows a large appetite effect. | benefits: Tiers and sizes added. | detailed_description: Replaces unsupported body-composition, sleep and tissue-repair claims. | recommended_dose: Literature doses overlap the community range; numeric fields unchanged. | dosing_notes: Removed unsourced comparative ranking and advice tone. | mechanism_of_action: Removed unsourced 'direct peripheral effects on adipose tissue'. Old value omitted for length. | clinical_studies: Old bullets cited Bowers 1991 and a Laferrere title that does not exist. | half_life: Primary human PK. | bioavailability: Old value was a GH-timing statement. | side_effects: Removed unsourced gynecomastia and mood claims. | amino_acid_sequence: One-letter format. | alternative_names: Adds lab code and Japanese trade name. | Compounding listing per decision 78, from batch 16 table-by-table read of the FDA page. | side_effects: Decision 78: FDA compounding listing found while auditing the blends (batch 16), carried to the single-peptide record.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/6918245","note":"amino_acid_sequence"},{"url":"https://www.kegg.jp/entry/D02040","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9849822/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15699539/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17609397/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15126555/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9661608/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9543135/","note":"half_life"},{"url":"https://pubmed.ncbi.nlm.nih.gov/7559885/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15230633/","note":"alternative_names"},{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"}],"data_version":3,"slug":"ghrp-2","url":"https://peptidelabs.app/peptides/ghrp-2/"},{"id":18,"name":"GHRP-6","description":"First synthetic GH-releasing hexapeptide (Bowers 1984); raised GH dose-dependently and synergized with GHRH in normal men (n=18). Appetite and gut-motility effects are documented in rodents.","benefits":"GH release and GHRH synergy (human, n=18), reduced myocardial infarct size (pig), safety and functional signal in acute stroke with EGF (human phase 1/2, n=36, open label), bone mineral content (rat), food intake and gut transit (rat)","categories":["growth hormone","muscle growth","appetite"],"recommended_dose":"0.1-1 mcg/kg IV in human GH studies (about 70 mcg at 1 mcg/kg); 90 mcg IV in the GHRH+GHRP-6 test; research-community range 100-300 mcg SC 1-3x daily","detailed_description":"GHRP-6 (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) is the first synthetic growth hormone-releasing peptide, described by Bowers in 1984 before its receptor (GHS-R1a) or its natural ligand ghrelin were known. In normal men, IV doses of 0.1-1 mcg/kg raised peak GH from 1 to 69 mcg/L and acted synergistically with GHRH; prolactin and cortisol roughly doubled at the 1 mcg/kg dose (Bowers 1990, n=18). GHRH plus GHRP-6 became a diagnostic stimulus whose GH response is preserved into old age (Micic 1998). Cuban groups report tissue-protective effects: a 400 mcg/kg dose cut infarct mass 78% in pigs (Berlanga 2007), and GHRP-6 combined with EGF was safe in a phase 1/2 randomized open-label stroke trial (Hernandez-Bernal 2024, n=36). Human PK exists for IV dosing (Cabrales 2013). It is not approved as a drug in any jurisdiction.","storage_temp":"Refrigerated (2-8°C)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"24+ months at room temperature","stacks_with":["CJC-1295","Ipamorelin"],"dose_min_mcg":100,"dose_max_mcg":300,"dose_unit":"mcg","dose_frequency":"2-3x daily","recon_volume_ml":2,"common_vial_sizes":[5,10],"dosing_notes":"Subcutaneous or IV in research; human GH studies used IV bolus. GH peak occurs within about 30 min. Prolactin and cortisol rose about 2-fold at 1 mcg/kg IV in men (Bowers 1990). Elimination half-life after IV bolus is about 2.5 h (Cabrales 2013).","mechanism_of_action":"GHRP-6 is an agonist at the growth hormone secretagogue receptor GHS-R1a, the receptor later found to bind ghrelin (Kojima 1999). It releases GH from pituitary somatotrophs by a pathway separate from GHRH, and the two stimuli synergize in men (Bowers 1990). At 1 mcg/kg IV it also roughly doubled prolactin and cortisol in men (Bowers 1990). In the heart, GHRPs bind CD36 as well as GHS-R1a; CD36 mediates the coronary effects of hexarelin in mice and is a proposed mechanism for the GHRP-6 cardioprotection seen in pigs (Berlanga 2007).","clinical_studies":["Raised peak GH from 1 to 69 mcg/L at 1 mcg/kg IV and synergized with GHRH in normal men, n=18 (Bowers et al., 1990)","GHRH + GHRP-6 (90 mcg each, IV) produced a preserved GH response in subjects aged 19-96 (Micic et al., 1998)","IV bolus 100-400 mcg/kg: distribution half-life 7.6 min, elimination half-life 2.5 h in nine healthy men (Cabrales et al., 2013)","400 mcg/kg reduced infarct mass 78% after coronary occlusion in pigs (Berlanga et al., 2007)","EGF + GHRP-6 (3.5-5 mg IV twice daily, 7 days) was safe in a phase 1/2 randomized open-label stroke trial, n=36 (Hernandez-Bernal et al., 2024)","Human-trial status: decades of acute human GH studies and one phase 1/2 combination trial; not approved anywhere"],"evidence_level":"clinical","references":[{"title":"On the in vitro and in vivo activity of a new synthetic hexapeptide that acts on the pituitary to specifically release growth hormone","authors":"Bowers CY, Momany FA, Reynolds GA, Hong A","journal":"Endocrinology","year":1984,"doi":"10.1210/endo-114-5-1537","pmid":"6714155"},{"title":"Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone","authors":"Bowers CY, Reynolds GA, Durham D, Barrera CM, Pezzoli SS, Thorner MO","journal":"Journal of Clinical Endocrinology & Metabolism","year":1990,"doi":"10.1210/jcem-70-4-975","pmid":"2108187"},{"title":"Pharmacokinetic study of Growth Hormone-Releasing Peptide 6 (GHRP-6) in nine male healthy volunteers","authors":"Cabrales A, Gil J, Fernandez E, et al.","journal":"European Journal of Pharmaceutical Sciences","year":2013,"doi":"10.1016/j.ejps.2012.10.006","pmid":"23099431"},{"title":"Preserved growth hormone (GH) secretion in aged and very old subjects after testing with the combined stimulus GH-releasing hormone plus GH-releasing hexapeptide-6","authors":"Micic D, Popovic V, Doknic M, et al.","journal":"Journal of Clinical Endocrinology & Metabolism","year":1998,"doi":"10.1210/jcem.83.7.4957","pmid":"9661645"},{"title":"Growth-hormone-releasing peptide 6 (GHRP6) prevents oxidant cytotoxicity and reduces myocardial necrosis in a model of acute myocardial infarction","authors":"Berlanga J, Cibrian D, Guevara L, et al.","journal":"Clinical Science (London)","year":2007,"doi":"10.1042/CS20060103","pmid":"16989643"},{"title":"Combination therapy of Epidermal Growth Factor and Growth Hormone-Releasing Hexapeptide in acute ischemic stroke: a phase I/II non-blinded, randomized clinical trial","authors":"Hernandez-Bernal F, Estenoz-Garcia D, Gutierrez-Ronquillo JH, et al.","journal":"Frontiers in Neurology","year":2024,"doi":"10.3389/fneur.2024.1303402","pmid":"38638315"},{"title":"The GH secretagogues ipamorelin and GH-releasing peptide-6 increase bone mineral content in adult female rats","authors":"Svensson J, Lall S, Dickson SL, et al.","journal":"Journal of Endocrinology","year":2000,"doi":"10.1677/joe.0.1650569","pmid":"10828840"},{"title":"Ghrelin is a growth-hormone-releasing acylated peptide from stomach","authors":"Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K","journal":"Nature","year":1999,"doi":"10.1038/45230","pmid":"10604470"}],"molecular_weight":873.01,"amino_acid_sequence":"H[D-W]AW[D-F]K[NH2]","alternative_names":["Growth Hormone Releasing Peptide 6","GHRP6","SKF-110679"],"half_life":"~2.5 h elimination, 7.6 min distribution (human, IV bolus; Cabrales 2013)","bioavailability":null,"side_effects":"In men, 1 mcg/kg IV produced no adverse clinical effects; prolactin and cortisol rose about 2-fold at that dose (Bowers 1990). Adverse events in the stroke trial did not exceed control (Hernandez-Bernal 2024). Appetite increase, water retention, tingling in the hands, lethargy and reduced insulin sensitivity are commonly reported (anecdotal) with repeated SC use. Regulatory: GHRP-6 is on FDA's 503B category 2 (significant safety risks) table, added 2023-09-29, page content as of 2026-04-22: https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","last_reviewed_at":"2026-10-06T08:18:03.656Z","reviewed_by":"audit-2026-10","review_notes":"description: Human appetite data in the located literature are for GHRP-2 and ghrelin, not GHRP-6; model systems added. | benefits: Muscle gain has no human source; tiers added. | detailed_description: Replaces vague 'healing properties' and 'caloric surplus' with cited findings and model systems. | recommended_dose: Literature doses sit at the bottom of the community range, so the numeric fields stand; the text now says which is which. | dosing_notes: Removed advice phrasing and the unsourced 'strongest hunger effect' ranking. | mechanism_of_action: Removed the unsourced claim that GHRP-6 stimulates ghrelin release from the stomach. Old value omitted for length; it is the current record text. | clinical_studies: Old bullets cited a 1991 Bowers paper and a 1996 Chapman appetite study that are not GHRP-6 papers (the Chapman 1996 paper is MK-677). | half_life: Primary human PK. | bioavailability: No SC bioavailability study located; the old value was a GH-timing statement, not a bioavailability figure. | side_effects: Separates literature from anecdote; removes unsourced gynecomastia claim. | amino_acid_sequence: One-letter format. | Compounding listing per decision 78, from batch 16 table-by-table read of the FDA page. | side_effects: Decision 78: FDA compounding listing found while auditing the blends (batch 16), carried to the single-peptide record.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/4345065","note":"amino_acid_sequence"},{"url":"https://pubmed.ncbi.nlm.nih.gov/10604470/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9849822/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11988484/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/19289567/","note":"dosing_notes"},{"url":"https://doi.org/10.1530/eje.0.1390552","note":"Raun 1998: GHRP-6 and GHRP-2 raised ACTH and cortisol in swine; not in references (8-reference cap)"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6714155/","note":"detailed_description"},{"url":"https://pubmed.ncbi.nlm.nih.gov/2108187/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/16989643/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/38638315/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/10828840/","note":"benefits"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9661645/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23099431/","note":"bioavailability"},{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"side_effects"}],"data_version":3,"slug":"ghrp-6","url":"https://peptidelabs.app/peptides/ghrp-6/"},{"id":46,"name":"Glutathione","description":"Endogenous tripeptide (Glu-Cys-Gly) and the main intracellular antioxidant, central to phase II detoxification and cellular redox defence.","benefits":"Raised blood, erythrocyte and lymphocyte glutathione stores and lowered the oxidized to reduced ratio at 250 to 1000 mg/day oral for 6 months (human RCT, n=54), lower melanin index at 500 mg/day oral for 4 weeks (human RCT, n=60), phase II detoxification cofactor (biochemistry, not a trial)","categories":["anti-aging","immune","skin health"],"recommended_dose":"200 to 600 mg by injection: clinic and community range. Published intravenous doses were higher: 1400 mg three times weekly (Hauser 2009) and 600 mg twice daily for 30 days (Sechi 1996)","detailed_description":"Glutathione is the endogenous tripeptide gamma-Glu-Cys-Gly (PubChem CID 124886), the main intracellular thiol antioxidant. The human trial record is mixed and route-dependent. Oral dosing at 250 or 1000 mg/day for 6 months raised glutathione in blood, erythrocytes, plasma, lymphocytes and buccal cells in 54 adults, with stores returning to baseline a month after stopping (Richie 2015). Oral 500 mg/day for 4 weeks lowered melanin index at 2 of 6 measured sites in 60 subjects (Arjinpathana 2012). By injection the picture is worse: a randomized trial of intravenous glutathione 1400 mg three times weekly for 4 weeks in 21 Parkinson patients found no significant UPDRS difference (Hauser 2009), and intranasal dosing was not superior to placebo (Mischley 2017). No parenteral glutathione product is approved for any systemic or cosmetic indication.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["NAD+","NMN"],"dose_min_mcg":200000,"dose_max_mcg":600000,"dose_unit":"mcg","dose_frequency":"1-3x weekly","recon_volume_ml":5,"common_vial_sizes":[200,600],"dosing_notes":"Intravenous or subcutaneous in research and clinic use. Published human doses, verbatim: 1400 mg intravenously three times a week for 4 weeks, randomized and placebo-controlled, no significant effect (Hauser 2009); 600 mg intravenously twice daily for 30 days, open label, 42% decline in disability (Sechi 1996); 100 or 200 mg intranasally three times daily for 3 months, not superior to placebo (Mischley 2017); 250 to 1000 mg/day orally for 6 months, which raised body stores (Richie 2015). No parenteral product is approved for a cosmetic indication anywhere, and compounded sterility is a documented problem.","mechanism_of_action":"Glutathione cycles between its reduced (GSH) and oxidized (GSSG) forms, serves as the cofactor for glutathione peroxidases, and is conjugated to electrophiles by glutathione-S-transferases for phase II elimination. The skin-lightening rationale is inhibition of tyrosinase and a shift from eumelanin to pheomelanin, which is in vitro pharmacology rather than a demonstrated mechanism in treated skin (Dlova 2026). One mechanistic claim in the old record is wrong in the other direction: parenteral dosing is justified by poor oral absorption, yet the one long randomized oral trial raised body stores at 250 and 1000 mg/day (Richie 2015), and liposomal oral dosing raised stores and natural killer activity (Sinha 2018). Direct cellular uptake of intact glutathione is limited; the gamma-glutamyl cycle normally breaks it down extracellularly and reassembles it inside cells.","clinical_studies":["Oral glutathione at 250 or 1000 mg/day for 6 months raised glutathione in blood, erythrocytes, plasma, lymphocytes and buccal cells in 54 adults, lowered the oxidized to reduced ratio, and more than doubled natural killer cytotoxicity in the high-dose group; levels returned to baseline after a 1-month washout (Richie et al., 2015)","Oral 500 mg/day for 4 weeks lowered melanin index at all six measured sites in 60 healthy subjects, reaching significance versus placebo at two sites (Arjinpathana et al., 2012)","Intravenous glutathione 1400 mg three times weekly for 4 weeks in 21 Parkinson patients was well tolerated but produced no significant UPDRS difference; a 2.8-unit mean improvement did not reach significance and reversed during follow-up (Hauser et al., 2009)","An earlier open-label series of 9 untreated early Parkinson patients given 600 mg intravenously twice daily for 30 days reported a 42% decline in disability lasting 2 to 4 months after stopping, with no control group (Sechi et al., 1996)","Intranasal glutathione at 100 or 200 mg three times daily for 3 months in 45 Parkinson patients improved UPDRS scores, but so did placebo, and neither dose separated from it; one high-dose participant developed cardiomyopathy (Mischley et al., 2017)","Human-trial status: the positive randomized evidence is oral. No randomized trial of injected glutathione has shown benefit for any indication, and a 2026 scoping review of systemic glutathione for skin lightening found the intravenous evidence base inadequate. The only US-approved product containing glutathione is an intraocular irrigating solution, BSS PLUS (NDA 018469)"],"evidence_level":"clinical","references":[{"title":"Randomized controlled trial of oral glutathione supplementation on body stores of glutathione","authors":"Richie JP Jr, Nichenametla S, Neidig W, Calcagnotto A, et al.","journal":"European Journal of Nutrition","year":2015,"doi":"10.1007/s00394-014-0706-z","pmid":"24791752"},{"title":"Glutathione as an oral whitening agent: a randomized, double-blind, placebo-controlled study","authors":"Arjinpathana N, Asawanonda P","journal":"Journal of Dermatological Treatment","year":2012,"doi":"10.3109/09546631003801619","pmid":"20524875"},{"title":"Randomized, double-blind, pilot evaluation of intravenous glutathione in Parkinson's disease","authors":"Hauser RA, Lyons KE, McClain T, Carter S, Perlmutter D","journal":"Movement Disorders","year":2009,"doi":"10.1002/mds.22401","pmid":"19230029"},{"title":"Reduced intravenous glutathione in the treatment of early Parkinson's disease","authors":"Sechi G, Deledda MG, Bua G, Satta WM, et al.","journal":"Progress in Neuro-Psychopharmacology and Biological Psychiatry","year":1996,"doi":"10.1016/s0278-5846(96)00103-0","pmid":"8938817"},{"title":"Phase IIb Study of Intranasal Glutathione in Parkinson's Disease","authors":"Mischley LK, Lau RC, Shankland EG, Wilbur TK, Padowski JM","journal":"Journal of Parkinson's Disease","year":2017,"doi":"10.3233/JPD-161040","pmid":"28436395"},{"title":"Oral supplementation with liposomal glutathione elevates body stores of glutathione and markers of immune function","authors":"Sinha R, Sinha I, Calcagnotto A, Trushin N, et al.","journal":"European Journal of Clinical Nutrition","year":2018,"doi":"10.1038/ejcn.2017.132","pmid":"28853742"},{"title":"Systemic glutathione for skin lightening: a scoping review of current evidence","authors":"Dlova NC, Enechukwu NA, Cole-Adeife O, Sagoe D","journal":"Journal of the European Academy of Dermatology and Venereology","year":2026,"doi":"10.1111/jdv.70514","pmid":"42183737"},{"title":"Glutathione Whitening Pills Induced Toxic Epidermal Necrolysis: An Unusual Case Confirmed by Enzyme-Linked Immunospot Assay and Liquid Chromatography-Mass Spectrometry","authors":"Chottawornsak N, Tansrisawad N, Tubtimrattana A, Thantiworasit P, et al.","journal":"Dermatitis","year":2022,"doi":"10.1097/DER.0000000000000782","pmid":"34608063"}],"molecular_weight":307.33,"amino_acid_sequence":"γ-Glu-Cys-Gly (γ-glutamyl bond, not standard peptide bond)","alternative_names":["GSH","L-Glutathione","Reduced glutathione","γ-L-glutamyl-L-cysteinyl-glycine"],"half_life":"Not reported in the published human trials. Oral dosing at 250 to 1000 mg/day for 6 months raised body stores, which returned to baseline within a 1-month washout (Richie 2015)","bioavailability":"Oral: absolute bioavailability has not been measured, but 250 to 1000 mg/day for 6 months raised blood, erythrocyte, plasma and lymphocyte stores (Richie 2015), and liposomal oral dosing raised stores and immune markers (Sinha 2018). Injection: no bioavailability or exposure data from the published trials","side_effects":"In the randomized trials glutathione was well tolerated: adverse events matched placebo at 1400 mg intravenously three times weekly (Hauser 2009) and at 250 to 1000 mg/day orally for 6 months (Richie 2015). Serious harms are documented in case reports and reviews of cosmetic use rather than in trials: toxic epidermal necrolysis after glutathione whitening pills, confirmed by ELISpot and mass spectrometry (Chottawornsak 2022), systemic inflammatory response syndrome after a high-dose intravenous glutathione revitalizing solution, reported as a single case in 2025, and one cardiomyopathy case in the intranasal trial. A 2026 scoping review concludes that the systemic skin-lightening evidence does not support the practice.","last_reviewed_at":"2026-10-06T08:17:37.850Z","reviewed_by":"audit-2026-10","review_notes":"storage: general guidance. Positive randomized evidence is oral; the injectable route has a negative randomized trial, which is stated in the bullets. FDA safety-warning claim removed as unverifiable. Molecular weight from PubChem CID 124886. | benefits: Each item now carries its tier and route. The two positive randomized trials are both oral, which matters because this record is the injectable. | detailed_description: Old text asserted benefits for oxidative stress conditions, skin health and cellular protection with no trial detail, and did not mention that the randomized intravenous trial was negative. Old value omitted for length. | mechanism_of_action: Old text asserted that IV and SC administration bypass poor oral bioavailability and that glutathione regenerates vitamins C and E, neither sourced. The oral trial contradicts the first. Old value omitted for length. | recommended_dose: Decision 24 in reverse: the published doses sit above the stored range, so the field names both. | dosing_notes: Decision 10: every published human dose now appears verbatim. The Philippine FDA advisory could not be resolved to a citable page in this pass, so the harm list moved to the peer-reviewed sources that document it. | clinical_studies: Old bullets claimed IV glutathione improved motor symptoms in Parkinson pilot studies, which inverts the randomized result, and credited the acetaminophen indication to glutathione when the approved drug is acetylcysteine. The insulin-sensitivity bullet had no identifiable study. | half_life: The 10 to 15 minute figure has no source in the cited literature. Replaced with the one measured persistence result. | bioavailability: \"Poor (<5%)\" has no source and is contradicted by the one long oral randomized trial. | side_effects: The FDA safety warning claim could not be verified against a citable fda.gov page in this pass, and a search of fda.gov.ph returned only product-specific advisories. The harms are real and now rest on resolved peer-re","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/124886/property/MolecularFormula,MolecularWeight,IUPACName/JSON","note":"molecular weight 307.33, C10H17N3O6S, reduced glutathione, CID 124886"},{"url":"https://api.fda.gov/drug/drugsfda.json?search=openfda.generic_name:%22glutathione%22","note":"clinical_studies"},{"url":"https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks","note":"glutathione is not named on the FDA compounding category 2 or withdrawn-nomination tables; content current as of 04/22/2026"},{"url":"https://www.fda.gov.ph/?s=glutathione","note":"Philippine FDA search returns product-specific advisories only; the general intravenous advisory could not be resolved in this pass"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42751591/","note":"Aloraini 2026 critical narrative review of glutathione skin lightening by all three routes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/24791752/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/20524875/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/19230029/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/28436395/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/28853742/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/42183737/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/8938817/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/40556995/","note":"side_effects"},{"url":"https://pubmed.ncbi.nlm.nih.gov/34608063/","note":"side_effects"},{"url":"https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/124886/property/MolecularFormula,MolecularWeight/JSON","note":"molecular_weight"}],"data_version":2,"slug":"glutathione","url":"https://peptidelabs.app/peptides/glutathione/"},{"id":47,"name":"Gonadorelin (GnRH)","description":"Synthetic GnRH decapeptide; pulsatile doses raise LH and FSH, continuous exposure suppresses them. US human products Factrel (1982) and Lutrepulse (1989) are discontinued.","benefits":"LH and FSH release test of pituitary reserve (approved diagnostic, US product discontinued), puberty and ovulation induction by pulsatile pump in hypogonadotropic hypogonadism (human trials), testicular support during TRT (community use, no trial)","categories":["hormonal","fertility"],"recommended_dose":"Community range 200 to 300 mcg subcutaneous (off-label; no current US human label).","detailed_description":"Gonadorelin is synthetic gonadotropin-releasing hormone, identical to the hypothalamic decapeptide. The FDA approved it as Factrel (NDA 018123, 1982) for testing pituitary gonadotropin reserve and as Lutrepulse (NDA 019687, 1989) for pulsatile pump induction of ovulation; both are discontinued. Every current gonadorelin label on DailyMed is veterinary (Factrel by Zoetis, Cystorelin, Fertagyl, used in cattle). Human trials used an infusion pump giving a pulse every 1 to 2 hours, which induced puberty in men and ovulation in women with hypogonadotropic hypogonadism (Hoffman 1982; Martin 1993). The once-daily subcutaneous use alongside TRT sold by vendors has no published trial.","storage_temp":"Refrigerate 2-8°C (36-46°F)","shelf_life_reconstituted":"28-30 days refrigerated","shelf_life_powder":"2+ years at room temp, 3+ years refrigerated","stacks_with":["Kisspeptin-10","HCG"],"dose_min_mcg":200,"dose_max_mcg":300,"dose_unit":"mcg","dose_frequency":"1x daily (before bed)","recon_volume_ml":2,"common_vial_sizes":[2,5],"dosing_notes":"Community protocols use 200 to 300 mcg subcutaneously to stimulate LH and FSH alongside TRT (off-label). The US human products Factrel and Lutrepulse are discontinued, so no current label gives a dose. Sustained exposure suppresses the gonadal axis rather than stimulating it.","mechanism_of_action":"Gonadorelin binds the GnRH receptor on pituitary gonadotrophs and releases LH and FSH (Conn 1991). The response depends on the pattern of exposure: in rhesus monkeys with hypothalamic lesions, hourly pulses restored LH and FSH secretion while a continuous infusion of the same hormone suppressed it (Belchetz 1978). That finding is the basis both for pulsatile pump therapy and for long-acting GnRH agonists used to shut the axis down. Native GnRH is cleared within minutes, which is why therapeutic use needed a pump rather than daily injections (Handelsman 1986).","clinical_studies":["Hourly GnRH pulses restored LH and FSH in rhesus monkeys with hypothalamic lesions, while continuous infusion suppressed them (Belchetz et al., 1978)","Long-term low-dose pulsatile GnRH induced puberty in men with hypogonadotropic hypogonadism (Hoffman and Crowley, 1982)","Pulsatile GnRH was compared with exogenous gonadotropins for ovulation induction in women with hypogonadotropic amenorrhea (Martin et al., 1993)","Review of GnRH and its analogue pharmacology in reproductive medicine (Conn and Crowley, 1991)","Human-trial status: approved by the FDA as Factrel (1982, diagnostic) and Lutrepulse (1989, ovulation induction), both discontinued; current US labels are veterinary only, and no trial has tested daily subcutaneous gonadorelin during TRT"],"evidence_level":"clinical","references":[{"title":"Gonadotropin-releasing hormone and its analogues","authors":"Conn PM, Crowley WF Jr","journal":"New England Journal of Medicine","year":1991,"doi":"10.1056/NEJM199101103240205","pmid":"1984190"},{"title":"Hypophysial responses to continuous and intermittent delivery of hypopthalamic gonadotropin-releasing hormone","authors":"Belchetz PE, Plant TM, Nakai Y, et al.","journal":"Science","year":1978,"doi":"10.1126/science.100883","pmid":"100883"},{"title":"Induction of puberty in men by long-term pulsatile administration of low-dose gonadotropin-releasing hormone","authors":"Hoffman AR, Crowley WF Jr","journal":"New England Journal of Medicine","year":1982,"doi":"10.1056/NEJM198211113072003","pmid":"6813732"},{"title":"Comparison of exogenous gonadotropins and pulsatile gonadotropin-releasing hormone for induction of ovulation in hypogonadotropic amenorrhea","authors":"Martin KA, Hall JE, Adams JM, Crowley WF Jr","journal":"Journal of Clinical Endocrinology & Metabolism","year":1993,"doi":"10.1210/jcem.77.1.8325934","pmid":"8325934"},{"title":"Pharmacokinetics of gonadotropin-releasing hormone and its analogs","authors":"Handelsman DJ, Swerdloff RS","journal":"Endocrine Reviews","year":1986,"doi":"10.1210/edrv-7-1-95","pmid":"3007081"}],"molecular_weight":1182.29,"amino_acid_sequence":"pGlu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2","alternative_names":["GnRH","LHRH","Luteinizing hormone-releasing hormone","Factrel","Lutrepulse","Gonadorelin acetate","Gonadorelin hydrochloride","Cystorelin (veterinary)","Fertagyl (veterinary)"],"half_life":"~2-4 minutes (very short)","bioavailability":"Subcutaneous: Rapid absorption; requires frequent pulsatile dosing for physiologic effect","side_effects":"Injection-site reactions, headache, nausea, and flushing are the most common effects. Continuous rather than pulsatile administration downregulates the pituitary and suppresses the gonadal axis, the opposite of the intended effect. Rare hypersensitivity reactions have been reported.","last_reviewed_at":"2026-10-06T08:31:00.354Z","reviewed_by":"audit-2026-10","review_notes":"claims_verified: FDA approvals of Factrel (NDA 018123, 1982) and Lutrepulse (NDA 019687, 1989), both discontinued; current DailyMed labels are veterinary. storage: general guidance. | description: Adds the US marketing status (decision 12). Old text was accurate on pharmacology but silent on the fact that no human product is sold in the US. | benefits: Decision 55: the approved uses carry their tier, and the TRT use is named as community practice. | detailed_description: Old text claimed studies \"demonstrate\" testosterone maintenance on TRT; no study does. Adds approval and discontinuation, the veterinary-only current labels, and what the human trials actually used. | mechanism_of_action: Old text asserted maintenance of testicular function during testosterone therapy as an established use. Rewritten to the receptor pharmacology and the primate pulse study, with model systems named. | clinical_studies: Old bullets said \"FDA-approved\" with no year or status and claimed TRT efficacy with no source. | alternative_names: Adds the two salt forms named in Drugs@FDA and the veterinary trade names on current DailyMed labels. | Batch 09 follow-up (decisions 4, 11, 15, 18). | recommended_dose: Decision 11. | dosing_notes: Unsourced half-life claim removed; regulatory status from batch 09.","sources":[{"url":"https://api.fda.gov/drug/drugsfda.json?search=products.active_ingredients.name:%22GONADORELIN%22","note":"alternative_names"},{"url":"https://api.fda.gov/drug/label.json?search=openfda.generic_name:%22GONADORELIN%22","note":"openFDA label: NOT_FOUND, no current human prescription label"},{"url":"https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=1451663c-b85a-4b45-8b27-6d572d0032f9","note":"detailed_description"},{"url":"https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=50cf9edb-f318-41d2-9b98-6ea3410e8128","note":"alternative_names"},{"url":"https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=0b4cad4e-df2a-4192-aee1-5d75c756632a","note":"alternative_names"},{"url":"https://pubmed.ncbi.nlm.nih.gov/100883/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/6813732/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/8325934/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/1984190/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/3007081/","note":"mechanism_of_action"}],"data_version":3,"slug":"gonadorelin-gnrh","url":"https://peptidelabs.app/peptides/gonadorelin-gnrh/"},{"id":12,"name":"GW501516","description":"Small-molecule PPAR-delta agonist (Cardarine), not a peptide. Raised HDL and lowered LDL and triglycerides in 2 to 12 week human trials; development stopped after rodent studies found tumours at all doses.","benefits":"Raised HDL cholesterol and lowered LDL, triglycerides and apoB (human RCTs, 2 to 12 weeks), increased fat oxidation and lowered liver fat (human, 2 weeks, n=6 per arm), running endurance (mouse)","categories":["fat loss","metabolic"],"recommended_dose":"2.5 to 10 mg once daily by mouth (doses used in 2 to 12 week human trials; development halted for rodent carcinogenicity)","detailed_description":"GW501516 is a selective PPAR-delta agonist from GlaxoSmithKline, described in 2003 (Sznaidman). In obese rhesus monkeys it raised HDL and lowered triglycerides and insulin (Oliver 2001). In healthy volunteers, 2.5 or 10 mg daily for 2 weeks raised HDL (Sprecher 2007); in moderately obese men, 10 mg daily for 2 weeks lowered triglycerides, LDL, insulin and liver fat and raised fat oxidation (Risérus 2008). A 12-week phase 2 trial in 268 people with low HDL found HDL up to 16.9% higher at 10 mg (Olson 2012). In mice it raised running endurance with exercise (Narkar 2008). Two-year GSK studies found treatment-related tumours in many tissues in rats and mice at every dose, and development was halted. WADA has prohibited it since 2009 and issued a health warning in 2013. No trial is active.","storage_temp":"Room temperature, dry, protected from light (general small-molecule guidance; no compound-specific CoA located)","shelf_life_reconstituted":null,"shelf_life_powder":"24+ months","stacks_with":[],"dose_min_mcg":2500,"dose_max_mcg":10000,"dose_unit":"mcg","dose_frequency":"1x daily","recon_volume_ml":null,"common_vial_sizes":null,"dosing_notes":"Oral. Human trials used 2.5, 5 or 10 mg once daily for 2 weeks (Sprecher 2007; Risérus 2008) or 12 weeks (Olson 2012). Rodent carcinogenicity studies dosed 3 to 80 mg/kg/day for 104 weeks and found tumours at every dose. No long-term human dosing has been studied.","mechanism_of_action":"GW501516 binds and activates PPAR-delta (PPARβ/δ), a nuclear receptor, with high selectivity over PPAR-alpha and PPAR-gamma (Sznaidman 2003). In human skeletal muscle cells it raised fatty acid oxidation and expression of CPT1, CD36 and the cholesterol efflux transporter ABCA1 (Sprecher 2007). In obese men it raised the share of dietary fat oxidised and muscle CPT1b expression (Risérus 2008). In primates, ABCA1 induction is the proposed basis of the HDL rise (Oliver 2001). In mice, combined with exercise, it induced oxidative muscle gene programmes (Narkar 2008). PPAR-delta activation also accelerated intestinal adenoma growth in Apc(min) mice, which is the proposed link to the rodent tumour findings (Gupta 2004).","clinical_studies":["12 weeks of 2.5 to 10 mg daily in 268 people with low HDL raised HDL up to 16.9% and lowered LDL 7.3% and triglycerides 16.9% (Olson et al., 2012)","10 mg daily for 2 weeks in moderately obese men lowered triglycerides 30%, LDL 23%, insulin 11% and liver fat 20%, and raised fat oxidation (Risérus et al., 2008)","First human report: 2.5 or 10 mg daily for 2 weeks raised HDL in healthy volunteers (Sprecher et al., 2007)","Raised running endurance in exercised mice; with AICAR it was the original 'exercise mimetic' paper (Narkar et al., 2008)","Increased the number and size of intestinal polyps in Apc(min) mice (Gupta et al., 2004); 104-week GSK studies found tumours in many tissues in rats and mice at all doses (Geiger and Newsholme, Toxicologist 2009)","Human-trial status: development halted after the rodent carcinogenicity findings; no active trials; WADA-prohibited since 2009"],"evidence_level":"clinical","references":[{"title":"Novel selective small molecule agonists for peroxisome proliferator-activated receptor delta (PPARdelta)--synthesis and biological activity","authors":"Sznaidman ML, Haffner CD, Maloney PR, et al.","journal":"Bioorganic & Medicinal Chemistry Letters","year":2003,"doi":"10.1016/s0960-894x(03)00207-5","pmid":"12699745"},{"title":"A selective peroxisome proliferator-activated receptor delta agonist promotes reverse cholesterol transport","authors":"Oliver WR Jr, Shenk JL, Snaith MR, et al.","journal":"Proceedings of the National Academy of Sciences of the United States of America","year":2001,"doi":"10.1073/pnas.091021198","pmid":"11309497"},{"title":"Triglyceride:high-density lipoprotein cholesterol effects in healthy subjects administered a peroxisome proliferator activated receptor delta agonist","authors":"Sprecher DL, Massien C, Pearce G, et al.","journal":"Arteriosclerosis, Thrombosis, and Vascular Biology","year":2007,"doi":"10.1161/01.ATV.0000252790.70572.0c","pmid":"17110604"},{"title":"Activation of peroxisome proliferator-activated receptor (PPAR)delta promotes reversal of multiple metabolic abnormalities, reduces oxidative stress, and increases fatty acid oxidation in moderately obese men","authors":"Risérus U, Sprecher D, Johnson T, et al.","journal":"Diabetes","year":2008,"doi":"10.2337/db07-1318","pmid":"18024853"},{"title":"Lipid effects of peroxisome proliferator-activated receptor-δ agonist GW501516 in subjects with low high-density lipoprotein cholesterol: characteristics of metabolic syndrome","authors":"Olson EJ, Pearce GL, Jones NP, Sprecher DL","journal":"Arteriosclerosis, Thrombosis, and Vascular Biology","year":2012,"doi":"10.1161/ATVBAHA.112.247890","pmid":"22814748"},{"title":"AMPK and PPARdelta agonists are exercise mimetics","authors":"Narkar VA, Downes M, Yu RT, et al.","journal":"Cell","year":2008,"doi":"10.1016/j.cell.2008.06.051","pmid":"18674809"},{"title":"Activation of nuclear hormone receptor peroxisome proliferator-activated receptor-delta accelerates intestinal adenoma growth","authors":"Gupta RA, Wang D, Katkuri S, et al.","journal":"Nature Medicine","year":2004,"doi":"10.1038/nm993","pmid":"14758356"},{"title":"Metabolic modulators of the exercise response: doping control analysis of an agonist of the peroxisome proliferator-activated receptor δ (GW501516) and 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR)","authors":"Pokrywka A, Cholbinski P, Kaliszewski P, et al.","journal":"Journal of Physiology and Pharmacology","year":2014,"pmid":"25179079"}],"molecular_weight":453.5,"amino_acid_sequence":null,"alternative_names":["Cardarine","GW-501516","Endurobol","GSK-516"],"half_life":"Not reported in peer-reviewed literature; human trials dosed once daily by mouth (Sprecher 2007; Olson 2012)","bioavailability":"Orally active in rodents, primates and humans (Oliver 2001; Sprecher 2007); no absolute bioavailability figure published","side_effects":"Published human trials (2 to 12 weeks, up to 10 mg daily) report lipid outcomes and no serious drug-related findings, but none ran long enough to address cancer risk. In 104-week GSK studies, rats given 3 to 40 mg/kg/day developed treatment-related tumours in liver, bladder, thyroid, stomach, tongue, skin, uterus and other tissues, with higher mortality in females at all doses; mice given 10 to 80 mg/kg/day developed liver and squamous stomach tumours. It enlarged intestinal polyps in Apc(min) mice. WADA issued a public health warning in 2013. No long-term human safety data exist.","last_reviewed_at":"2026-10-06T08:17:29.477Z","reviewed_by":"audit-2026-10","review_notes":"N/A-by-design: oral. storage: general guidance. Carcinogenicity sources are conference abstracts (no DOI), listed in sources. | description: Decision 20: class in the first clause. Old text was accurate in spirit; now names the trial durations and the all-doses tumour finding from the GSK carcinogenicity abstracts. | benefits: Each item now carries its model system. | detailed_description: Old text used 'dramatic effects' and 'potential cardiovascular benefits' without model systems and understated the carcinogenicity findings. Old value omitted for length. | mechanism_of_action: Keeps the pathway but attributes each step. Drops the unsourced 'slow-twitch fibre development' and the 'NOT a peptide' note, which now lives in description. Old value omitted for length. | clinical_studies: Old bullets cited 'Olson et al., 2012' under the wrong journal, claimed tumours at '40-100x human equivalent' (the rat abstract reports tumours from 3 mg/kg/day) and gave a 2007 discontinuation date no source supports. | side_effects: Replaces 'should not be considered safe' with the specific findings, doses and species from the primary carcinogenicity abstracts. | half_life: No published human or animal PK paper located; the 16 to 24 h figure has no source. | bioavailability: 'High' was unsourced. | dose_min_mcg: Human trials used 2.5, 5 and 10 mg daily; the range now matches the text. | recommended_dose: Adds route and duration; agrees with dose_min/dose_max. | dosing_notes: Old note was close; adds the trial citations and the rodent dose range, drops the 'explicit health warning' wording now carried by side_effects. | storage_temp: Labelled as general guidance. | stacks_with: Decision 14: no published combination with either compound and no documented community protocol located.","sources":[{"url":"https://pubchem.ncbi.nlm.nih.gov/compound/9803963","note":"C21H18F3NO3S2, MW 453.5; synonyms GW501516, Cardarine, Endurobol, GSK-516"},{"url":"https://www.toxicology.org/pubs/docs/Tox/2009Tox.pdf","note":"dosing_notes"},{"url":"https://www.wada-ama.org/en/news/wada-issues-alert-gw501516","note":"side_effects"},{"url":"https://clinicaltrials.gov/study/NCT00158899","note":"GSK phase 2, low HDL, n=424 enrolled, completed 2004 start"},{"url":"https://pubmed.ncbi.nlm.nih.gov/22814748/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17110604/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18024853/","note":"dosing_notes"},{"url":"https://pubmed.ncbi.nlm.nih.gov/18674809/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/12699745/","note":"mechanism_of_action"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11309497/","note":"bioavailability"},{"url":"https://pubmed.ncbi.nlm.nih.gov/25179079/","note":"clinical_studies"},{"url":"https://pubmed.ncbi.nlm.nih.gov/14758356/","note":"side_effects"}],"data_version":2,"slug":"gw501516","url":"https://peptidelabs.app/peptides/gw501516/"}],"meta":{"total":134,"page":1,"per_page":50,"generated_at":"2026-10-21T05:39:25.876Z","source":"https://peptidelabs.app","attribution":"Data from PeptideLab (https://peptidelabs.app). Link back required.","license":"CC BY-NC 4.0","disclaimer":"PeptideLab does not provide medical advice, diagnosis, or treatment recommendations. The information here is for educational and research purposes only."}}