Longevity Peptides

01Epitalonsmall human studies, no aging outcome

the guide

the telomere claim. a four-amino-acid peptide, Ala-Glu-Asp-Gly, built at the St Petersburg Institute of Bioregulation and Gerontology from the amino acid content of epithalamin, a polypeptide complex extracted from cattle pineal gland. FDA treats epitalon and epithalamin as different substances, which matters because the long-lived-human claims come from epithalamin studies.

evidence: the telomerase result is cell culture: human fetal lung fibroblasts given the peptide expressed telomerase, lengthened telomeres and passed the Hayflick limit by about ten divisions (Khavinson 2003, Khavinson 2004). in people FDA found three studies, two sublingual and one an injection beside the eye, none by the subcutaneous route proposed to FDA for compounding, and none measuring sleep or any aging outcome. a 2025 group at Brunel University in London repeated the telomere lengthening in normal and breast cancer cell lines, a paper whose three result figures were replaced by a correction in November 2025, and it is the first replication outside the originating institute that i could find.

watch for: FDA's 2026 evaluation says the mechanism cuts both ways: activating telomerase and lengthening telomeres is also how a cell can evade senescence and become cancerous, long telomeres are associated with higher cancer risk, and no two-year carcinogenicity study of epitalon exists. FDA found no pharmacokinetic data and no clinical safety study, and concluded the balance weighs against adding it to the compounding list.

02MOTS-cno completed human trial

the guide

the mitochondrial signal. a 16-amino-acid peptide encoded inside mitochondrial DNA, in the 12S rRNA region, discovered by Changhan Lee and Pinchas Cohen at USC in 2015. it reaches AMPK indirectly, by blocking the folate cycle and the purine synthesis tied to it.

evidence: mice and cells. MOTS-c prevented diet-induced obesity and age-dependent insulin resistance in mice (Lee 2015), and raised running performance in young, middle-aged and old mice, with treatment started at 23.5 months still increasing physical capacity (Reynolds 2021). the first human trial of the peptide itself is a phase 2a in prediabetes that plans 120 participants, started 2 February 2026 and has no results (NCT07505745). CB4211, studied in 88 people, is an engineered analogue, not MOTS-c.

watch for: the age story is not settled: circulating MOTS-c fell with age in healthy men while muscle MOTS-c ran about 1.5 times higher in older and middle-aged men than in young men (D'Souza 2020), and a doping-control lab could not confirm ELISA-measured blood levels by mass spectrometry (Knoop 2019). the same lab found MOTS-c is hydrolysed quickly in human blood, which FDA raised as a reason the injected peptide may not reach useful concentrations. prohibited in sport at all times as an AMPK activator.

03Humaninno human trials

the guide

the cell-survival signal. a peptide of 24 amino acids from the mitochondrial 16S rRNA region, found in 2001 in a screen for things that protected neurons from Alzheimer-related toxicity. a 2003 Nature paper showed it binds the pro-apoptotic protein Bax and stops it moving to mitochondria, which blocks the intrinsic death pathway (Guo 2003).

evidence: rodent and cell work. in rats, humanin infused into the brain improved insulin sensitivity, and the paper that reported it also found humanin lower with age in rodent tissue and in human blood (Muzumdar 2009). no interventional trial of humanin in people has been published.

watch for: the age direction is contested. measured in 693 people aged 21 to 113, humanin was higher in old age and highest in centenarians; the three mitokines that study measured, humanin among them, went with worse handgrip strength and insulin sensitivity most clearly at age 70, and higher levels tracked shorter survival in the oldest subjects (Conte 2019). that is the opposite of the decline the sales story needs. the anti-apoptosis mechanism is also the reason cancer history is a question nobody has studied.

04FOXO4-DRIno human trials

the guide

the senescent-cell claim. a peptide built in all-D amino acids in reverse order so human enzymes cannot cut it, with a cationic tail that carries it into cells. it blocks FOXO4 from holding p53 in the nucleus of a senescent cell, which lets p53 reach mitochondria and kill the cell.

evidence: cells and mice, from the 2017 Cell paper by Baar and colleagues at Erasmus MC: senescent cells died while their neighbours mostly did not, and in mice aged 115 to 130 weeks the peptide improved fur density, raised running wheel activity and lowered blood urea, a measure of kidney filtering. no human trial has been registered or published. other groups have since reproduced the senescent-cell killing in human chondrocytes and in several mouse disease models.

watch for: clearing senescent cells is not uniformly good. in a 2022 Circulation study, removing senescent cells with this peptide or with a drug senolytic worsened pulmonary blood pressure measures in mice and killed off lung endothelial cells, and the authors asked the field to reconsider senolytic strategies for that reason. the sequence sold is also worth checking: the Methods of the original paper give a 46-residue D-isoform with a molecular weight of 5358.2.

05GHK-Cusmall topical human trials only

the guide

the skin and matrix claim, and the only compound here with randomized human trials of a clinical outcome. a copper-bound tripeptide, glycyl-L-histidyl-L-lysine, present in human plasma, saliva and urine, sold as a lyophilized research vial and used for decades as a topical cosmetic ingredient.

evidence: the human trials are topical. a multicentre randomized evaluator-blinded trial in diabetic neuropathic foot ulcers found faster closure than vehicle (Mulder 1994). a randomized trial in venous stasis ulcers found silver sulfadiazine beat placebo and the copper tripeptide cream did not (Bishop 1992). after CO2 laser resurfacing, 13 completers showed no objective improvement in wrinkles or skin quality and only higher self-reported satisfaction (Miller 2006). no controlled human trial of injected GHK-Cu has been published, and the one registered GHK-Cu trial is a topical gel study still recruiting.

watch for: the gene-expression claim people quote comes from the Broad Institute Connectivity Map: a signature of emphysema severity in lung tissue from eight smokers' lungs nominated GHK by computer, and the effect was then shown in cultured fibroblasts (Campbell 2012). the thousands-of-genes figure comes from review articles by the peptide's own proponents. no vendor publishes the elemental copper dose a vial carries, and in Wilson disease copper build-up is the disease itself.

epitalon, MOTS-c, humanin, FOXO4-DRI and GHK-Cu get sold for longer life, each on a different claim. the claims are telomeres, mitochondria, senescent cells and skin. for each one the question is whether any aging outcome has ever been measured in a person. no amounts, no schedules. the Longevity Peptides bench covers 5 compounds: Epitalon, MOTS-c, Humanin, FOXO4-DRI, GHK-Cu, and BodyHackGuide publishes no protocol for any of them.