Best Peptides for Longevity

Educational content only. Not medical advice. Consult a licensed healthcare provider before starting any protocol.

Overview

Longevity peptides are short amino acid sequences marketed as slowing, halting, or partially reversing the cellular mechanisms of aging. The category sits at the intersection of gerontology research, the biohacker community, and a considerable amount of marketing. The purpose of this hub is to keep those three apart.

The realistic expectation: no peptide has been shown in a well-controlled human trial to extend human lifespan, and the one compound in this category with a completed phase 3 trial did not meet its primary endpoints. That is not a rhetorical hedge — MMPOWER-3, a 218-patient, randomized, double-blind, placebo-controlled phase 3 trial of elamipretide (SS-31) in primary mitochondrial myopathy, failed both of its primary endpoints: the difference from placebo in six-minute walk distance was −3.2 metres (95% CI −18.7 to 12.3, p = 0.69) and the fatigue score difference was likewise non-significant (PMID 37268435).

That result matters more than any mechanistic story on this page, because SS-31 was the category's strongest clinical candidate in a disease population where the mechanism should have been easiest to demonstrate.

What several of these compounds do have is mechanistic and biomarker data, some of it genuinely interesting. This hub covers what the evidence actually supports, compound by compound, and where each claim came from. If you are researching the best peptides for anti-aging, the epithalon vs ghk-cu question, or how telomere peptides fit into a longevity stack, start here — and expect the answers to be more modest than the ones you have been reading.

Who this hub is for

• Health optimizers building a longevity protocol
• People over 40 considering peptides as part of a broader strategy
• Readers comparing peptides against rapamycin, metformin, NAD+ precursors, and senolytics
• Anyone trying to reconcile the Khavinson research claims with Western evidence standards
• Practitioners wanting a reference framework

What you'll learn

1. How longevity peptides map onto the hallmarks-of-aging framework
2. Honest evidence levels for each compound, with the primary sources named
3. Which biomarkers are worth tracking and which are noise
4. Where peptides sit alongside interventions with better evidence

The Hallmarks of Aging Framework

The dominant scientific framework here is Hallmarks of Aging, whose 2023 update by López-Otín, Blasco, Partridge, Serrano, and Kroemer expanded the original list to twelve (PMID 36599349):

1. Genomic instability
2. Telomere attrition
3. Epigenetic alterations
4. Loss of proteostasis
5. Disabled macroautophagy
6. Deregulated nutrient sensing
7. Mitochondrial dysfunction
8. Cellular senescence
9. Stem cell exhaustion
10. Altered intercellular communication
11. Chronic inflammation
12. Dysbiosis

Longevity peptides are aimed at hallmarks 2, 3, 7, and 10–11. They do not clear senescent cells — that is the senolytics category — and they do not modulate mTOR the way rapamycin does. One caution worth stating: mapping a compound onto a hallmark establishes that its proposed mechanism is coherent with the framework. It does not establish that the compound does anything in a human. Most of the mapping on this page is at the first level.

For a protocol combining several of these mechanisms, see the longevity peptide protocol guide.

The Longevity Peptide Family

Read that table as a ranking of evidence, not of popularity. The popularity ordering in the community is close to the reverse.

Epithalon — The Telomerase Peptide

Epithalon (also spelled Epitalon) is a tetrapeptide, Ala-Glu-Asp-Gly, developed by Vladimir Khavinson's group in St. Petersburg. It is the most-discussed telomere peptide in the biohacker community and the most contested.

What the primary source actually reports

The foundational telomerase paper is specific and narrow. Adding Epithalon to telomerase-negative human fetal fibroblast culture induced expression of the telomerase catalytic subunit, telomerase enzymatic activity, and telomere elongation — which the authors read as reactivation of the telomerase gene in somatic cells, indicating "the possibility" of prolonging the life span of a cell population and of the whole organism (PMID 12937682). A companion paper reported the peptide promoting cells past their division limit (PMID 15455129).

Note the three qualifiers: cell culture, fetal fibroblasts, and "the possibility." Those are the authors' own framing, published in Bulletin of Experimental Biology and Medicine, from the institute that developed and sells the compound. That is the whole of the direct telomerase evidence.

The same group has separately reported that pineal peptide preparations — Epithalamin and Epitalon — restored night-time melatonin release and normalized the plasma melatonin rhythm in old monkeys and in elderly people with pineal insufficiency (PMID 17969590). Again: same research tradition, specialist gerontology journal, no independent Western replication.

The honest assessment

• Replication. Few Western labs have attempted the key findings, and none has published a confirmation.
• Methodology. The human reports predate and do not meet modern trial reporting standards.
• Conflict of interest. The institute that produced the research is the primary commercial source of the peptide. That does not make the findings wrong; it does mean independent replication carries more weight than additional papers from the same group.
• The telomerase target cuts both ways. Telomerase reactivation is a well-studied target in cancer biology, where it is something tumours do. Anyone with a personal or family cancer history should weigh that carefully rather than treating telomere lengthening as unambiguously good.

Practical use

Doses are not listed here. The pulse-dosing pattern people use — a short daily course repeated once or twice a year — derives from how Khavinson's group originally administered it, and the milligram figures circulating in the community do not trace to a published human dose-finding study. See the Epithalon protocol guide, which carries the amounts alongside their provenance, and its dated FDA row on our tracker as Epitalon.

Two practical notes that do not require a dose. Subcutaneous injection is the route used in the published protocols. And if you are measuring telomere length to evaluate it, leukocyte telomere length by qPCR is noisy run to run, so a single reading before and after a course cannot tell you anything — which is a reason to be sceptical of any before-and-after telomere result you are shown.

GHK-Cu — The Multi-Pathway Regenerator

GHK-Cu is a copper-binding tripeptide, glycyl-L-histidyl-L-lysine, first described by Loren Pickart. It has the most extensive Western literature in this category, and the most important thing to understand about that literature is who wrote it.

The 4,000-gene claim, sourced

The claim originates in a review by Pickart and colleagues, which states that GHK is present in human plasma, saliva, and urine but declines with age; that it stimulates synthesis and breakdown of collagen and glycosaminoglycans; that it restores replicative vitality to fibroblasts after radiation therapy; that it accelerates wound healing across skin, hair follicles, gastrointestinal tract, bone, and — in animals — induces systemic wound healing in rats, mice, and pigs; and that it "is capable of up- and downregulating at least 4,000 human genes, essentially resetting DNA to a healthier state" (PMID 26236730).

Three things to hold onto. The gene-regulation figure is real and published. It is a transcriptomic count, not an outcome — 4,000 genes changing expression is a measure of how promiscuous a signal is, not of how beneficial it is. And the review's authors are affiliated with Skin Biology, the company that commercialized GHK-Cu, which is disclosed in the paper and should be disclosed here.

The specific claim that plasma GHK "declines roughly 60% between age 20 and age 60" has been removed from this page: the cited review states that GHK declines with age, without that figure, and no source for the 60% number could be located.

Topical versus systemic

• Topical. The paper reports that in cosmetic products GHK has been found to tighten loose skin, improve elasticity, density and firmness, reduce fine lines, wrinkles, photodamage and hyperpigmentation, and increase keratinocyte proliferation (PMID 26236730). This is the best-supported use.
• Systemic subcutaneous. Reported benefits — hair regrowth, wound healing, reduced inflammation, general rejuvenation — rest on the wound-healing and transcriptomic work above plus user report. No randomized human trial of subcutaneous GHK-Cu for a longevity endpoint has been published.

Epithalon vs GHK-Cu

The community frames this as a choice. On the evidence it is not a close contest: GHK-Cu has peer-reviewed Western literature including cosmetic and wound-healing work, while Epithalon's direct evidence is a cell-culture study from the institute that sells it. Both fall well short of a longevity claim. Most stacks include both because they act on different proposed mechanisms, not because either has been shown to extend anything.

Practical notes

• Copper balance. GHK-Cu delivers copper into tissue, so stacking it with high-dose oral copper supplements is unnecessary. Specific milligram figures are left to the protocol guide.
• Colour. Reconstituted GHK-Cu is a vivid blue-violet from the copper-peptide complex. A clear or pale solution is likely copper-free GHK or improperly synthesized product — a rare case where you can sanity-check a vial by eye.
• Best-supported use cases. Skin elasticity and wound healing. The systemic longevity case is inferential.

Because the route matters to its regulatory position, GHK-Cu carries two rows on our status tracker rather than one — injectable and non-injectable, stated separately under GHK-Cu.

MOTS-c — The Exercise Mimetic

MOTS-c is a 16-amino-acid peptide encoded within the mitochondrial 12S rRNA rather than the nuclear genome, identified in 2015 as a member of the mitochondrial-derived peptide class.

What the founding paper showed

MOTS-c regulates insulin sensitivity and metabolic homeostasis; its primary target organ appears to be skeletal muscle; its cellular actions inhibit the folate cycle and tethered de novo purine biosynthesis, leading to AMPK activation; and MOTS-c treatment in mice prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity (PMID 25738459).

The AMPK link is the origin of the "exercise mimetic" framing, and the framing is defensible as mechanism. What it is not is a demonstration in humans: no randomized controlled trial of exogenous MOTS-c in humans for any endpoint has been published. The human case rests on extrapolation from that mouse work plus observational data on endogenous MOTS-c levels. "Exercise in a bottle" is a marketing phrase, and the actual exercise comparison is unflattering — see the fitness data in the lifestyle section below.

Doses and cycling patterns are left to the MOTS-c protocol; the figures circulating in the community are not derived from a human dose-finding study. Its regulatory position, including the July 2026 advisory-committee recommendation, is on our tracker as MOTS-c.

Where MOTS-c plausibly helps most

If the mouse mechanism translates at all, it would translate in someone whose insulin sensitivity is drifting — borderline fasting glucose, rising HbA1c, accumulating visceral fat — who is already doing the lifestyle work. There is less mechanistic room in an already metabolically healthy person. That is reasoning from mechanism, not from a trial.

SS-31 and Humanin — The Mitochondrial Thesis, and Its Reality Check

This is where mainstream biotech invested the most, which is exactly why the result matters.

SS-31 (elamipretide): the phase 3 outcome

SS-31 is a tetrapeptide that binds cardiolipin in the inner mitochondrial membrane and is proposed to stabilize electron transport chain function. Stealth BioTherapeutics advanced it through a full clinical program in primary mitochondrial myopathy, and the pivotal trial reported out.

MMPOWER-3 did not work. In 218 genetically confirmed PMM participants randomized 1:1 to 24 weeks of elamipretide 40 mg/day subcutaneously or placebo, the trial did not meet either primary endpoint. The difference between groups in six-minute walk distance from baseline to week 24 was −3.2 metres (95% CI −18.7 to 12.3, p = 0.69), and the total fatigue score difference was also non-significant (PMID 37268435). A later post hoc analysis explored genotype-specific effects (PMID 39574155) — which is a hypothesis-generating exercise on a failed trial, not a rescue of it. Earlier phase work had been more encouraging: a dose-escalation trial (PMID 29500292) and a randomized crossover trial (PMID 32096613) both preceded it, which is the ordinary pattern of a promising early signal that does not survive a pivotal trial.

This page previously listed SS-31 as the category's strongest evidence on the grounds that it "has Phase 3 trial data." It does. The data is negative on its primary endpoints, and presenting "in phase 3" as validation without saying how the trial ended is the kind of omission this site should not make.

None of that means cardiolipin stabilization is a dead end, and elamipretide has been studied in other indications. It does mean the mitochondrial-peptide thesis has now been tested at pivotal scale in its most favorable population and did not deliver.

Humanin

Humanin is a 24-amino-acid mitochondrial-derived peptide, the first member of that class to be identified, with neuroprotective and metabolic effects described in preclinical models and levels that decline with age in human serum. No interventional human trial of exogenous humanin has been published. It is used less than MOTS-c in practice, largely for cost and supply reasons.

For both compounds, see the Humanin & SS-31 protocol guide.

Why the thesis still attracts attention

Mitochondrial dysfunction is one of the twelve hallmarks and is often argued to sit upstream of several others (PMID 36599349). A compound that restored mitochondrial efficiency would plausibly cascade. That biological logic — not the human evidence, which now includes a failed pivotal trial — is why the sub-family keeps drawing research money.

The Khavinson Bioregulator Stack

The Khavinson peptides are widely used and widely misunderstood, so they get an honest section. Working at the St. Petersburg Institute of Bioregulation and Gerontology, Khavinson's group developed dozens of short peptides, typically two to four amino acids, each claimed to selectively regulate a corresponding organ:

• Pinealon — pineal gland, sleep, cognition
• Thymalin — thymus, immune function (see the Thymulin & Thymogen protocol)
• Cortexin — brain cortex, cognition (see the P21 & Cortexin protocol)
• Prostamax — prostate
• Vesugen — vascular endothelium

What is actually published

Take the most popular one as the test case. The published Pinealon work is cell-culture work: the tripeptide Glu-Asp-Arg restricted reactive oxygen species accumulation in a dose-dependent manner in cerebellar granule cells, neutrophils and PC12 cells, and decreased necrotic cell death (PMID 21978084). That is an antioxidant and cell-viability result in vitro. There is no published human trial of Pinealon for sleep, cognition, or any longevity endpoint.

Evidence caveats

• Replication. Independent Western replication is essentially nonexistent across the family.
• Mechanism. Short cell-penetrating peptides regulating organ-specific gene expression is plausible but underspecified.
• Methodology. Much of the human literature does not meet modern reporting standards.
• Commercial entanglement. The same group sells the peptides.

A reasonable interpretation: the bioregulators have a long use record without prominent safety signals, which is weak positive evidence about safety and no evidence about efficacy. Treat them as low-risk experimental adjuncts, not foundational protocol elements — and note that "no reported harm from decades of use" is a much weaker statement than "studied and found safe."

How Longevity Stacks Are Built

The tiers below describe structure. Dosing tables and annual cost projections that previously appeared here have been removed: the milligram figures did not derive from human dose-finding studies, and the cost numbers were unsourced and stale.

For the fully sequenced version see the longevity peptide protocol guide, and for the GH-axis component the GH secretagogue protocol; both sit in the wider protocol library.

Stacking principles worth keeping

• Do not start everything at once. Introduce one compound at a time so you can attribute effects and side effects.
• Pulse the pulsed compounds together so that any biomarker review afterwards covers a coherent window.
• Reassess on a schedule and be willing to drop things. Given how little human evidence supports most of this category, a compound that has produced no detectable biomarker or subjective change after a couple of courses is a cost, not a protocol element.
• Mind the IGF-1 trade-off. Adding a GH secretagogue raises IGF-1, and higher circulating IGF-I is associated with a moderately increased risk of prostate cancer in pooled data from 12 prospective studies (PMID 18838726). In a longevity protocol specifically, deliberately raising IGF-1 for body composition is a trade against a documented association, not a free addition.

Biomarkers to Track

A serious protocol includes a baseline panel and periodic rechecks. Target ranges have been removed from this table where they were not sourced — "optimal" ranges circulating in the longevity community frequently differ from laboratory reference ranges without a trial behind them, and publishing them here would be presenting convention as evidence. Bring the numbers to a clinician who can interpret them against your own history.

The two entries at the bottom deserve their scepticism. Telomere length and epigenetic clocks are the measurements most often used to sell this category, and they are the two least suited to detecting a real effect in an individual over a short period.

What the Evidence Actually Shows

Ranked honestly, strongest to weakest:

• Best documented, and negative. SS-31 / elamipretide is the only compound here with a completed pivotal trial, and it missed both primary endpoints in 218 patients (PMID 37268435).
• Best documented, and positive but narrow. Topical GHK-Cu for skin, and GHK's wound-healing work (PMID 26236730) — reported largely by the compound's developer, and about skin rather than lifespan. GH secretagogues have real human pharmacology, for body composition rather than longevity, with an IGF-1 trade-off.
• Preclinical and promising. MOTS-c, on mouse data (PMID 25738459).
• Single-source and in vitro. Epithalon's telomerase result, in fetal fibroblast culture, from the selling institute (PMID 12937682).
• Weakest. The remaining Khavinson bioregulators. Pinealon's published record is cell culture (PMID 21978084).

The summary: no longevity peptide has been shown in a rigorous trial to extend human lifespan or healthspan, and the category's best clinical shot missed. What exists is mechanistic plausibility and biomarker movement. That is a legitimate reason for some people to experiment, with eyes open and a budget they can afford to be wrong about. It is not a reason to reorganize your health strategy around it.

Longevity Peptides vs Other Interventions

Peptides are one tool, and on current evidence not the best-supported one.

Costs have been removed from this comparison. The monthly figures previously listed were unsourced and vary too much by supplier and jurisdiction to be useful.

The honest ordering is uncomfortable for a peptide site to publish: the intervention with by far the strongest human mortality data in this table is aerobic fitness, and it is free.

Lifestyle Foundation (Required)

This is not a courtesy section. It is where the evidence is.

• Cardiorespiratory fitness. In the 122,007-patient cohort above, mortality fell continuously with fitness and the penalty for low fitness exceeded that of coronary artery disease, diabetes, or smoking in the same adjusted model (PMID 30646252). Nothing else on this page has data of that weight.
• Resistance training. Lean mass and strength are strongly associated with healthspan in older adults, and a DEXA scan will tell you whether you are holding yours.
• Sleep. The largest growth hormone pulse of the day occurs in association with slow-wave sleep, and the amount of SW sleep tracks the amount of GH secreted (PMID 10984255). If you are paying for a GH secretagogue while sleeping five hours, you have the order of operations wrong. See the Sleep Hub.
• Protein intake. Adequate protein defends against sarcopenia in older adults. Specific gram-per-kilogram targets vary by guideline and by individual and belong with a clinician or dietitian rather than on a hub page.
• Metabolic health. HbA1c, fasting insulin and visceral fat are the endpoints the mitochondrial peptides are proposed to improve in mice. Improving them by diet and training first is both cheaper and better evidenced.
• Stress and social connection. Both are associated with mortality in observational data.

Peptides build on this. They are not a workaround for skipping it, and in this category more than any other on the site, the foundation has better evidence than the product.

Cycling Strategy

The week-count table that used to sit here has been removed. None of the cycle lengths circulating for these compounds — for Epithalon, GHK-Cu, MOTS-c, Pinealon or Humanin — derives from a human study, and presenting them in a table implied a precision that does not exist.

What can be said from the published work:

• Pulse-dosed compounds (Epithalon, the bioregulators) are pulsed because that is the pattern the originating research tradition used, not because a pulsed schedule was ever compared against a continuous one. No source is offered for the specific schedule here, because the papers behind these compounds do not establish one — the foundational Epithalon result is a cell-culture experiment with no dosing regimen at all, and the pineal-peptide report in monkeys and elderly people (PMID 17969590) does not compare schedules either.
• SS-31 was dosed continuously in its trials — 40 mg daily for 24 weeks in MMPOWER-3 (PMID 37268435) — which is the one dosing schedule on this page that comes from a controlled trial, and it did not produce the primary outcome.
• GH-axis compounds need IGF-1 monitoring more than they need a particular calendar. After multiple doses of the long-acting CJC-1295, IGF-I remained above baseline for up to 28 days (PMID 16352683), which is a real constraint on how fast a washout happens.

The defensible general principle: deliberate off periods exist so that you can see your own baseline. If you never stop, you cannot tell whether anything is working. See Peptide Cycling Strategies.

Frequently Asked Questions: Longevity Peptides

Do longevity peptides actually extend lifespan? Not in humans, and the strongest test so far was negative: the phase 3 trial of elamipretide in 218 patients missed both primary endpoints. In animals, several compounds have shown healthspan or lifespan effects, and MOTS-c prevented diet-induced obesity and insulin resistance in mice. The honest answer is that we have mechanistic and biomarker data, one failed pivotal trial, and no human lifespan endpoints.

Epithalon vs GHK-Cu — which should I start with? On evidence rather than popularity, GHK-Cu, because it has peer-reviewed Western literature including cosmetic and wound-healing work — with the caveat that the key review was written by the compound's commercial developer. Epithalon's direct telomerase evidence is a cell-culture study in fetal fibroblasts from the institute that sells it. Neither has a longevity outcome trial.

Are longevity peptides safe long-term? Long-term human safety data does not exist for any of them. The Khavinson family has the longest use record without prominent safety signals, which is weak positive evidence about safety rather than a substitute for a safety study. Elamipretide has the most formal safety data because it went through a full clinical program.

Can I take longevity peptides with rapamycin or metformin? People do, and no major interactions are documented — but formal interaction studies are essentially nonexistent, so "no known interaction" here means "not studied" rather than "checked and clear." One real tension is worth naming: rapamycin inhibits mTOR while GH secretagogues raise IGF-1, which signals through that axis. Discuss the combination with whoever prescribes the rapamycin.

Will peptides reverse my biological age clocks? Epigenetic clocks remain research tools rather than validated clinical endpoints, and no randomized trial has shown that any peptide on this page moves one. Anyone quoting a specific number of years of biological age reversal from peptides is quoting something other than a trial result.

Do I need a doctor to use these? Strongly recommended, and specifically for the labs. The GH-axis adjuncts raise IGF-1, which carries a documented cancer association, and several compounds here touch insulin sensitivity. Those are the drifts you cannot feel and a clinician can measure.

What about cancer risk? This is the most important risk in the category and it is not hypothetical in one respect. Higher circulating IGF-I is associated with a moderately increased risk of prostate cancer across 12 pooled prospective studies, so deliberately raising IGF-1 with a GH secretagogue is a real trade-off. Separately, telomerase reactivation — Epithalon's proposed mechanism — is something cancer cells characteristically do, which is a reason for caution rather than a demonstrated harm. Anyone with a personal or strong family cancer history should discuss this before starting anything here.

Can women take longevity peptides? None of the core compounds is sex-specific, and none has been studied well enough in either sex to give sex-specific guidance. Pregnancy and breastfeeding are absolute contraindications across the category.

How quickly will I notice anything? Subjective reports of sleep, skin and energy changes typically come within weeks, and those are user reports rather than trial endpoints. Biomarker changes take months to rise above measurement noise, and the two biomarkers most often used to market this category — telomere length and epigenetic age — are the noisiest of all over short periods. Treat any dramatic short-term result with suspicion.

Where do GH secretagogues fit in a longevity stack? They address sarcopenia, body composition and recovery, which are genuine healthspan components with real human pharmacology behind them. They also raise IGF-1, which carries the cancer association above, and growth hormone administration in healthy young subjects improved body composition without improving strength. They are an adjunct with a trade-off, not a foundation. See the GH secretagogue protocol and the Muscle Hub.

Featured Protocols on Peptides.NYC

• Epithalon Protocol — telomere and pineal-axis pulse dosing
• GHK-Cu Protocol — topical and systemic use, copper considerations
• MOTS-c Protocol — the mitochondrial-derived peptide
• Humanin & SS-31 Protocol — including the MMPOWER-3 outcome
• Pinealon Protocol — the Khavinson bioregulator, and what is published about it
• Thymulin & Thymogen Protocol — the thymic bioregulators
• P21 & Cortexin Protocol — the cortical bioregulators
• GH Secretagogue Protocol — body composition, with the IGF-1 trade-off
• Longevity Peptide Protocol — the sequenced annual program
• Bloodwork Checklist — what to test and why
• Peptide Cycling Strategies

Related Hubs

• Sleep Peptide Hub — why sleep precedes any GH-axis intervention
• Cognitive Peptide Hub — the nootropic overlap with the bioregulators
• Muscle & Performance Peptide Hub — the GH axis and the IGF-1 evidence in full
• Immune Peptide Hub — thymic peptides and immunosenescence

Reminder: This content is for educational purposes only. The peptides discussed are research compounds and are not FDA-approved for anti-aging or longevity indications. Human clinical evidence is limited or absent for most of them, and the one compound with a completed pivotal trial did not meet its primary endpoints. Consult a licensed healthcare provider before starting any protocol, especially if you have a personal or family history of cancer, are pregnant, breastfeeding, or taking other medications. Peptides.NYC does not sell peptides.

Selected References

Every PMID linked above points to the PubMed record for that paper, so you can check the claim against the abstract yourself.

1. López-Otín C, Blasco MA, Partridge L, et al. Hallmarks of aging: an expanding universe. Cell. 2023. PMID 36599349 · doi:10.1016/j.cell.2022.11.001
2. Khavinson VKh, Bondarev IE, Butyugov AA. Epithalon peptide induces telomerase activity and telomere elongation in human somatic cells. Bulletin of Experimental Biology and Medicine. 2003. PMID 12937682 · doi:10.1023/a:1025493705728
3. Khavinson VKh, Bondarev IE, Butyugov AA, et al. Peptide promotes overcoming of the division limit in human somatic cell. Bulletin of Experimental Biology and Medicine. 2004. PMID 15455129 · doi:10.1023/b:bebm.0000038164.49947.8c
4. Korkushko OV, Lapin BA, Goncharova ND, et al. Normalizing effect of the pineal gland peptides on the daily melatonin rhythm in old monkeys and elderly people. Advances in Gerontology. 2007. PMID 17969590
5. Pickart L, Vasquez-Soltero JM, Margolina A. GHK peptide as a natural modulator of multiple cellular pathways in skin regeneration. BioMed Research International. 2015. PMID 26236730 · doi:10.1155/2015/648108
6. Lee C, Zeng J, Drew BG, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism. 2015. PMID 25738459 · doi:10.1016/j.cmet.2015.02.009
7. Karaa A, Bertini E, Carelli V, et al. Efficacy and safety of elamipretide in individuals with primary mitochondrial myopathy: the MMPOWER-3 randomized clinical trial. Neurology. 2023. PMID 37268435 · doi:10.1212/WNL.0000000000207402
8. Karaa A, Haas R, Goldstein A, et al. Randomized dose-escalation trial of elamipretide in adults with primary mitochondrial myopathy. Neurology. 2018. PMID 29500292 · doi:10.1212/WNL.0000000000005255
9. Karaa A, Haas R, Goldstein A, et al. A randomized crossover trial of elamipretide in adults with primary mitochondrial myopathy. Journal of Cachexia, Sarcopenia and Muscle. 2020. PMID 32096613 · doi:10.1002/jcsm.12559
10. Karaa A, Bertini E, Carelli V, et al. Genotype-specific effects of elamipretide in patients with primary mitochondrial myopathy: a post hoc analysis of the MMPOWER-3 trial. Orphanet Journal of Rare Diseases. 2024. PMID 39574155 · doi:10.1186/s13023-024-03421-5
11. Khavinson V, Ribakova Y, Kulebiakin K, et al. Pinealon increases cell viability by suppression of free radical levels and activating proliferative processes. Rejuvenation Research. 2011. PMID 21978084 · doi:10.1089/rej.2011.1172
12. Mandsager K, Harb S, Cremer P, et al. Association of cardiorespiratory fitness with long-term mortality among adults undergoing exercise treadmill testing. JAMA Network Open. 2018. PMID 30646252 · doi:10.1001/jamanetworkopen.2018.3605
13. Harrison DE, Strong R, Sharp ZD, et al. Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature. 2009. PMID 19587680 · doi:10.1038/nature08221
14. Martens CR, Denman BA, Mazzo MR, et al. Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nature Communications. 2018. PMID 29599478 · doi:10.1038/s41467-018-03421-7
15. Hickson LJ, Langhi Prata LGP, Bobart SA, et al. Senolytics decrease senescent cells in humans: preliminary report from a clinical trial of dasatinib plus quercetin in individuals with diabetic kidney disease. EBioMedicine. 2019. PMID 31542391 · doi:10.1016/j.ebiom.2019.08.069
16. Justice JN, Nambiar AM, Tchkonia T, et al. Senolytics in idiopathic pulmonary fibrosis: results from a first-in-human, open-label, pilot study. EBioMedicine. 2019. PMID 30616998 · doi:10.1016/j.ebiom.2018.12.052
17. Gonzales MM, Garbarino VR, Kautz TF, et al. Senolytic therapy in mild Alzheimer's disease: a phase 1 feasibility trial. Nature Medicine. 2023. PMID 37679434 · doi:10.1038/s41591-023-02543-w
18. Roddam AW, Allen NE, Appleby P, et al. Insulin-like growth factors, their binding proteins, and prostate cancer risk: analysis of individual patient data from 12 prospective studies. Annals of Internal Medicine. 2008. PMID 18838726 · doi:10.7326/0003-4819-149-7-200810070-00006
19. Van Cauter E, Copinschi G. Interrelationships between growth hormone and sleep. Growth Hormone & IGF Research. 2000. PMID 10984255 · doi:10.1016/s1096-6374(00)80011-8
20. Teichman SL, Neale A, Lawrence B, et al. 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. Journal of Clinical Endocrinology and Metabolism. 2006. PMID 16352683 · doi:10.1210/jc.2005-1536

Inclusion here is not endorsement — reference 7 is cited precisely because it is a failed pivotal trial, and reference 5 because its authors are the compound's commercial developers. Nothing on this page is medical advice.

Source: https://peptides.nyc/learn/goal/longevity