BRAK LABS Peptide research, plainly written

group

Longevity compounds

Six compounds sold for ageing and mitochondrial health, covered one at a time: what each substance is, what the published work measured, and what the registry actually contains when the records are opened.

Last Reviewed Editorial policy Methodology

This is the group where the labels come apart. Six substances are sold here as longevity peptides. Two of them are not peptides at all: NAD+ is a dinucleotide coenzyme and 5-Amino-1MQ is a small ring molecule. One of them, sold under the research name SS-31, is an FDA-approved drug called Forzinity. Two of them, MOTS-c and humanin, are genuine peptides written by mitochondrial DNA rather than by the DNA in the cell nucleus, which is the most interesting piece of biology on this page.

What people research them for is roughly the same story in each case: mitochondrial function, energy, body composition and the general idea of slowing ageing. What sits behind those claims varies more than any other group in this catalog, from an accelerated FDA approval with a published run of missed primary endpoints to a compound with a single much-cited mouse paper and nothing else.

Every entry states what was measured, in what species, and what the registry returned when it was searched for this page on 2 August 2026. Twenty numbered sources sit at the foot of the page: seventeen primary papers and reviews, including one paper cited together with its published correction, and three agency documents. Two counting rules do most of the work here, and both are set out before the entries so the numbers on this page can be checked rather than believed.

Not medical advice

This page reports what has been documented about a compound. It is not medical advice, not a diagnosis, not a dosing protocol, and not a recommendation to obtain or use anything described here. Talk to a licensed clinician about anything concerning your health. Read the full disclaimer.

Reviewed against editorial standards Updated

The compounds in this group

Each row names what the compound is and what its published work covers. The evidence level is the strongest tier of evidence about that compound for the use it is sold for. It is a single figure for a whole entry rather than a claim by claim grading, so an entry may also describe work that is weaker, or that tested a different route or a different molecule, and each of those carries its own citation in the text. Where a compound's own review has been run, its page grades every claim area separately.

Compounds covered on this page, what each one is, and what the published record on it covers
CompoundAlso known asWhat the published work coversWhere it standsEvidence level
EpitalonEpithalon, epithalamin, AEDG peptideTelomere and telomerase work in cultured human cells, plus a Russian body of work that has not been independently replicatedNo registered study under any of its three names. Put to the FDA compounding advisory committee on 24 July 2026[In-vitro]
MOTS-cMitochondrial ORF of the 12S rRNA type-cMouse metabolic studies, and nine registrations of which eight measure the body's own MOTS-c rather than giving anyNamed on the 2026 WADA Prohibited List. Put to the FDA compounding advisory committee on 23 July 2026[Animal]
SS-31Elamipretide, MTP-131, Bendavia, ForzinityRandomised trials in Barth syndrome, primary mitochondrial myopathy, dry age-related macular degeneration and heart failure, with the primary endpoint missed in eachApproved by FDA on 19 September 2025 as Forzinity for one rare genetic condition. Twenty-one registrations under elamipretide, two under SS-31, one molecule[Human RCT]
NAD+Nicotinamide adenine dinucleotide, NADA 2026 systematic review that went looking for outcomes trials of infused or injected NAD+ itself and reported finding noneNot a peptide. The oral precursors are sold as supplements. Infusions are caught by the WADA rule on infusion volume[Anecdote]
5-Amino-1MQ5-amino-1-methylquinoliniumOne much-cited 2018 mouse study of NNMT inhibition, and a 2014 mouse study of the same target by a different methodUnapproved, no registered study, and not a peptide[Animal]
HumaninHN, HNG, S14G-humaninCell work on nerve cell survival, and seven registrations, every one of which measures the body's own humanin as a markerUnapproved. No human study has given humanin to anyone[In-vitro]

Two counting rules, before any number on this page is read

The first rule is that one molecule with two names has one trial programme. SS-31 and elamipretide are the same four amino acid peptide. On 2 August 2026 ClinicalTrials.gov returned 21 registrations under elamipretide and 2 under SS-31, and those numbers describe the same drug indexed twice. Adding them produces 23 and invents a programme that was never run. Where a vendor page quotes a trial count for SS-31, the number to check is which name it was searched under.

The second rule is that a registration which measures something is not a trial of giving it to anyone. MOTS-c and humanin are both molecules the body already makes, so a great deal of clinical research measures how much of them a person has, as a marker of something else. Those studies appear in a registry search under the compound's name. They administer nothing. On this page the two kinds of registration are counted separately, and every record behind the counts was opened.

Kisspeptin, in the sexual health group, has the same problem, and so does every other endogenous molecule sold as a supplement. The general form of the rule: before quoting a registry count, ask whether the studies gave the substance or looked for it.

Two of these six are not peptides

NAD+ is nicotinamide adenine dinucleotide, a dinucleotide coenzyme built from two nucleotides joined at their phosphates. Every cell uses it to shuttle electrons through metabolism. It contains no amino acids and no peptide bonds, and calling it a peptide is a straightforward chemistry error rather than a matter of framing.

5-Amino-1MQ is 5-amino-1-methylquinolinium, a small molecule built on a two-ring aromatic system carrying a permanent positive charge. It is also not a peptide, and it is not a precursor of NAD+ either: it acts on the enzyme that consumes one of NAD+'s building blocks, which is a different idea entirely.

This matters beyond pedantry, because the rules that govern a peptide, a small molecule and a coenzyme sold as a supplement are not the same rules. The regulatory line under each entry below states which one applies.

The six compounds, one at a time

Epitalon

Also known as Epithalon, Epithalamin, AEDG peptide

Plain-English version: A four amino acid peptide made to mimic an extract of the pineal gland, sold for ageing and sleep.

Strongest evidence, and what it covers [In-vitro] Ageing, telomeres and sleep [1] [2] [3] [4]

Epitalon is four amino acids long, alanine-glutamate-aspartate-glycine, which is where the alternative name AEDG comes from. It was synthesised to reproduce the activity of epithalamin, an extract of the pineal gland, and it is the anchor compound of the whole longevity category.

ClinicalTrials.gov returned nothing on 2 August 2026 under epitalon, under epithalon or under epithalamin. The body of work behind the compound comes from Vladimir Khavinson's group in St Petersburg, is largely unavailable in indexed English-language journals, and has not been reproduced by an independent laboratory. The telomere claim rests on cell work: a 2003 report of telomerase activity and telomere elongation in cultured human somatic cells [3], and a 2025 paper in Biogerontology reporting increased telomere length in human cell lines through telomerase upregulation or ALT activity [1]. That 2025 paper carries a published correction, and both records are cited here so anyone checking it lands on the corrected version rather than on the original alone [2]. A 2025 review collects what exists [4].

Where it stands Epitalon is not an approved drug in the United States and it holds no registered trial under any of its three names. FDA put epitalon-related bulk drug substances to its Pharmacy Compounding Advisory Committee on 24 July 2026, in separate votes on the free base and the acetate [20]. A committee recommendation is advisory: FDA has published no vote record. Reporting says the committee recommended inclusion, against FDA staff's own written proposal, and the 503A record on this site sets out what that did and did not change.

Our takeA telomere claim resting on cultured cells, from a group with a commercial interest in the peptide class, in journals most readers cannot obtain. The 2025 cell work is the most checkable thing on the record, and it is still a dish.

MOTS-c

Also known as Mitochondrial ORF of the 12S rRNA type-c

Plain-English version: A sixteen amino acid peptide encoded by mitochondrial DNA rather than by the DNA in the cell nucleus.

Strongest evidence, and what it covers [Animal] Metabolic health, body composition and exercise capacity [5] [6]

MOTS-c is sixteen amino acids long and it is written by the mitochondrion's own DNA, not by the nucleus. That is the genuinely novel piece of biology here: the organelle encodes a signalling peptide that acts outside itself. The founding paper, in Cell Metabolism in 2015, reported that MOTS-c given to mice changed measures of insulin sensitivity and fat mass, and traced the effect to a folate and AMPK pathway [5].

The registry count is where care is needed. ClinicalTrials.gov returned 9 registrations on 2 August 2026, and eight of them measure the body's own MOTS-c as a marker inside a study about something else: exercise after a breast cancer diagnosis, anaesthesia technique, diabetes and coronary disease, Ramadan fasting, dialysis, deafness screening, vestibular implants. Measuring how much MOTS-c a person already makes is not a trial of giving MOTS-c to anyone. One registration does administer it, NCT07505745, a phase 2 study in adults with prediabetes and overweight or obesity, which was recruiting on that date with no results posted. Circulating levels of mitochondrial-derived peptides also rise after endurance exercise in people, which is where much of the athletic interest comes from [6].

Where it stands MOTS-c is named on the 2026 WADA Prohibited List under S4.4.1, the class covering AMPK activators, and substances in that class are prohibited at all times rather than in competition only [19]. FDA put MOTS-c-related bulk drug substances to its Pharmacy Compounding Advisory Committee on 23 July 2026, in separate votes on the free base and the acetate [20]. FDA has published no vote record. Reporting says the committee recommended inclusion, against FDA staff's own written proposal, and the 503A record on this site sets out what that did and did not change.

Our takeNine registrations reads like a programme. One of them gives anyone the peptide, it is still recruiting, and it has posted nothing. The other eight are measuring a molecule people already have.

SS-31

Also known as Elamipretide, MTP-131, Bendavia, Forzinity

Plain-English version: A four amino acid peptide that concentrates in mitochondria, approved in 2025 for one rare condition.

Strongest evidence, and what it covers [Human RCT] Mitochondrial function, muscle strength and energy [7] [8] [9] [10] [11]

SS-31 and elamipretide are the same molecule: a four amino acid aromatic-cationic peptide that concentrates in the inner mitochondrial membrane. It has also carried the names MTP-131 and Bendavia, and since 2025 it has a brand name, Forzinity. Those names split its registry record in two. On 2 August 2026 ClinicalTrials.gov returned 21 registrations under elamipretide and 2 under SS-31, describing one drug indexed twice.

The trial record is both large and negative, which is rare enough to be worth stating precisely. TAZPOWER, a phase 2 and 3 crossover trial in Barth syndrome, missed its primary endpoints in the randomised part and continued as an open-label extension that ran to 168 weeks [7] [8]. MMPOWER-3, a phase 3 trial in primary mitochondrial myopathy with 218 participants, was terminated, and the registry's own stop reason reads that the double blind portion of the trial did not meet the primary end points [9]. ReCLAIM-2, a randomised phase 2 trial in dry age-related macular degeneration, missed [10]. PROGRESS-HF, a phase 2 trial in heart failure with reduced ejection fraction, missed [11]. The 2025 accelerated approval rests on the open-label extension of the trial whose randomised phase failed.

Where it stands FDA granted elamipretide accelerated approval on 19 September 2025 under the brand name Forzinity, application 215244, to improve muscle strength in patients with Barth syndrome weighing at least 30 kg, as recorded on the agency's 2025 novel drug approvals table [18]. That approval covers one rare genetic condition. It carries no statement about mitochondrial health, energy or ageing in anyone else.

Our takeThe clearest approved-drug-sold-under-a-research-name case in this catalog, and the trial history is the opposite of what the research name implies. Every adequately powered randomised trial this molecule ran missed its primary endpoint, and all of it is on the public record.

NAD+

Also known as Nicotinamide adenine dinucleotide, NAD

Plain-English version: Not a peptide. A dinucleotide coenzyme every cell uses, sold as an injectable and, separately, as an oral supplement.

Strongest evidence, and what it covers [Anecdote] Energy, ageing and recovery [12]

NAD+ is nicotinamide adenine dinucleotide, a coenzyme built from two nucleotides joined at their phosphates, and every cell in the body uses it to move electrons through metabolism. It contains no amino acids. Filing it under peptides is a chemistry error, and it is the single most common one in this catalog.

It reaches people in two quite different forms. The oral precursors, nicotinamide mononucleotide and nicotinamide riboside, are sold as dietary supplements and carry most of the human trial record: registry searches on those names return dozens of studies. The injected and infused form is what the peptide storefronts sell, and it is a different object. A 2026 systematic review in Ageing Research Reviews went looking for outcomes trials of intravenous or intramuscular NAD+ itself for an ageing or wellness indication, and reported finding none that met its inclusion criteria [12]. Registry searches on infusion terms return dozens of records, and reading them shows the same split: the studies are largely on the precursors rather than on NAD+ itself.

Where it stands The 2026 WADA Prohibited List caps intravenous infusions at 100 mL per 12 hour period under M2.2, so a large-volume infusion is a prohibited method for a tested athlete whatever is in the bag [19]. NAD+ was not among the seven substances FDA put to its Pharmacy Compounding Advisory Committee on 23 and 24 July 2026 [20].

Our takeThe human trial literature people cite for NAD+ is a literature about two oral precursors. A systematic review looked specifically for trials of the infused form and came back with nothing, which is the most informative sentence written about this compound in years.

5-Amino-1MQ

Also known as 5-amino-1-methylquinolinium

Plain-English version: Not a peptide. A small molecule that blocks an enzyme involved in how cells use NAD+.

Strongest evidence, and what it covers [Animal] Fat loss and NAD+ availability [13] [14]

5-Amino-1MQ is 5-amino-1-methylquinolinium, a small molecule built on a two-ring aromatic system carrying a permanent positive charge. It has no amino acids and no peptide bonds. It is sold for fat loss, and usually alongside NAD+ products, which is where the confusion about what it does starts.

The idea behind it is an enzyme called nicotinamide N-methyltransferase, NNMT, which attaches a methyl group to nicotinamide and takes it out of circulation. Nicotinamide is one of the building blocks cells use to make NAD+, so the hypothesis is that blocking NNMT leaves more of that building block available, particularly in fat tissue. The compound is an inhibitor of that enzyme rather than a source of NAD+, which is a different mechanism from the one most listings describe.

Two mouse studies carry the whole story. In 2014, a Nature paper knocked NNMT down in diet-induced obese mice using an antisense oligonucleotide and reported protection against weight gain [14]. That study is about the target and it did not use this compound. In 2017 and 2018 a group publishing in Biochemical Pharmacology reported that selective, membrane-permeable small-molecule NNMT inhibitors reversed high-fat-diet-induced obesity in mice [13]. That is the paper the marketing is built on, and it is frequently described online as a Nature paper. It is not: the Nature paper is the 2014 knockdown study, and the two used different methods on the same enzyme.

ClinicalTrials.gov returned no registered study of 5-Amino-1MQ on 2 August 2026, and no human study of any design has been published. What the mouse work covers is a measurable change in body composition in animals made obese on purpose by their diet, on a target that was engaged two different ways in two different papers. What it does not cover is any measurement in a person, at any exposure, by any route. Nothing has been published about how much of the compound survives being swallowed, what dose scale would correspond to the mouse work, or what happens on repeated exposure.

Where it stands 5-Amino-1MQ is not an approved drug anywhere, it holds no registered trial, and it was not among the seven substances FDA put to its Pharmacy Compounding Advisory Committee on 23 and 24 July 2026 [20].

Our takeTwo mouse papers on one enzyme, one of which does not involve this molecule, and a widely repeated citation error about which journal published which. That is the entire basis for a compound sold as a fat-loss agent.

Humanin

Also known as HN, HNG, S14G-humanin

Plain-English version: A 24 amino acid peptide, also encoded by mitochondrial DNA, sold on the same reasoning as MOTS-c.

Strongest evidence, and what it covers [In-vitro] Cell survival, ageing and metabolic health [15] [16] [17]

Humanin is 24 amino acids long and, like MOTS-c, it is written by mitochondrial DNA rather than by the nucleus. It was found in 2001 in a screen for factors that keep nerve cells alive under Alzheimer's-related insults, and the paper that described it appeared in the Proceedings of the National Academy of Sciences [15]. A more potent laboratory analog, S14G-humanin, is usually written HNG, and vendor listings use the two names interchangeably even though they are different sequences.

The registry position is the same as MOTS-c's and it is stricter. ClinicalTrials.gov returned 7 registrations on 2 August 2026. Every one of them measures the body's own humanin as a marker: humanin isoforms in cardiac muscle and plasma after cardiac surgery, plasma humanin in acute kidney injury, humanin in IVF outcomes in polycystic ovary syndrome, humanin in muscle biopsies taken during orthopaedic surgery in cerebral palsy, and two studies where it is one readout among several in exercise and anaesthesia protocols. None of them gives humanin to anybody. There is no registered interventional trial of administering humanin, and there is no published one either.

What the human numbers do show is what the body does with its own supply. Levels of humanin rise in plasma and in muscle after high-intensity interval exercise in men [16], and humanin has been examined alongside MOTS-c and telomere length as a candidate biomarker in Alzheimer's disease [17]. Both of those are measurements of an endogenous peptide in people who were given nothing, and neither says anything about what happens if the peptide is supplied from outside.

The original 2001 work, and most of what followed it, was done in cultured cells and in animals: nerve cells challenged with amyloid and with familial Alzheimer's mutations, where humanin in the medium changed survival [15]. Those results come from dishes, at concentrations the experimenters chose, and cell and tissue work is a further step removed from a person than animal work is, because the concentrations that produce an effect in a dish are often far above anything a body reaches.

Where it stands Humanin is not an approved drug anywhere, it holds no interventional registration, and it was not among the seven substances FDA put to its Pharmacy Compounding Advisory Committee on 23 and 24 July 2026 [20].

Our takeSeven registrations, zero of which administer anything. It is the cleanest example in this catalog of a trial count that describes a measurement programme and gets read as a treatment programme.

What we do not know about this group

No published human study has given epitalon, MOTS-c, 5-Amino-1MQ or humanin to a person and measured an ageing-related outcome. For MOTS-c one registered study proposes to give it, and it was recruiting rather than reporting on 2 August 2026. For the other three there is nothing registered at all.

The one compound here with a large human record is also the one whose record is negative. Elamipretide missed the primary endpoint of every adequately powered randomised trial it ran, across four different conditions [7] [9] [10] [11]. Why an accelerated approval followed, and what the open-label extension can and cannot establish on its own, is the question this page exists to set out, and it is the one any page selling SS-31 leaves out.

Telomere length is the claim area with the widest gap between what is measured and what is claimed. The epitalon work reports telomerase activity and telomere length in cultured cells [1] [2] [3]. Whether telomere length in a dish tracks anything a person experiences is a separate scientific question that these papers do not address and were not designed to.

For NAD+ the unknown is basic pharmacology rather than outcome. How much of an infused dinucleotide survives, where it goes, and whether it enters cells intact are not settled, and the 2026 systematic review found no outcomes trial of the infused form to reason from [12].

And the two mitochondrial peptides raise a question nobody has answered: both are molecules the body already makes and regulates, and levels of both move with exercise, illness and age [6] [16] [17]. What supplying more of an endogenous signalling peptide does to the system that normally sets its level has not been measured in a person for either one.

What this evidence can and cannot show

These results come from mice and rats in diet-induced obesity, genetic models of mitochondrial disease, and cultured human cell lines, not from people. An animal model is a deliberate simplification: the injury is created on purpose, the animal is young and healthy, the dose is scaled to body weight in a way that does not translate directly, and the outcome is measured at a fixed point rather than lived with. Cell and tissue work is a further step removed, because the concentrations that produce an effect in a dish are often far above anything a body reaches. Mechanism is a reason to run a trial. It is not a substitute for one, and compounds that looked mechanistically convincing have failed in people many times.

Frequently asked questions

Is SS-31 the same thing as elamipretide?

Yes. One molecule, several names: SS-31, elamipretide, MTP-131, Bendavia, and since 2025 the brand name Forzinity. The names split its registry record, and on 2 August 2026 ClinicalTrials.gov returned 21 registrations under elamipretide and 2 under SS-31. Those are the same drug indexed twice, and adding them together produces a trial count that does not exist.

Is SS-31 FDA approved?

The molecule is, under the brand name Forzinity, granted accelerated approval on 19 September 2025 as application 215244, to improve muscle strength in patients with Barth syndrome weighing at least 30 kg [18]. That approval covers one rare genetic condition. It is not an approval for mitochondrial health, energy or ageing, and a product sold as SS-31 is not the approved product.

Does MOTS-c have nine clinical trials?

It has nine registrations, which is a different statement. Eight of them measure the body's own MOTS-c as a marker inside studies about exercise, anaesthesia, diabetes, fasting, dialysis and other topics. One administers it: NCT07505745, a phase 2 study in adults with prediabetes and overweight or obesity, recruiting with no results posted as of 2 August 2026.

Has anyone been given humanin in a study?

Not in any registered or published study. All seven registrations returned on 2 August 2026 measure the humanin a person already makes, as a biomarker in cardiac surgery, kidney injury, IVF, muscle biopsy and exercise research. The work behind the marketing is cell and animal work [15].

Is NAD+ a peptide?

No. NAD+ is nicotinamide adenine dinucleotide, a coenzyme made of two nucleotides joined at their phosphates. It has no amino acids and no peptide bonds. 5-Amino-1MQ is not a peptide either: it is a small ring molecule that inhibits an enzyme.

What is the evidence for NAD+ infusions?

A 2026 systematic review in Ageing Research Reviews searched for outcomes trials of intravenous or intramuscular NAD+ itself for anti-ageing or wellness indications and reported that none met its inclusion criteria [12]. The substantial human trial literature people cite is on the oral precursors, nicotinamide mononucleotide and nicotinamide riboside, which are different substances taken by a different route.

Will any of these show up on a drug test?

MOTS-c is named on the 2026 WADA Prohibited List under S4.4.1, the AMPK activator class, prohibited at all times [19]. Separately, WADA's M2.2 rule caps intravenous infusions at 100 mL per 12 hour period, which makes a large-volume NAD+ infusion a prohibited method for a tested athlete regardless of its contents [19].

Was the epitalon telomere paper corrected?

Yes. The 2025 Biogerontology paper reporting increased telomere length in human cell lines carries a published correction, and both records are cited on this page so anyone checking it reaches the corrected version [1] [2].

What happened at the FDA advisory committee in July 2026?

The committee worked through seven substances over two days, voting twice on each, once for the free base and once for the acetate. The agency's own questions document names them: BPC-157, KPV, TB-500, MOTS-c, emideltide, epitalon and semax [20]. Two of the seven, MOTS-c and epitalon, are on this page. A recommendation is advisory in either direction, and FDA has published no vote record. The 503A record on this site sets out what the agency put to the committee and what would have to happen next.

References

  1. Al-Dulaimi S, Thomas R, Matta S, Roberts T. Epitalon increases telomere length in human cell lines through telomerase upregulation or ALT activity. Biogerontology. 2025. PMID 40908429 DOI 10.1007/s10522-025-10315-x
  2. Al-Dulaimi S, Thomas R, Matta S, Roberts T. Correction: Epitalon increases telomere length in human cell lines through telomerase upregulation or ALT activity. Biogerontology. 2025. PMID 41240216 DOI 10.1007/s10522-025-10326-8
  3. Khavinson VKh, Bondarev IE, Butyugov AA. Epithalon peptide induces telomerase activity and telomere elongation in human somatic cells. Bull Exp Biol Med. 2003. PMID 12937682 DOI 10.1023/a:1025493705728
  4. Araj SK, Brzezik J, Mądra-Gackowska K, Szeleszczuk Ł. Overview of Epitalon-Highly Bioactive Pineal Tetrapeptide with Promising Properties. Int J Mol Sci. 2025. PMID 40141333 DOI 10.3390/ijms26062691
  5. Lee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, Cohen P. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015. PMID 25738459 DOI 10.1016/j.cmet.2015.02.009
  6. von Walden F, Fernandez-Gonzalo R, Norrbom J, Emanuelsson EB, Figueiredo VC, Gidlund EK, Norrbrand L, Liu C, Sandström P, Hansson B, Wan J, Cohen P, Alkner B. Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans. J Appl Physiol (1985). 2021. PMID 34351816 DOI 10.1152/japplphysiol.00706.2019
  7. Reid Thompson W, Hornby B, Manuel R, Bradley E, Laux J, Carr J, Vernon HJ. A phase 2/3 randomized clinical trial followed by an open-label extension to evaluate the effectiveness of elamipretide in Barth syndrome, a genetic disorder of mitochondrial cardiolipin metabolism. Genet Med. 2021. PMID 33077895 DOI 10.1038/s41436-020-01006-8
  8. Thompson WR, Manuel R, Abbruscato A, Carr J, Campbell J, Hornby B, Vaz FM, Vernon HJ. Long-term efficacy and safety of elamipretide in patients with Barth syndrome: 168-week open-label extension results of TAZPOWER. Genet Med. 2024. PMID 38602181 DOI 10.1016/j.gim.2024.101138
  9. Karaa A, Bertini E, Carelli V, Cohen BH, Enns GM, Falk MJ, Goldstein A, Gorman GS, Haas R, Hirano M, Klopstock T, Koenig MK, Kornblum C, Lamperti C, Lehman A, Longo N, Molnar MJ, Parikh S, Phan H, Pitceathly RDS, Saneto R, Scaglia F, Servidei S, Tarnopolsky M, Toscano A, Van Hove JLK, Vissing J, Vockley J, Finman JS, Brown DA, Shiffer JA, Mancuso M, MMPOWER-3 Trial Investigators. 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
  10. Ehlers JP, Hu A, Boyer D, Cousins SW, Waheed NK, Rosenfeld PJ, Brown D, Kaiser PK, Abbruscato A, Gao G, Heier J, ReCLAIM-2 (SPIAM-202) Study Investigators. ReCLAIM-2: A Randomized Phase II Clinical Trial Evaluating Elamipretide in Age-related Macular Degeneration, Geographic Atrophy Growth, Visual Function, and Ellipsoid Zone Preservation. Ophthalmol Sci. 2025. PMID 39605874 DOI 10.1016/j.xops.2024.100628
  11. Butler J, Khan MS, Anker SD, Fonarow GC, Kim RJ, Nodari S, O'Connor CM, Pieske B, Pieske-Kraigher E, Sabbah HN, Senni M, Voors AA, Udelson JE, Carr J, Gheorghiade M, Filippatos G. Effects of Elamipretide on Left Ventricular Function in Patients With Heart Failure With Reduced Ejection Fraction: The PROGRESS-HF Phase 2 Trial. J Card Fail. 2020. PMID 32068002 DOI 10.1016/j.cardfail.2020.02.001
  12. Gallagher C, Emmanuel OO. NAD⁺ supplementation for anti-aging and wellness: A PRISMA-guided systematic review of preclinical and clinical evidence. Ageing Res Rev. 2026. PMID 41655607 DOI 10.1016/j.arr.2026.103057
  13. Neelakantan H, Vance V, Wetzel MD, Wang HL, McHardy SF, Finnerty CC, Hommel JD, Watowich SJ. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2018. PMID 29155147 DOI 10.1016/j.bcp.2017.11.007
  14. Kraus D, Yang Q, Kong D, Banks AS, Zhang L, Rodgers JT, Pirinen E, Pulinilkunnil TC, Gong F, Wang YC, Cen Y, Sauve AA, Asara JM, Peroni OD, Monia BP, Bhanot S, Alhonen L, Puigserver P, Kahn BB. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014. PMID 24717514 DOI 10.1038/nature13198
  15. Hashimoto Y, Niikura T, Tajima H, Yasukawa T, Sudo H, Ito Y, Kita Y, Kawasumi M, Kouyama K, Doyu M, Sobue G, Koide T, Tsuji S, Lang J, Kurokawa K, Nishimoto I. A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer's disease genes and Abeta. Proc Natl Acad Sci U S A. 2001. PMID 11371646 DOI 10.1073/pnas.101133498
  16. Woodhead JST, D'Souza RF, Hedges CP, Wan J, Berridge MV, Cameron-Smith D, Cohen P, Hickey AJR, Mitchell CJ, Merry TL. High-intensity interval exercise increases humanin, a mitochondrial encoded peptide, in the plasma and muscle of men. J Appl Physiol (1985). 2020. PMID 32271093 DOI 10.1152/japplphysiol.00032.2020
  17. Rodríguez-Esparragón F, Cazorla-Rivero SE, Torrealba E, Cánovas-Molina Á, González-Hernández AN, Martín-Alfaro R, Afonso-Medina MP, Martínez de Saavedra-Álvarez MT, Pérez-Santana CG, Bartolomé C, Estupiñán L, González-Martín JM, Clavo B. Insights into the Biomarker Potential of Humanin and Mots-c Expression and Telomere Length in Alzheimer's Disease. Int J Mol Sci. 2025. PMID 41303353 DOI 10.3390/ijms262210866
  18. US Food and Drug Administration. Novel drug approvals for 2025. Records Forzinity (elamipretide), approved 19 September 2025 under application 215244, to improve muscle strength in patients with Barth syndrome weighing at least 30 kg. FDA, Center for Drug Evaluation and Research. 2025. Source document
  19. World Anti-Doping Agency. The 2026 Prohibited List, international standard, effective 1 January 2026. WADA. 2026. Source document
  20. US Food and Drug Administration. Questions for PCAC regarding whether FDA should include certain bulk drug substances on the 503A Bulks List, Pharmacy Compounding Advisory Committee, 23 and 24 July 2026. The document names all seven substances put to a vote: BPC-157, KPV, TB-500, MOTS-c, emideltide, epitalon and semax. FDA advisory committee materials. 2026. Source document