Peptides for Mitochondrial Dysfunction: SS-31, MOTS-c, Humanin

Peptides for mitochondrial dysfunction: SS-31 is FDA-approved for one rare disease only. MOTS-c and humanin are unproven biomarkers, not treatments.

Written bySebastian Hunter, Founder and EditorI'm a 42-year-old senior advisor and distance runner who came to peptides as a sceptic. I'm not a doctor: I read the research, run my own experiment and keep honest notes. Read full bio

Published September 27, 2026

The short version

One mitochondria-targeted peptide has reached FDA approval, and the approval is narrow: elamipretide (SS-31), approved as Forzinity for Barth syndrome only. That is one ultra-rare genetic disorder, not general mitochondrial dysfunction. Its largest trial, in a more common mitochondrial disease, did not meet its primary endpoints. Your own mitochondria already make MOTS-c and humanin. The human research on each measures natural levels, not the effect of injecting more.

SS-31 (elamipretide) is FDA-approved as Forzinity, but only for Barth syndrome, an ultra-rare genetic disorder. It is not approved for general mitochondrial dysfunction.
SS-31's largest trial, in primary mitochondrial myopathy, did not meet its primary endpoints.
MOTS-c human studies measure the peptide your body already produces, rising with exercise. No completed trial has tested injecting it.
Humanin's human data is also observational blood levels, not a dosing trial. Its treatment evidence is cells and rodents only.

One mitochondria-targeted peptide is FDA-approved, and the approval covers one ultra-rare disease. Mitochondrial dysfunction gets marketed as a broad, fixable problem across three peptides (SS-31, MOTS-c and humanin), with very different evidence behind each. This page reports what was tested, in whom, compound by compound. None of it supports treating mitochondrial dysfunction as a general, self-directed condition.

SS-31 (elamipretide): approved for one disease only

SS-31, or elamipretide, is sold as the prescription drug Forzinity. It is the most heavily trialled compound on this page, with a real programme of randomised, controlled, multicentre human trials behind it Karaa 2018 - Karaa A, Haas R, Goldstein A et al. Randomized dose-escalation trial of elamipretide in adults with primary mitochondrial myopathy. Neurology. 2018;90(14):e1212-e1221., in the references below Karaa 2020 - Karaa A, Haas R, Goldstein A et al. A randomized crossover trial of elamipretide in adults with primary mitochondrial myopathy. J Cachexia Sarcopenia Muscle. 2020;11(4):909-918., in the references below. In September 2025 the FDA granted it accelerated approval for Barth syndrome, an ultra-rare X-linked genetic disorder. The approval is to improve muscle strength in adults and children who weigh at least 30 kg. It rests on an intermediate endpoint, not confirmed clinical benefit. It does not extend to mitochondrial dysfunction more broadly.

Its largest trial ran in a more common mitochondrial disease, primary mitochondrial myopathy, and did not meet its primary endpoints. The trial states that subcutaneous elamipretide did not improve the six-minute walk test or fatigue scores it measured Karaa 2023 - 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;101(3):e238-e252., in the references below Thompson 2024 - Thompson WR, Manuel R, Abbruscato A et al. Long-term efficacy and safety of elamipretide in patients with Barth syndrome: 168-week open-label extension results of TAZPOWER. Genet Med. 2024;26(7):101138., in the references below. Full detail, including the trial doses and side-effect data: SS-31 (elamipretide).

MOTS-c: a biomarker, not yet a treatment

MOTS-c is a peptide encoded inside mitochondrial DNA. It was first described in 2015 as promoting metabolic homeostasis largely through the AMPK pathway Lee 2015 - Lee C, Zeng J, Drew BG et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015;21(3):443-54., in the references below. The human research on it measures the MOTS-c your body already produces. It shows levels rising with endurance and resistance exercise, metformin and heat stress von 2021 - von Walden F, Fernandez-Gonzalo R, Norrbom J et al. Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans. J Appl Physiol (1985). 2021;131(3):1035-1042., in the references below. Reviews describe proposed roles in metabolism, insulin sensitivity and aging Zheng 2023 - Zheng Y, Wei Z, Wang T. MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation. Front Endocrinol (Lausanne). 2023;14:1120533., in the references below Kong 2023 - Kong BS, Lee C, Cho YM. Mitochondrial-Encoded Peptide MOTS-c, Diabetes, and Aging-Related Diseases. Diabetes Metab J. 2023;47(3):315-324., in the references below. Those roles come from the biomarker research and from cell and animal work, not from a completed trial that gave anyone injected MOTS-c.

One placebo-controlled trial giving subcutaneous MOTS-c to adults with prediabetes is currently recruiting and has not reported results. Until it does, no completed human trial tests MOTS-c as an administered treatment for insulin sensitivity, fat loss or any mitochondrial outcome. Full detail: MOTS-c.

Humanin: cells and rodents, not a human trial

Humanin is also encoded inside mitochondrial DNA rather than by a conventional nuclear gene. The evidence behind its neuroprotection and metabolic-signalling claims is cell culture and rodent work.

The human research is observational. It measures the humanin someone’s body already produces, circulating in blood, and correlates that level with age or a disease state. It does not measure what happens when someone is given more, because no completed human trial has administered humanin to anyone. Full detail: humanin.

What mitochondrial dysfunction treatment looks like today

A specialist manages diagnosed mitochondrial disease. They can test mitochondrial function directly and monitor a patient over time. It is not something to self-direct with a research chemical bought online. For Barth syndrome, an approved prescription option (Forzinity) now exists. For every other form of mitochondrial dysfunction discussed on this page, no peptide has cleared that bar.

Common questions

Is there a peptide for mitochondrial dysfunction?

One peptide, elamipretide (SS-31), is FDA-approved, but only for Barth syndrome, an ultra-rare genetic mitochondrial disorder. It is not approved for mitochondrial dysfunction generally. MOTS-c and humanin are naturally occurring mitochondrial peptides with real research behind them. Neither has a completed human trial testing it as an administered treatment for any form of mitochondrial dysfunction.

What is SS-31 approved for?

SS-31, as the drug Forzinity, received FDA accelerated approval in September 2025 to improve muscle strength in adults and children with Barth syndrome who weigh at least 30 kg. That is the entire approved indication. Its largest trial, in primary mitochondrial myopathy (a more common condition than Barth syndrome), did not meet its primary endpoints. Full detail is on the SS-31 page.

Does MOTS-c treat mitochondrial disease?

This is not established. Published human MOTS-c research measures the peptide your body already produces, rising in response to exercise, heat stress and other stimuli. That is biomarker research, not treatment research. One placebo-controlled trial giving injected MOTS-c to adults with prediabetes is currently recruiting and has not reported results. No completed human trial has tested injected MOTS-c for any mitochondrial disease.

Does humanin treat mitochondrial dysfunction?

No completed human trial has tested giving humanin to anyone for any indication. The human research that exists measures the humanin someone already produces in their own blood and correlates it with age or disease state. Everything describing humanin as neuroprotective or as helping mitochondrial function comes from cell cultures and rodent models.

Is any peptide FDA-approved for general mitochondrial disease?

No. The one FDA approval in this space, Forzinity (elamipretide/SS-31), is specific to Barth syndrome, a single ultra-rare genetic disorder affecting a tiny population and diagnosed by a specialist. No peptide is approved for mitochondrial dysfunction as a general category. Diagnosed mitochondrial disease should be managed by a physician who can test mitochondrial function, not self-directed with a research chemical.

References (9 sources)

Bibliographic detail is fetched from PubMed, not written by me - so a citation here cannot drift from the paper it names. Study design comes from PubMed's own tags rather than my judgement.