A mitochondrial-derived peptide researched as an 'exercise mimetic' for insulin sensitivity, metabolic health and aging — largely in animals.
Research use only / investigational — not approved for any indication. A phase 2a trial in adults with prediabetes is a notably early clinical step; most existing data are preclinical or observational.
Also known as: Mitochondrial ORF of the twelve S rRNA type-c, mitochondrial-derived peptide
Encoded within mitochondrial 12S rRNA; inhibits the folate cycle to raise AICAR and activate AMPK, the master energy sensor. AMPK activation promotes glucose uptake, fatty-acid oxidation and mitochondrial biogenesis; also raises NAD+ with partial SIRT1 involvement.
MOTS-c is a 16-amino-acid peptide encoded by mitochondrial DNA that acts as an exercise mimetic, activating AMPK and influencing glucose use and fat oxidation in animal models. In humans the evidence is largely correlational: exercise raises endogenous MOTS-c in muscle and blood, and in one study of breast-cancer survivors a 16-week exercise programme raised MOTS-c levels that tracked with fat-mass and insulin-resistance improvements. Crucially, there are essentially no completed randomised trials of giving exogenous MOTS-c. It remains interesting biology, not established therapy — and claims that it replaces exercise are unsupported.
We report both positive and negative trial results. For exact study protocols, read the sources — we cite them rather than repackage them.
Bars reflect the strength & volume of research evidence for each use — not a guarantee of results.
Largely uncharacterised in humans. Controlled dosing studies are only now beginning, so the adverse-effect profile, long-term safety and even reliable pharmacokinetics of injected MOTS-c are not established.
SS-31 — complementary: SS-31 repairs existing mitochondria while MOTS-c drives biogenesis. Humanin — another mitochondrial-derived peptide. NAD+ precursors — grouped by shared energy-metabolism framing.
Mechanistic context only — we don't publish combinations, amounts or protocols.
Versus NAD+ precursors (NMN/NR), MOTS-c is likewise a mitochondrial signalling agent, but with even less human interventional data — NMN at least has multiple RCTs, whereas exogenous MOTS-c efficacy in people is essentially untested.
No. It is called an exercise mimetic in cell and animal work, but there is no human evidence that injecting it reproduces the benefits of training.
Not yet. Most human data are observational — exercise raises natural MOTS-c. Controlled trials of giving it are only starting.
Its human safety profile is largely unknown because rigorous dosing studies are still early.
No reviews yet. If you've used MOTS-c, be the first to share what it helped with and any side effects.
⚠️ Educational research information only — not medical advice. Many peptides are sold strictly for laboratory research and are not approved treatments. The evidence scores reflect research interest and strength, not efficacy or safety for any individual. Always consult a qualified professional.