MOTS-c is a mitochondrial-derived peptide studied for its role in cellular energy metabolism and exercise-related signaling. Research is still largely preclinical, with interest driven by its proposed link to metabolic and longevity pathways.
The only human clinical data in this space is for CB4211, described as "a novel analog of MOTS-c" developed by CohBar — not MOTS-c itself. Same related-but-different-molecule pattern found repeatedly across this research project.
MOTS-c is a 16-amino-acid mitochondrial-derived peptide, encoded within the mitochondrial genome itself (the 12S rRNA region) rather than nuclear DNA. It's produced in skeletal muscle in response to exercise (in a reactive-oxygen-species-dependent manner) and is reported to act mainly through the folate-AICAR-AMPK pathway, affecting glucose metabolism, insulin resistance, and exercise adaptation. This mechanistic picture comes from animal/cell studies, not human trials of MOTS-c itself.
CB4211 (MOTS-c analog), Phase 1a/1b (healthy volunteers + NAFLD patients, 28 days, 25mg subcutaneous daily, n=11 treated vs. 9 placebo): met its primary safety outcome; liver enzymes ALT and AST were reduced 25% and 17% respectively vs. placebo in the NAFLD subgroup. Development of CB4211 was subsequently discontinued, and as of this research pass there are no active Phase 2/3 trials for MOTS-c or any MOTS-c analog.
No dose for MOTS-c itself has been clinically established — the only human dosing data (25mg/day subcutaneous) is for the CB4211 analog, not the native peptide sold as "MOTS-c."
CB4211 was reported safe and well-tolerated in its Phase 1 trial. No safety data exists for MOTS-c itself in humans.
Studies focus on mitochondrial function, metabolic regulation, and exercise-adaptation signaling.
No, it is not an approved drug and is sold for research use only.
Yes, it is encoded within mitochondrial DNA and occurs naturally in the body; the research compound is a synthesized version of that sequence.
Not in the usual sense — it's encoded by your mitochondrial DNA rather than your regular genome, discovered only in 2015. It's a signal your mitochondria produce themselves under stress or exercise, and production naturally declines with age.
Yes — exercise induces your body to produce MOTS-c on its own, in muscle tissue and circulating in blood, confirmed in humans specifically, not just animal models.
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