MOTS-c
Also known as Mitochondrial ORF of the 12S rRNA type-c
Evidence comes from rodents or other animal models, with no published controlled human trials. Most compounds that look promising in animals do not replicate in people — the attrition rate from animal model to approved drug is well over 90%.
What it is
A peptide encoded within mitochondrial DNA rather than the nuclear genome — one of a small group of mitochondrial-derived peptides identified since 2015. The underlying biology is genuinely interesting and independently studied.
How it is thought to work
Reported to activate AMPK and influence the folate-methionine cycle, positioning it as a signal from mitochondria to the rest of the cell about metabolic state.
What the studies found
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Metabolic effects in mice
Mouse studies report improved insulin sensitivity, resistance to diet-induced obesity and improved exercise capacity in older animals.
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Observational human associations
Circulating levels have been associated with exercise and with metabolic status in observational studies. Association is not causation, and these are not interventional trials.
What the evidence does not show
- No published randomised controlled trials in humans.
- Human evidence is observational — measuring natural levels, not administering it.
- The mouse metabolic literature is a poor predictor of human outcomes; this is the field where translation most often fails.
Reported risks and adverse effects
- No human safety data from controlled administration.
- Adverse effect profile in humans is unknown.
This is a summary of what has been reported in the literature, not a complete safety profile. For anything concerning your own health, speak to a doctor.
Regulatory status
Not approved anywhere. An active research subject, not a treatment.