MOTS-c
Compound snapshot
Class
Mitochondrial-derived peptide
FDA approved
No — recommended 7–5 by the FDA advisory committee in July 2026; the vote is advisory and does not permit compounding
Clinical development
Preclinical
Last reviewed
September 2026
Research areas
Mitochondrial function / Glucose metabolism / Exercise physiology
Regulatory status
Research use only — not approved
Internet attention
High
Registry query
MOTS-c
A 16-amino-acid peptide encoded by mitochondrial DNA rather than the cell nucleus — one of the 'mitochondrial-derived peptides' discovered in the last 15 years.
Reality check — what we actually know
Supported by human evidence
- No adequately powered randomised human trials establish the outcomes this compound is marketed for.
Animal research only
- Improved insulin sensitivity and prevented diet-induced obesity in mouse models
- Increased exercise capacity in aged mice — a widely cited 'exercise-mimetic' finding
- Higher endogenous MOTS-c levels associate with metabolic health and longevity in human cohort studies
Mechanistically plausible
- Activates AMPK, the cell's low-energy sensor, shifting the cell toward glucose uptake and fat oxidation. Translocates to the nucleus under metabolic stress to regulate adaptive gene expression.
Common internet claims
- Online discussion frequently presents MOTS-c as a proven treatment rather than a research compound.
Not established
- Human efficacy for the outcomes commonly claimed
- Optimal route, quantity and duration in humans
- Long-term human safety
Evidence distribution
Each band is a live PubMed search for MOTS-c, filtered to that kind of study. Top is the strongest evidence; the base is reasoning, not proof. A band with no records means that kind of study has not been published for this compound yet.
Mechanism and reported findings
Activates AMPK, the cell's low-energy sensor, shifting the cell toward glucose uptake and fat oxidation. Translocates to the nucleus under metabolic stress to regulate adaptive gene expression.
- Improved insulin sensitivity and prevented diet-induced obesity in mouse models
- Increased exercise capacity in aged mice — a widely cited 'exercise-mimetic' finding
- Higher endogenous MOTS-c levels associate with metabolic health and longevity in human cohort studies
- Anti-inflammatory and mitochondrial-stress-protective effects in cell work
Strength of the evidence: Strong mechanistic biology and mouse data; human interventional evidence is minimal. Early human trials in metabolic disease have been discussed but not concluded.
Safety and known cautions
No established human dosing or safety profile. WADA-prohibited.
Evidence at a glance
No single score, on purpose. The line beside each bar shows how much reported outcomes vary between studies.
Development stage
- Discovery
- PreclinicalCurrent
- Phase 1
- Phase 2
- Phase 3
- Regulatory review
- Approved