MOTS-c

Mitochondrial-derived peptide encoded within the 12S rRNA gene. Activates AMPK signaling, enhancing glucose uptake and fatty acid oxidation independent of insulin. Regulates the folate-methionine cycle, linking cellular metabolism to epigenetic function. Acts as an exercise mimetic at the molecular level.

Half-life

4 hours (estimated)

Bioavailability

Systemic via subcutaneous injection

Route

subcutaneous

Evidence tier

T2 — Single-RCT or mechanistic

Optimization pillars

cellular-health · fat-loss

References

2 peer-reviewed

Dose ranges

Three tiers ordered by aggressiveness. Tier chips on every OPTIMIZE intervention let you filter the catalog by your evidence tolerance.

conservative

5 mg/week

Metabolic support

moderate

5–10 mg/week

Metabolic optimization

aggressive

10–15 mg/week

Insulin resistance intervention

Monitoring

fasting-glucose
fasting-insulin
hba1c
homa-ir
triglycerides

Contraindications

type-1-diabetes
pregnancy

References

PMID:25738459The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance — Cell Metab, 2015
PMID:30948246MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline — Nat Commun, 2019

Notes

MOTS-c is the most intellectually interesting peptide in the metabolic space. Your mitochondria are encoding signaling peptides that regulate your metabolism. This is not a pharmaceutical — it is a molecule your cells already produce, declining with age. The AMPK activation mirrors exercise at the molecular level. The question is whether exogenous administration recapitulates the endogenous signal. Early evidence says yes. The metabolic markers move in the right direction.

This is not medical advice

Discuss with a licensed clinician before starting, stopping, or changing any compound. This page documents what the research literature describes — it is not a prescription.

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