MOTSC

MOTS-c

Metabolic Anti-Aging Preclinical (animal)

Mitochondria-derived peptide that regulates metabolic homeostasis; in mice it prevented diet-induced obesity and insulin resistance.

Regulatory status (as of Sept 2026)

Not FDA-approved. Removed from 503A Category 2 on April 15, 2026. PCAC recommended for the 503A Bulks List (advisory); awaiting FDA rulemaking; not lawfully compoundable under 503A as of Sept 17, 2026. PCAC vote: 7–5–2 (yes–no–abstain), July 23, 2026.

See the FDA peptide regulatory tracker · Read our July 27, 2026 dispatch on the FDA PCAC peptide vote
Educational summary. Every effect described below is drawn from the cited published research and describes what was observed in research subjects — not a promise of results, a dose recommendation, or an endorsement for human use. Many peptides are not FDA-approved. Consult a licensed healthcare provider before making any health decision. Full disclaimer.

2 studies referenced · Last reviewed Oct 1, 2026 · Reviewed by The Peptide Dispatch Editorial Team · How we research & label content

TL;DR — MOTS-c at a Glance

MOTS-c is a compound studied only in animals and lab experiments so far. Mitochondria-derived peptide that regulates metabolic homeostasis; in mice it prevented diet-induced obesity and insulin resistance.

Half-lifeNot established in published research
How it's given in studiesSubcutaneous injection
Research stagePreclinical (animal)
Dosing
Published research: No published human dosing
detailsi.p. injection in mice fed high-fat diet and aged mice (Lee et al. 2015); exact mg/kg in full text, not in abstract
Community-reportedCommunity-reported: 5–10 mg weekly, subcutaneous injection

Published-research dosing is what was given in the cited studies (species and units as reported). Community-reported dosing is what users describe, not from clinical studies. Neither is a recommendation. Not medical advice.

Where each point comes from: Clinicalhuman trials and FDA labels   Lab / animalrodent, cell and ex vivo studies   Community-reporteduser experience and commonly used protocols, not from clinical studies

How It Works

In plain terms: It is a small peptide made by mitochondria that acts mainly on muscle energy use, based on mouse and cell studies. Proposed mechanism, from mouse and cell studies (Lee 2015): a mitochondrial-derived peptide whose primary target appears to be skeletal muscle; it inhibits the folate cycle and de novo purine biosynthesis, leading to AMPK activation. In mice it prevented age-dependent and high-fat-diet-induced insulin resistance and diet-induced obesity.

Effects Reported in Research

How to read this: Each item below is an effect observed in research subjects in the cited studies — think of Dexter, our stand-in research subject. These are findings from the literature, not results you should expect, and not medical advice.

  • Lab / animalIn animal studies: metabolic regulation
  • Lab / animalExercise-mimetic effects in mouse studies
  • Lab / animalPrevented diet-induced obesity and insulin resistance in mice

What Users Report (Community, Not Clinical)

Commonly reported protocol

Community-reportedSome users report running MOTS-c at 5–10 mg weekly (subcutaneous injection). This is not a recommendation.

Community reports are anecdotal, vary widely in product quality and purity, and are not medical advice. Talk to a licensed provider.

Side Effects and Safety Notes

  • No published human safety data for exogenous MOTS-c

References

  1. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance
    Lee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J et al. Cell metabolism. 2015. PMID: 25738459.
    Study type: Mouse (HFD and aged) + cell studies.
    DOI: 10.1016/j.cmet.2015.02.009 · PubMed
  2. MOTS-c in type 2 diabetes mellitus: From risk factors to cardiac complications and potential treatment
    Fang T, Han JC, Taberner A, Pham T. Life sciences. 2025. PMID: 41083123.
    Study type: Review.
    DOI: 10.1016/j.lfs.2025.124009 · PubMed

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How MOTS-c Compares

PeptideHalf-LifeRouteResearch Status
MOTS-cUnknownSubcutaneous injectionPreclinical (animal)
5-Amino-1MQUnknownOralPreclinical (animal)
AOD-9604No published PK data foundSubcutaneous injectionDiscontinued
Adipotide (FTPP)No published PK data foundSubcutaneous injectionPreclinical (animal)
Dulaglutide~5 daysSubcutaneous injectionFDA-approved

Values reflect figures reported in published research. Compare any peptides side-by-side →

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Frequently Asked Questions

What is MOTS-c?
Mitochondria-derived peptide that regulates metabolic homeostasis; in mice it prevented diet-induced obesity and insulin resistance.
How does MOTS-c work?
In plain terms: It is a small peptide made by mitochondria that acts mainly on muscle energy use, based on mouse and cell studies. Proposed mechanism, from mouse and cell studies (Lee 2015): a mitochondrial-derived peptide whose primary target appears to be skeletal muscle; it inhibits the folate cycle and de novo purine biosynthesis, leading to AMPK activation. In mice it prevented age-dependent and high-fat-diet-induced insulin resistance and diet-induced obesity.
What is the research status of MOTS-c?
MOTS-c is at the following stage in the published literature: Preclinical (animal). All information is for research and educational purposes only.
What is the half-life of MOTS-c?
Reported half-life: Unknown.
How is MOTS-c administered in research?
Reported administration route in the literature: Subcutaneous injection. This is not a recommendation for human use.

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Category

This peptide belongs to the Metabolic category. View All Metabolic Peptides

Related Categories

Anti-Aging

Related Peptides

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Sources & Methodology

Dosing, half-life figures, and mechanism descriptions on this page are compiled from peer-reviewed published research, with the species and study type stated where reported. Figures labeled “Dosing used in published research” describe what was given in those studies and do not constitute dosing recommendations for any human use. Each cited paper is listed with DOI and PubMed links in the References section above. Found an error? Contact us.

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