MOTS-c is a 16-amino-acid peptide encoded by a short open reading frame within the mitochondrial genome's 12S rRNA region, rather than by nuclear DNA. Published research identified skeletal muscle as its primary studied target tissue.

What does published research study MOTS-c for?

The literature has investigated MOTS-c in relation to AMPK activation via folate-cycle inhibition, prevention of diet-induced obesity and insulin resistance in mice, nuclear gene regulation under metabolic stress, and exercise-induced expression and physical-performance effects in mice. These are studied mechanisms and animal-model observations, not established human effects.

Is there human clinical evidence for MOTS-c?

The human evidence is limited: exercise was shown to induce endogenous MOTS-c expression in human skeletal muscle and circulation, and a cross-sectional study of 54 adults found plasma MOTS-c correlated with insulin sensitivity in lean but not obese participants. No completed human interventional trial of administered MOTS-c has been published.

How does MOTS-c compare to Humanin?

Both are peptides encoded directly by mitochondrial DNA, but published research links them to different pathways — Humanin to cell-survival and neuroprotective signaling, and MOTS-c to metabolic regulation via AMPK and nuclear gene expression.

How is research-grade MOTS-c supplied?

Typically as a lyophilized (freeze-dried) powder for reconstitution in a laboratory setting, accompanied by a Certificate of Analysis confirming HPLC-verified purity.

Materials described here are for laboratory research only and are not for human consumption. Nothing here is medical advice.

Research Library ·

MOTS-c: Research Overview, Mechanism & Published Studies

References

Lee C, Zeng J, Drew BG, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015;21(3):443-454.
Kim KH, Son JM, Benayoun BA, Lee C. The mitochondrial-encoded peptide MOTS-c translocates to the nucleus to regulate nuclear gene expression in response to metabolic stress. Cell Metab. 2018;28(3):516-524.
Reynolds JC, et al. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nat Commun. 2021;12(1):470.
Cataldo LR, Fernández-Verdejo R, Santos JL, Galgani JE. Plasma MOTS-c levels are associated with insulin sensitivity in lean but not in obese individuals. J Investig Med. 2018;66(6):1019-1022.
Kim SJ, Miller B, Kumagai H, et al. Mitochondrial-derived peptides in aging and age-related diseases. GeroScience. 2021;43(3):1113-1121.

Go Deeper

Related research

MOTS-c: Mechanism of Action in Published Studies
A research-framed look at the AMPK-activation and nuclear-translocation pathways published studies have associated with MOTS-c, a mitochondrial-DNA-encoded peptide.
MOTS-c vs Humanin: What the Research Compares
A research-framed comparison of how published studies characterize MOTS-c against Humanin, the other best-known peptide encoded directly by mitochondrial DNA.
MOTS-c Research FAQ
Common questions about MOTS-c answered in a research context — what it is, what studies examine, and the limits of the evidence.

Research Materials

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MOTS-c

Compliance & Disclaimer

This product is supplied strictly for research purposes only. It is not intended for human or animal consumption and is not intended for therapeutic, dietary, cosmetic, diagnostic, or veterinary use.

Statements on this page have not been evaluated by the U.S. Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Human/animal consumption prohibited. Laboratory/in-vitro experimental use only.