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Mitochondrial-derived peptide that directly translocates to the nucleus under metabolic stress.

Dose ranges reflect commonly studied amounts in published research models. This is not medical advice. For research use only. Not for human consumption.
Protocol Comparison
Mitochondrial
Research dose range
Standard research range
5 - 10 mg
Primary investigative range for sustained AMPK activation and glucose disposal kinetics.
Research focus
Mitochondrial metabolic signaling & AMPK activation
Observed window
4-12 weeks
Administration
2-3x weekly protocol
Primary pathway
Mitochondrial 12S rRNA / AMPK / Folate cycle
Dosing compiled from peer-reviewed scientific literature (Lee et al., Cell Metabolism 2015). For laboratory research only.
PROTOCOL BENEFITS
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Mitochondrial-derived peptide that directly translocates to the nucleus under metabolic stress.
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Activates AMPK and enhances systemic glucose disposal and insulin sensitivity in animal models.
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Promotes metabolic flexibility, mimicking exercise-induced cellular signaling.
SCIENCE
MOTS-c is an exceptional 16-amino acid peptide encoded within the mitochondrial 12S rRNA gene. Discovered in 2015 by Lee et al. at USC, it acts as an endocrine-like mitochondrial messenger that translocates into the nucleus to regulate nuclear gene expression.
By activating 5'-AMP-activated protein kinase (AMPK) and modulating the folate-methionine cycle, MOTS-c prevents AICAR accumulation and stimulates cellular glucose uptake independently of insulin, representing a novel axis of cellular energetics.
WHAT TO EXPECT
Acute cellular energetic shifts are typically observed within hours to days in in-vitro assays, while functional exercise capacity outcomes are evaluated across 4–12 week protocols.
PROTOCOL NOTE
Available in 10 mg vials. Strictly for research and laboratory development use.
FAQ
MOTS-c originates directly within mitochondrial DNA, functioning as an endocrine metabolic signal that targets AMPK activation, cellular glucose uptake, and mitochondrial respiration.
It engages identical downstream metabolic pathways to endurance exercise, notably GLUT4 translocation and enhanced muscle insulin sensitivity, without requiring physical exertion.
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