MOTS-c
About
About MOTS-c
A mitochondrial-derived peptide encoded by the 12S rRNA gene, MOTS-c functions as a signaling molecule that regulates metabolic homeostasis by activating AMPK and influencing glucose uptake, insulin sensitivity, and fatty acid oxidation. This peptide has demonstrated effects on cellular metabolism and exercise mimetic properties in preclinical studies. Current research focuses on its potential applications in metabolic dysfunction, age-related decline, and insulin resistance.
Science
Mechanism of Action
MOTS-c activates AMPK (AMP-activated protein kinase) by interfering with the folate-methionine cycle and generating ZMP (an AICAR analog). AMPK activation inhibits mTORC1, stimulates fatty acid oxidation, promotes mitochondrial biogenesis via PGC-1α, and upregulates autophagy. Under cellular stress, MOTS-c translocates to the nucleus and acts as a transcriptional co-regulator of stress-response genes. Net effects include improved insulin sensitivity, enhanced energy utilization, and metabolic resilience.
Dosing
Typical Protocol
5–10 mg subcutaneously daily or 3–5 times weekly. Cycles of 4–8 weeks. Some practitioners combine with other mitochondrial support compounds (NAD+, SS-31) for a mitochondrial optimization stack. Best administered in the morning given its exercise-mimetic effects.
⚠ Protocol information is for educational purposes only. Dosing must be determined by a licensed physician based on individual health status and goals.
Regulatory
Legal Status in 2026
This compound occupies a regulatory grey area in 2026. It is neither explicitly FDA-approved nor clearly illegal for personal use, but it lacks formal clinical approval and may not be legally sold for human use in all contexts. Proceed with caution: source quality is variable, and regulatory status can change. Always consult a physician.
Evidence
Evidence Tier
Evidence primarily from animal studies, cell cultures, or small pilot human trials. Results are promising but have not yet been confirmed in large-scale human RCTs. Effects in humans may differ from animal models.
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