MOTS-C
the mitochondrial peptideMitochondrial-derived peptide — cellular energy metabolismA mitochondrial peptide protocol aimed at energy metabolism and training adaptation — screened against your baseline and monitored through the course.
Roughly 90% of your cellular energy comes from mitochondria — MOTS-C is a peptide your mitochondria produce themselves, acting as an exercise signal. Human evidence is early, and your physician will be direct about what is and isn’t established.
Who this is for
Adults with declining training capacity, energy, or metabolic markers — where labs support a mitochondrial indication. Candidacy is decided by your physician against your history and baseline, never by a checkout flow.
What’s included
No prices on this site by design — your program is quoted in full after your consultation, before anything is dispensed.
Common questions
Some athletes report changes in endurance and recovery within weeks; for others it is gradual. Progress is read from your labs and training data at weeks 6 and 12 rather than promised.
A peptide written in mitochondrial DNA
MOTS-c regulates cellular metabolism in an AMPK-dependent manner. AMPK (AMP-activated protein kinase) is the master metabolic switch that responds to cellular energy state. The AMPK-dependent mechanism underpins the metabolic homeostasis effects reported in the Lee 2015 discovery paper.
Kim and colleagues (Cell Metab, 2018;28(3):516-524) reported that MOTS-c translocates to the nucleus in response to metabolic stress and regulates nuclear gene expression. The nuclear translocation provides a mechanism by which a mitochondrial-encoded peptide influences nuclear-genome gene expression.
Lee and colleagues (Cell Metab, 2015;21(3):443-454) reported that MOTS-c administration in mice promoted metabolic homeostasis and reduced obesity and insulin resistance in diet-induced obese models. The published findings provide the basis for insulin sensitivity research applications.
Reynolds and colleagues (Nat Commun, 2021;12:470) reported that exercise induces endogenous MOTS-c expression in human skeletal muscle and that intermittent MOTS-c treatment increased physical capacity in mouse models across multiple age groups. The work supports the "exercise mimetic" framing common in MOTS-c commentary.
MOTS - C is also searched as MOTSC, Mitochondrial-derived peptide.