MOTS-c is a peptide produced by mitochondria themselves. It is researched as an exercise mimetic, with published work covering metabolism, insulin sensitivity, mitochondrial signalling and endurance in preclinical models.
PEPTIDE · RESEARCH MONOGRAPH · MITOCHONDRIAL-DERIVED 16-AMINO-ACID PEPTIDE
Mechanisms described in the published preclinical literature.
Activates AMPK in skeletal muscle, adipose tissue and liver. AMPK is the master metabolic sensor responding to cellular energy status, and its activation was associated with increased glucose uptake, fatty acid oxidation and mitochondrial biogenesis signalling in preclinical models.
Encoded within the 12S rRNA gene of the mitochondrial genome, a finding that established mitochondria as capable of producing bioactive peptides. Under metabolic stress it translocates to the nucleus and acts as a transcriptional regulator.
Endogenous levels rise with exercise, and administration in mouse models replicated several exercise-associated adaptations, including improved insulin sensitivity, reduced adiposity and greater endurance, even in sedentary animals.
Findings from the published literature, as the studies reported them. Where a finding comes from a human trial, it says so. None is a claim about the material supplied here.
In high-fat diet mouse models, administration improved insulin sensitivity, reduced fat accumulation and normalised glucose tolerance, mediated principally through skeletal muscle AMPK activation.
Lee C et al. 2015
Circulating levels decline with age in humans and rodents. Administration restored age-related declines in physical performance and metabolic flexibility in aged mouse models.
Reynolds JC et al. 2021
Circulating levels increase significantly with aerobic exercise in humans. In sedentary mouse models, administration replicated exercise-related improvements in energy metabolism and endurance.
Kim SJ et al. 2022
Population studies identified variants, particularly R150Q, enriched in elderly Japanese populations, linking mitochondrial peptide biology to human longevity phenotypes.
Zempo H et al. 2016
A sixteen-residue peptide encoded within the 12S rRNA gene of mitochondrial DNA, rather than in the cell nucleus like most peptides. Its discovery established that mitochondria can produce bioactive signalling molecules.
Endogenous levels rise with aerobic exercise, and in sedentary mouse models administration reproduced several exercise-associated metabolic adaptations. It is a description of what the preclinical literature reports, not a claim that it substitutes for training.
Circulating levels decline with age in both humans and rodents, and administration restored some age-related declines in physical performance and metabolic flexibility in aged mice. Population studies also link sequence variants to longevity.
Reported to act via folate cycle inhibition, which alters metabolic flux and activates AMPK independently of the AICAR route. AMPK is the same energy sensor exercise engages.
Human work is largely observational: circulating levels have been measured in relation to exercise and age. The interventional findings cited here are from animal and cell models, not human trials.
Store the sealed vial at −20°C for long-term stability. Once reconstituted, hold at 2–8°C and protect from light; we do not publish an in-use shelf life for reconstituted material because we have not measured one on this material. Protect from light and avoid repeated freeze-thaw cycles.
Each entry opens a PubMed search for that title rather than a fixed identifier, so the link resolves to the current record.
For laboratory research use only. Not a drug, supplement or medical product, and not for human or animal use. Every finding referenced on this page comes from published preclinical or laboratory research and is not a claim about this product.
