Description
MOTS-C (Mitochondrial Open Reading Frame of the 12S rRNA-c) is a 16-amino-acid peptide encoded by mitochondrial DNA, placing it among a small class of mitochondrially encoded peptides. MOTS-C was discovered by Lee et al. in 2015 in the laboratory of Pinchas Cohen at USC. It has since become one of the most extensively studied compounds in mitochondrial research.
The central research mechanism lies in AMPK signaling. In research models, MOTS-C activates the AMPK axis via the folate-methionine-one-carbon pathway system. AMPK is the central energy sensor of the cell and, in its activated form, regulates glucose uptake, fatty acid oxidation and mitochondrial biogenesis. This makes MOTS-C a research tool for studies on insulin sensitivity, metabolic flexibility and age-related metabolic changes.
In preclinical studies, MOTS-C levels in multiple tissues have been associated with aging, physical activity and metabolic status. The research hypothesis: MOTS-C functions as an endocrine signaling molecule between mitochondria and nucleus, communicating cellular energy status. This makes MOTS-C one of the first well-characterized mitokines.
In research setups, MOTS-C is typically used in cell cultures or animal models at defined concentrations over several weeks to observe chronic metabolic effects.
MOTS-C is available in 10mg vials as 10-vial packs.
This information is for research and educational purposes only. No medical recommendations.
Risks & Safety
MOTS-C is considered well tolerated per study reports. As an endogenous, mitochondrially encoded peptide, the available preclinical studies do not describe a pronounced toxicity profile.
Observed in studies and user reports:
- Injection site: mild redness, pressure or transient irritation at the injection site is the most common observation with subcutaneous use.
- Circulation: isolated reports of brief warmth, mild dizziness or fatigue shortly after application.
- AMPK effect on metabolism: through the AMPK axis MOTS-C modulates glucose uptake and energy metabolism. Possible effects on blood sugar are discussed in the literature.
- No long-term data: robust human studies barely exist. Most of the available evidence comes from cell cultures and animal models.
This classification does not replace medical advice. Risk and responsibility for any actual use lie entirely with the buyer.
Studies
- The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis - Cell Metabolism 2015: Original characterization of the compound.
- The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress - Cell Metabolism 2018: Under metabolic stress, MOTS-c translocates to the nucleus in an AMPK-dependent manner and regulates stress-response genes there, in part by interacting with the transcription factor NRF2.
- MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis - Nature Communications 2021: MOTS-c enhanced physical performance in young, middle-aged and old mice. In humans, exercise increased endogenous MOTS-c expression in skeletal muscle and in circulation.
- Mitochondrial-Encoded Peptide MOTS-c, Diabetes, and Aging-Related Diseases - Diabetes & Metabolism Journal 2023: Review of mitochondrial-encoded peptides focusing on recent MOTS-c data on type 1 and type 2 diabetes and age-related diseases.
