MOTS-c
Mitochondrial Open Reading Frame of the 12S rRNA-c
Half-life: ~30 min–2 hours (estimated)
Research Profile
Relative research assessments — educational reference only.
Target Receptors
Critical Research Warning
MOTS-c is an experimental mitochondrial peptide. No human clinical trials for obesity or metabolic syndrome have been completed. For in-vitro and in-vivo animal research use only.
"A 16-amino acid peptide encoded within the mitochondrial genome — a newly discovered class of signaling molecule. Regulates metabolic homeostasis via AMPK and FOXO1 pathways."
Full Description
MOTS-c is a 16-amino acid mitochondrial-derived peptide (MDP) encoded in the 12S rRNA region of the mitochondrial genome — making it one of a small class of peptides with mitochondrial DNA origin. It translocates from mitochondria to the nucleus in response to metabolic stress, directly activating AMPK (AMP-activated protein kinase) and FOXO1, regulating glucose and lipid metabolism. Research in mice shows improved insulin sensitivity, exercise capacity, and reversal of diet-induced obesity and high-fat diet metabolic dysfunction. MOTS-c levels decline with age, suggesting potential roles in metabolic aging.
Mechanism of Action
Translocates from mitochondria to nucleus under metabolic stress. Activates AMPK and FOXO1, increasing glucose uptake, fatty acid oxidation, and mitochondrial biogenesis. Reduces ROS and inflammatory signaling.
Reported Benefits
- • Mimics the metabolic effects of exercise via AMPK activation
- • Improves cellular insulin sensitivity and glucose uptake
- • Promotes fatty acid oxidation and prevents diet-induced obesity
- • Protects against age-related metabolic decline
Potential Side Effects
- • Potential hypoglycemia in fasted states
- • Injection site irritation
- • Long-term human side effects remain unknown due to lack of RCTs
- • Unknown interactions with mitochondrial disorders
Frequently Asked Questions
How do researchers use MOTS-c?▼
Does it actually replace exercise?▼
What results have been seen in animal models?▼
For Research Reference Only
Not medical advice. Peptides may be regulated or restricted in your jurisdiction.
References
- 1.Mitochondrial-derived peptide MOTS-c activates metabolic signaling but blunts reparative function in human mesenchymal stromal cells. PubMed (2026). Xing L, et al.. pubmed.ncbi.nlm.nih.gov/42324588/ ↑
- 2.Mitochondrial peptide MOTS-c suppresses systemic and cardiac inflammasome activation in a diabetic rat model. PubMed (2026). Mills AR, et al.. pubmed.ncbi.nlm.nih.gov/42321010/ ↑
- 3.Reduced Circulating MOTS-c Levels in Hashimoto's Thyroiditis Reflect Integrated Autoimmune and Metabolic Dysregulation: A Cross-Sectional Study. PubMed (2026). Sonay HO, et al.. pubmed.ncbi.nlm.nih.gov/42278864/ ↑
- 4.MOTS-c partially protects against skeletal muscle deterioration in C26 cachexia. PubMed (2026). Jamnick NA, et al.. pubmed.ncbi.nlm.nih.gov/42266945/ ↑
Where to Source MOTS-c
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