MOTS-c
For laboratory and research purposes only. Not for human consumption, veterinary use, or medical applications.
What is MOTS-c?
MOTS-c (Mitochondrial Open reading frame of the Twelve S rRNA type-c) is a mitochondrial-derived peptide consisting of 16 amino acids. This peptide is released from mitochondria in response to cellular stress and has been studied for its effects on metabolic regulation, insulin sensitivity, exercise capacity, and aging research.
How Does MOTS-c Work?
MOTS-c is encoded within the mitochondrial 12S rRNA gene and translocates to the nucleus under metabolic stress conditions, where it directly regulates nuclear gene expression. It activates the AMPK pathway, a master regulator of cellular energy homeostasis, thereby improving glucose uptake in skeletal muscle and suppressing de novo lipogenesis. Research has also shown MOTS-c inhibits the folate cycle and de novo purine synthesis, redirecting metabolic flux toward energy production and away from biosynthesis during nutrient scarcity.
Research Applications
- Metabolic regulation and insulin sensitivity studies
- Exercise capacity and skeletal muscle research
- Mitochondrial stress response investigations
- Longevity and cellular aging models
- Nuclear gene expression regulation research
Specifications
Storage & Handling
Store lyophilized peptide at -20°C. Once reconstituted, store at 4°C for up to 1 week or at -20°C for up to 3 months. Avoid repeated freeze-thaw cycles. Recommended reconstitution solvent: sterile water or bacteriostatic water.
For laboratory and research purposes only. Not for human consumption, veterinary use, or medical applications.
Scientific References
- Lee C, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015;21(3):443-54.
- Reynolds JC, et al. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nat Commun. 2021;12(1):470.
- Lu H, et al. MOTS-c peptide regulates adipose homeostasis to prevent ovariectomy-induced metabolic dysfunction. J Mol Med. 2019;97(4):473-85.
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