MOTS-c
Mitochondrial peptide
Research overview
A mitochondrial-DNA-derived peptide studied in models of metabolic homeostasis and insulin sensitivity.
Descriptions reference published research areas for laboratory context only and are not claims of efficacy, safety, or intended use in humans or animals.
- Price
- $170 CAD
- Purity
- ≥98.6% (HPLC)
- Presentation
- 10 mg lyophilized vial
Order / inquire about MOTS-c
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For laboratory research use only — not for human or veterinary use
MOTS-c is a chemical reference material sold strictly for in-vitro laboratory research by qualified professionals. It is not a drug, food, cosmetic, or natural health product; it has not been evaluated or approved by Health Canada; and it must never be ingested, injected, or applied to humans or animals. Sold in Canada only, to purchasers 18+. See our Research Use Policy.
Research encyclopedia
Everything the literature has studied.
For laboratory research use only — not for human or veterinary use. The content below summarizes published research context only. It is not medical advice, makes no therapeutic claims, and describes no intended use in humans or animals. These materials have not been evaluated or approved by Health Canada.
What it is
MOTS-c (Mitochondrial ORF of the Twelve S rRNA type-c) is a 16-amino-acid mitochondrial-derived peptide (MDP) encoded within the mitochondrial 12S rRNA gene. It acts as a mitochondria-to-nucleus signaling molecule regulating systemic metabolism and is frequently described in the literature as an 'exercise mimetic'.
Mechanism of action
Functions as a mitochondria-derived hormone that activates AMP-activated protein kinase (AMPK) via the folate-methionine/AICAR-AMPK axis, increasing skeletal-muscle glucose uptake and fatty-acid oxidation. Under metabolic stress it translocates to the nucleus and regulates nuclear antioxidant-response and adaptive stress genes (e.g., NRF2-linked programs).
Research areas
- Insulin sensitivity and metabolic homeostasis
- Physical performance and exercise capacity (exercise-mimetic biology)
- Healthy aging and skeletal-muscle bioenergetics
- Inflammatory and oxidative-stress response
Studied effects in research models
- Improved insulin sensitivity and glucose uptake in rodent models
- Increased mitochondrial bioenergetic efficiency and fatty-acid oxidation
- Attenuation of diet-induced and age-related metabolic decline (preclinical)
- AMPK-dependent metabolic reprogramming in cell culture
Effects listed describe observations reported in laboratory or animal research models only — not outcomes claimed for humans or animals.
Biomarkers tracked in related research
Discovery & background
Identified and characterized around 2015 by the laboratories of Changhan (David) Lee and Pinchas Cohen (University of Southern California) as a bioactive peptide encoded within mitochondrial DNA. Its discovery expanded the concept of the mitochondrial genome encoding functional signaling peptides that translocate to the nucleus under metabolic stress.
Considerations & limitations
Research-use-only reference material; not approved by Health Canada or the FDA. Evidence is almost exclusively preclinical (rodents and cell culture); human clinical data are very limited and metabolic/exercise benefits in humans remain unconfirmed extrapolations. Because it converges on AMPK and glucose metabolism, theoretical overlap with metabolic agents (e.g., metformin) is noted in models but human interactions are unstudied.
References
- [1]Lee et al., 2015 (MOTS-c identification) — Cell Metab; 21:443-454; PMID: 25738459
- [2]Reynolds et al., 2021 (MOTS-c and exercise) — Nat Commun; 12:470; PMID: 33473109
- [3]Kim et al., 2018 (MOTS-c nuclear translocation) — Cell Metab; 28:516-524; PMID: 29983246