Overview
MOTS-c is classified as a mitochondrial peptide peptide. Energy, metabolism, fat loss, longevity.
Regulates mitochondrial function and AMPK. Enhances glucose uptake and fatty acid oxidation, improves insulin sensitivity, and protects against age-related metabolic decline.
Also known as: Mitochondrial ORF of 12S rRNA Type-c
Category
Mitochondrial Peptide
Half-Life
4h
Route
SubQ
FDA Status
Not Approved
How Does MOTS-c Work?
Regulates mitochondrial function and AMPK. Enhances glucose uptake and fatty acid oxidation, improves insulin sensitivity, and protects against age-related metabolic decline.
At the molecular level, MOTS-c operates through pathways characteristic of the Mitochondrial Peptide class, interacting with target receptors and downstream signaling cascades to produce its observed effects.
Published Research
The following studies are indexed from PubMed and peer-reviewed journals:
[1]MOTS-c regulates metabolic homeostasis (Cell Metabolism)
Lee et al. (Cell Metabolism): Discovery paper showing MOTS-c is a mitochondrial-derived peptide that regulates insulin sensitivity and metabolic homeostasis via AMPK activation.
Evidence: emerging[2]MOTS-c prevents age-related insulin resistance in mice
Lee et al.: MOTS-c treatment prevents both age-dependent and high-fat-diet-induced insulin resistance and diet-induced obesity in mouse models.
Evidence: preclinical[3]MOTS-c improves skeletal muscle glucose metabolism
Study demonstrating MOTS-c specifically targets skeletal muscle glucose metabolism, providing molecular basis for metabolic benefits and exercise-mimetic properties.
Evidence: preclinical[4]Circulating MOTS-c levels decline with age and obesity
Human observational study linking decreased circulating MOTS-c levels with aging, obesity, and type 2 diabetes suggesting therapeutic rationale for supplementation.
Evidence: emerging[5]The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress.
A study published in Cell metabolism investigating the effects and mechanisms.
Evidence: preclinical[6]Mitochondrial-Encoded Peptide MOTS-c, Diabetes, and Aging-Related Diseases.
A study published in Diabetes & metabolism journal investigating the effects and mechanisms.
Evidence: preclinical[7]The mitochondrial-derived peptide MOTS-c suppresses ferroptosis and alleviates acute lung injury induced by myocardial ischemia reperfusion via PPARγ signaling pathway.
A study published in European journal of pharmacology investigating the effects and mechanisms.
Evidence: preclinical[8]MOTS-c attenuates lung ischemia-reperfusion injury via MYH9-Dependent nuclear translocation and transcriptional activation of antioxidant genes.
A study published in Redox biology investigating the effects and mechanisms.
Evidence: preclinical[9]MOTS-c attenuates mitochondrial dysfunction induces pyroptosis and cartilage degradation in osteoarthritis via an Nrf2-Dependent Mechanism.
A study published in Free radical biology & medicine investigating the effects and mechanisms.
Evidence: preclinical[10]Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging.
A study published in Journal of translational medicine investigating the effects and mechanisms.
Evidence: preclinical[11]MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism.
A study published in Free radical biology & medicine investigating the effects and mechanisms.
Evidence: preclinical[12]MOTS-c Functionally Prevents Metabolic Disorders.
A study published in Metabolites investigating the effects and mechanisms.
Evidence: preclinical[13]MOTS-c, the Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases.
A study published in International journal of molecular sciences investigating the effects and mechanisms.
Evidence: moderate[14]Mitochondria-derived peptide MOTS-c and its role in OSA pathogenesis: a potential therapeutic target?
A study published in Sleep and biological rhythms investigating the effects and mechanisms.
Evidence: preclinical[15]The mitochondrial genome-encoded peptide MOTS-c interacts with Bcl-2 to alleviate nonalcoholic steatohepatitis progression.
A study published in Cell reports investigating the effects and mechanisms.
Evidence: preclinical[16]MOTS-c regulates the ROS/TXNIP/NLRP3 pathway to alleviate diabetic cardiomyopathy.
A study published in Biochemical and biophysical research communications investigating the effects and mechanisms.
Evidence: preclinical[17]Circulating PGC-1α and MOTS-c Peptide as Potential Mitochondrial Biomarkers in Patients Undergoing Aortic Valve Replacement.
A study published in Biologics : targets & therapy investigating the effects and mechanisms.
Evidence: moderate[18]Mitochondrial-derived peptides and exercise.
A study published in Biochimica et biophysica acta. General subjects investigating the effects and mechanisms.
Evidence: preclinical[19]Mitochondrial-Derived Peptides Exacerbate Senescence.
A study published in Rejuvenation research investigating the effects and mechanisms.
Evidence: preclinical[20]MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation.
A study published in Frontiers in endocrinology investigating the effects and mechanisms.
Evidence: preclinicalSafety Profile
Promising but limited human data. As an endogenous peptide, theoretical biocompatibility favorable.
| Side Effect | Incidence | Severity |
|---|---|---|
| Injection site reaction | ~5% of users | mild |
| Generally well-tolerated | Very limited human data | mild |
Sourcing MOTS-c for Research
If you're looking to source MOTS-c for laboratory research, our vendor directory compares pricing, purity testing, and COA verification from independently vetted suppliers.
* Research vendor — verify your regional regulations before purchase.
Full Research Profile
MOTS-c — dosing, interactions, timelines & more
Comprehensive compound profile with sourcing information, stacking synergies, and outcome timelines.