β οΈΒ RESEARCH PURPOSES ONLY β This compound is not FDA authorized for human consumption. All referenced data is presented for informational and educational purposes only.
MOTS-c 15MG
$50.00
How It Works
Mitochondrial-derived peptide signaling studied in metabolic, aging, and exercise biology research
AMP-Activated Protein Kinase Signaling
MOTS-c activates AMP-activated protein kinase (AMPK) in skeletal muscle, adipose tissue, and liver. AMPK is a master metabolic sensor that responds to cellular energy status. MOTS-cβinduced AMPK activation in preclinical models was associated with increased glucose uptake, fatty acid oxidation, and mitochondrial biogenesis signaling.
- Direct AMPK phosphorylation (Thr172) in skeletal muscle
- Downstream activation of PGC-1Ξ± and mitochondrial biogenesis
- Enhanced GLUT4 translocation and glucose uptake
Mitochondria-to-Nucleus Retrograde Signaling
MOTS-c is encoded within the 12S rRNA gene of the mitochondrial genome β a discovery that established mitochondria as an endocrine organ capable of producing bioactive peptides. Under metabolic stress, MOTS-c translocates from mitochondria to the nucleus where it acts as a transcriptional regulator, modulating antioxidant response element (ARE) gene expression.
- Encoded in mitochondrial DNA (12S rRNA gene region)
- Nuclear translocation under metabolic stress conditions
- Modulates ARE-driven antioxidant gene expression
Metabolic Homeostasis & Exercise Signaling
MOTS-c levels naturally rise in response to exercise, and exogenous MOTS-c administration in mouse models replicated several exercise-associated metabolic adaptations including improved insulin sensitivity, reduced adiposity, and increased physical endurance β even in sedentary animals. It inhibits the folate cycle and purine synthesis under stress, redirecting metabolic flux.
- Endogenous levels increase with aerobic exercise
- Improves insulin sensitivity in rodent obesity models
- Inhibits AICAR-independent AMPK activation via folate cycle
What Research Has Shown
Key preclinical findings from published mitochondrial peptide studies
Research Applications
Primary areas of investigation
Insulin Resistance & Obesity
MOTS-c administration in high-fat diet mouse models improved insulin sensitivity, reduced fat accumulation, and normalized glucose tolerance β effects mediated primarily through skeletal muscle AMPK activation.
Lee C et al. 2015 βAge-Related Metabolic Decline
Circulating MOTS-c levels decline with age in both humans and rodents. Exogenous MOTS-c restored age-related declines in physical performance and metabolic flexibility in aged mouse models, suggesting its role in mitochondrial-nuclear communication during aging.
Reynolds JC et al. 2021 βExercise Mimicry
Circulating MOTS-c increases significantly with aerobic exercise in humans. In sedentary mouse models, exogenous MOTS-c replicated exercise-related improvements in energy metabolism, mitochondrial biogenesis markers, and physical endurance.
Kim SJ et al. 2022 βmtDNA Variation & Longevity
Population studies identified MOTS-c variants (particularly R150Q) enriched in elderly Japanese populations. Genetic variation in MOTS-c sequence correlates with metabolic disease risk, linking mitochondrial peptide biology to human longevity phenotypes.
Zempo H et al. 2016 βCompound Information
Technical specifications