The Mot-C lived up to my expectations and then some! There was a bit of a shipping mix up and I can’t say enough about the great and responsive customer service. The folks at Bioinfinity have my business!
MOTS-c — clinical & mechanistic profile
MOTS-c is a 16-amino-acid mitochondrial-derived peptide encoded within the 12S rRNA gene. 2025 studies show it restores cardiac mitochondrial OXPHOS respiration and reduces fasting glucose/hypertrophy in T2D rat models, protects against acute lung injury, and delays weight gain in high-fat diet models. Analog CB411 shows superior stability for obesity/NASH. Levels decline 21% in elderly vs young adults.
Research status
preclinical
Sequence
MRWQEMGYIFYPRKLR
Molecular weight
2174.64 Da
Molecular formula
C101H152N28O22S2
Studied applications
- •Exercise mimetic: causes cells to behave as if exercise has occurred, with older mice doubling running capacity on treadmill tests
- •AMPK activation: potent activator of the 'metabolic master switch' AMP-activated protein kinase, increasing glucose uptake and fat burning
- •NAD+ and sirtuin elevation: increases NAD+ levels and activates SIRT1, metabolic cofactors critical for cell survival and energy metabolism
- •Insulin sensitivity: improves glucose uptake and insulin responsiveness in muscle and adipose tissue
- •Folate-methionine regulation: modulates folate and methionine metabolism, pathways connected to DNA methylation and cellular stress
- •Bioregulator association: centenarians maintain higher MOTS-c levels than shorter-lived peers; levels decline 21% in 70-81 year olds vs 18-30 year olds
Mechanisms of action
- •AMPK pathway activation: directly activates AMP-activated protein kinase in skeletal muscle, triggering metabolic adaptations and glucose uptake
- •NAD+/SIRT1 activation: elevates NAD+ levels and activates sirtuins (particularly SIRT1), critical metabolic cofactors for cell survival
- •Nuclear translocation: unique ability to travel to nucleus and influence gene expression related to metabolism via ARE/TFAM pathways
- •Glucose metabolism: enhances glucose uptake in muscle and adipose tissue, improving whole-body glucose homeostasis
- •Fatty acid oxidation: promotes lipid catabolism and reduces fat accumulation through metabolic gene activation
- •Methionine restriction mimetic: promotes methionine restriction effects (which extends mouse lifespan by 45% and reduces age-related diseases)
- •Most data from rodent models—human translation not established
- •Endogenous production declines with age, complicating supplementation logic
- •Optimal dosing and administration routes for research not standardized
- •Long-term effects of exogenous MOTS-c administration unknown
- •Not FDA approved for any therapeutic use
Peer-reviewed references
- Lee C, et al. — Original MOTS-c discovery and metabolic effects in Cell Metabolism (2015)PMID: 25738459View
- Reynolds JC, et al. — MOTS-c exercise and aging study (2019)PMID: 30948516View
- Kim SJ, et al. — MOTS-c and metabolic homeostasis reviewPMID: 33037436View
- Mitochondrial-derived peptides cellular functionsPMID: 27239947View
- MOTS-c in skeletal muscle metabolismPMID: 32958710View
For research use only. This summary is a research-scientific overview compiled from peer-reviewed sources. It is not medical advice and is not intended for human or veterinary consumption.
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