(4-Pack) MOTS-C – 10mg
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For research use only — not for human consumption, therapeutic, or diagnostic use. By adding to cart you acknowledge these terms.
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About This Compound
Deep technical insights for clinical research
Primary Research Applications
This compound is supplied strictly for in-vitro and preclinical research use only. Research focuses on the modulation of cellular repair mechanisms and upregulation of specific growth factor receptors in laboratory models.
Evaluation of metabolic activity and proliferation rates in relevant cell lineages.
Investigation of intracellular signaling cascades in controlled laboratory settings.
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Synthetics Quality Control
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Applied Peptide Research
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Pairs & Supplies
The compounds and tools researchers stack with (4-Pack) MOTS-C - 10mg.
Peer-Reviewed Literature
Related Studies
MOTS-c Is an Exercise-Induced Mitochondrial-Encoded Regulator of Age-Dependent Physical Decline and Muscle Homeostasis
Nature Communications
MOTS-c enhanced physical performance across the lifespan; in aged mice (equivalent to 65+ years), it doubled running capacity by regulating nuclear gene expression in skeletal muscle.
The Mitochondrial-Derived Peptide MOTS-c Promotes Metabolic Homeostasis and Reduces Obesity and Insulin Resistance
Cell Metabolism
Foundational study identifying MOTS-c as a novel mitochondrial-derived peptide that prevents age- and diet-induced insulin resistance through AMPK activation via folate cycle inhibition.
Mitochondrial-Encoded Peptide MOTS-c Prevents Pancreatic Islet Cell Senescence to Delay Diabetes
Experimental & Molecular Medicine
MOTS-c reduced senescence markers in aged pancreatic islets and improved glucose intolerance in diabetic mice. Circulating MOTS-c levels are lower in T2D patients versus healthy controls.
MOTS-c Is an Exercise-Induced Mitochondrial-Encoded Regulator of Age-Dependent Physical Decline and Muscle Homeostasis
Nature Communications
MOTS-c levels increase with exercise, and exogenous MOTS-c administration in aged mice improved physical capacity, grip strength, gait, and thermogenesis to levels approximating young controls.
MOTS-c Peptide Regulates Adipose Homeostasis to Prevent Ovariectomy-Induced Metabolic Dysfunction
Journal of Molecular Medicine
MOTS-c treatment prevented ovariectomy-induced obesity and insulin resistance by promoting brown adipose tissue activation, improving glucose tolerance, and reducing visceral fat accumulation.
The Mitochondrial-Derived Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress
Cell Metabolism
MOTS-c translocates to the nucleus under metabolic stress to directly regulate ARE-containing genes via AMPK-dependent chromatin remodeling — establishing a novel mito-nuclear communication pathway.