MOTS-C 10mg
Mitochondrial exercise mimetic — activates AMPK, improves insulin sensitivity, enhances fat metabolism. Standard dose vial.
In Stock (20 available)
SKU: ML-MOTSC-20MG
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Buy 3+ vials = 10% off · Buy 5+ vials = 15% off
Description
What It Is
MOTS-C is a mitochondrial-derived peptide encoded within the mitochondrial genome (12S rRNA). Discovered in 2015 by researchers at the University of Southern California, it is one of the first mitochondrial peptides identified to have systemic hormonal effects. MOTS-C activates AMPK (AMP-activated protein kinase) — the master metabolic switch — producing effects that closely mimic those of aerobic exercise. It is nicknamed the "exercise mimetic peptide." It also translocates to the cell nucleus in response to metabolic stress, directly regulating gene expression.
Key Benefits
- AMPK activation — mimics the metabolic benefits of aerobic exercise at the cellular level
- Insulin sensitivity — improves glucose uptake and reduces insulin resistance
- Fat metabolism — enhances fatty acid oxidation and metabolic flexibility
- Longevity signalling — associated with healthy ageing; circulating MOTS-C is elevated in centenarians
- Anti-obesity effects — shown to prevent diet-induced obesity in animal models
- Muscle endurance — improves exercise performance and reduces fatigue
- Anti-inflammatory — modulates metabolic inflammation
Dosing Protocol
| Reconstitution | Add 3 mL bacteriostatic water |
| Dose per injection | 500 mcg (4 IU on a 100-unit syringe) |
| Injection site | Subcutaneous |
| Frequency | Daily |
| Best timing | Pre-workout in a fasted state for maximum effect |
| 1 vial lasts | ~15 days |
| Recommended cycle | 8 weeks on, then as needed |
| Vials for an 8-week cycle | ~4 vials |
New to MOTS-C? Start with the standard 500 mcg dose for at least 2 weeks before assessing. See the 40mg vial for higher-dose protocols and longer cycles.
Research Notes
MOTS-C was first described by Lee et al. (2015) in Cell Metabolism, where it was shown to regulate insulin sensitivity and prevent diet-induced obesity. Follow-up studies have shown that circulating MOTS-C levels decline with age and are significantly elevated in long-lived individuals, including centenarians.
Research References
Mitochondrial open reading frame of the 12S rRNA type-c (MOTS-c) primes adrenal cortex metabolism.
Investigates MOTS-c's effects on adrenal cortex metabolic priming.
Mitochondria-derived peptide MOTS-c alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice by activating Nrf2 pathway.
Demonstrates MOTS-c protects against lung injury through Nrf2 antioxidant pathway activation.
MOTS-c Protects Against Acetaminophen-induced Liver Injury through the MAPK Signaling Pathway.
Shows MOTS-c provides hepatoprotection against acetaminophen-induced liver damage via MAPK signaling.
Mitochondrial-derived peptides MOTS-c and humanin attenuate dexamethasone-induced atrophy in human skeletal muscle cells.
Demonstrates MOTS-c protects against corticosteroid-induced muscle wasting in human cells.
Aerobic exercise and MOTS-c attenuate diabetic myocardial fibrosis via inhibition of the THBS1/TGF-beta signaling pathway.
Shows MOTS-c reduces cardiac fibrosis in diabetic models by inhibiting the THBS1/TGF-beta pathway.
Therapeutic Effects of MOTS-c in the Valproic Acid-Induced Autism Model in Rats.
Explores MOTS-c as a therapeutic agent in an autism model with effects via BDNF pathways.
Reduced serum and skeletal muscle MOTS c levels in women with polycystic ovary syndrome are associated with mitochondrial dysfunction.
Identifies reduced MOTS-c levels in women with PCOS linked to mitochondrial dysfunction.
MOTS-c attenuates cardiac dysfunction following high altitude exposure by promoting mitophagy.
Demonstrates MOTS-c protects the heart from high-altitude dysfunction by enhancing mitophagy.
Exogenous MOTS-c mitigates myocardial ischemia-reperfusion injury in rat heart models.
Provides evidence that exogenous MOTS-c protects against heart ischemia-reperfusion injury.
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