MOTS-C Dosage Calculator

• Low (5.0mg): Often utilized in baseline longevity models and studies assessing preliminary mitochondrial function and baseline AMP-activated protein kinase (AMPK) activation without severe metabolic stress.¹ 
• Mid (10.0mg): The standard median dosage frequently cited in experimental literature, widely used in protocols observing significant shifts in glucose regulation, enhanced insulin sensitivity, and the prevention of diet-induced obesity.²
• High (15.0mg): The upper threshold typically reserved for acute phases of research focusing on severe metabolic dysfunction or studies measuring extreme physiological stress and exercise capacity over a compressed timeframe.³
  

In experimental systemic protocols, MOTS-C is most commonly administered one to three times weekly. Because it functions as an exercise-mimetic and a mitochondrial-derived regulator of metabolism, researchers often time the administration prior to physical exertion or metabolic stress testing to observe its synergistic effects on fatty acid oxidation and physical endurance.³

Research literature documents administration routes based on whether the study is tracking systemic metabolic shifts or localized muscle uptake:

• Subcutaneous (SubQ): The benchmark route for systemic research targeting general metabolic flexibility, insulin resistance, and overall mitochondrial biogenesis.
• Intramuscular (IM): Occasionally utilized when studies specifically target direct skeletal muscle uptake, as skeletal muscle is the primary target organ for MOTS-C’s AMPK-activating effects.²

MOTS-C research generally follows sub-acute to longitudinal timelines to accurately track metabolic remodeling:

• Acute/Exercise Models: 2 to 6 weeks is the standard timeline for observing initial shifts in physical endurance, exercise capacity, and immediate glucose clearance rates.
• Longitudinal/Obesity Models: 12 to 24 weeks for observing the sustained prevention of diet-induced obesity, the stabilization of systemic insulin sensitivity, and long-term mitochondrial optimization without altering the subject’s caloric intake.²
  

While in vivo animal models demonstrate MOTS-C’s profound ability to act as a mitochondrial-encoded regulator of aging, enhance exercise capacity, and protect against diet-induced metabolic dysfunction, large-scale human clinical trials are currently limited. MOTS-C is not approved by the FDA for treating obesity, diabetes, metabolic syndrome, or age-related physical decline. All data provided is strictly for educational context, and all compounds are restricted to Research Use Only (RUO).

1. Kim SJ, Xiao J, Wan J, Cohen P, Yen K. Mitochondrially derived peptides as novel regulators of metabolism. J Physiol. 2017;595(21):6613-6621. https://pubmed.ncbi.nlm.nih.gov/28124443/
2. Lee C, Zeng J, Drew BG, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015;21(3):443-454. https://pubmed.ncbi.nlm.nih.gov/25738459/
3. Reynolds JC, Lai RW, Woodhead JST, et al. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nat Commun. 2021;12(1):470. https://pubmed.ncbi.nlm.nih.gov/33473109/