Research library
Longevity & MitochondrialPlausible but unproven in humans
Mitochondrial derived peptide
MOTS-c, 16 aa mitochondrial peptide
A 16-amino acid peptide encoded by the mitochondrial 12S rRNA gene, discovered as a signaling molecule that activates AMPK to regulate metabolism and insulin sensitivity.
16
AMPK
12S rRNA
How MOTS-c works
A peptide encoded inside mitochondrial DNA that acts like an exercise signal, switching on AMPK to improve insulin sensitivity and metabolism.
MOTS-c
AMPK
Glucose / fat
Insulin sensitivity
Research applications
Insulin sensitivity
Glucose metabolism
Obesity / metabolism
Diet induced
Exercise capacity
Healthspan
Bars indicate how far the evidence has progressed (in vitro to animal to human), not the size of any effect.
Molecular profile
Key studies
The Mitochondrial Derived Peptide MOTS-c Promotes Metabolic Homeostasis and Reduces Obesity and Insulin Resistance
Lee C, et al.
Identified MOTS-c (16 aa, 12S rRNA) as an AMPK activating regulator that improves insulin sensitivity and prevents diet induced obesity in mice.
Evidence, safety & status
Claimed benefits & evidence
Improves insulin sensitivity, reduces obesity, and increases physical capacity/healthspan in mice. In humans, exercise induces endogenous MOTS-c, but there are no human trials of exogenous MOTS-c administration for any endpoint, all therapeutic data is rodent.
Safety & dangers
Human safety profile unestablished; gray market risk.
Regulatory status
Not FDA approved; Category 2 (2023), removed April 2026; PCAC review July 23, 2026 (obesity and osteoporosis). WADA: S0.
Administration
Subcutaneous/intraperitoneal (in animal studies).
Source: Fnx Performance Peptide Research Database, a synthesis of the scientific and regulatory literature, not medical advice. For medical questions, consult a qualified physician.
For research use only
For Research Use Only. Not for human or animal consumption. Products are sold strictly for in vitro laboratory research, not for compounding or therapeutic application.