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.

Metabolism Insulin sensitivity Longevity Mitochondria

Amino acids

AMPK

Primary target

12S rRNA

Gene origin

Mechanism of action

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

12S rRNA peptide

AMPK

Activation

Glucose / fat

Metabolism

Insulin sensitivity

Healthspan

Also studied

Activates AMPK to improve insulin sensitivity and prevent diet induced and age related insulin resistance, in mice.

See related compounds

An exercise induced peptide: endogenous MOTS-c rises in muscle and blood with exercise in humans.

See related compounds

Circulating MOTS-c declines with age, with implications for metabolic disease and longevity science.

See related compounds

Applications

Research applications

Insulin sensitivity

Glucose metabolism

Animal (rodent) model

Mouse models

Obesity / metabolism

Diet induced

Animal (rodent) model

Rodent

Exercise capacity

Healthspan

Animal (rodent) model

Human exercise induces endogenous

Bars indicate how far the evidence has progressed (in vitro to animal to human), not the size of any effect.

Compound data

Molecular profile

CAS number1627580-64-6

Molecular formulaC101H152N28O22S2

Molecular weight2174.6 g/mol

Type16 aa mitochondrial derived peptide

SequenceMet-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg

AppearanceWhite lyophilized powder

Literature

Key studies

Cell Metabolism2015

The Mitochondrial Derived Peptide MOTS-c Promotes Metabolic Homeostasis and Reduces Obesity and Insulin Resistance

Lee C, et al.

Key finding

Identified MOTS-c (16 aa, 12S rRNA) as an AMPK activating regulator that improves insulin sensitivity and prevents diet induced obesity in mice.

View study

Full profile

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. Anyone considering these compounds should 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.