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MOTS-c

Also known as: Mitochondrial Open reading frame of the 12S rRNA-c

9.8k views/week 156 citations 0 edits Updated 4/6/2026

MOTS-c is a 16-amino-acid mitochondria-derived peptide encoded within the 12S ribosomal RNA gene of the mitochondrial genome — one of the first peptides discovered to be encoded by mitochondrial rather than nuclear DNA. It acts as an exercise-mimetic, activating AMPK to improve insulin sensitivity, metabolic flexibility, and physical endurance.

STRUCTURE

Molecular Composition

FORMULA
C₁₀₁H₁₈₀N₃₄O₂₉S
MOL. WEIGHT
2174.82 Da
SEQUENCE LENGTH
16 amino acids
CAS NUMBER
1627580-64-6
ORIGIN
Mitochondrial 12S rRNA
WADA STATUS
Banned since 2024
AMINO ACID CHAIN VISUALIZATION
M
Met
N-terminal start
NH-CO
R
Arg
nuclear localisation
NH-CO
W
Trp
AMPK pathway interaction
NH-CO
L
Leu
hydrophobic core
NH-CO
T
Thr
phosphorylation site
NH-CO
L
Leu
hydrophobic core
NH-CO
T
Thr
metabolic signalling
SEQUENCEM-R-W-L-T-L-T
MECHANISMS

How It Works

Mitochondrial-Nuclear Signalling
MOTS-c is unique as the only known peptide encoded by mitochondrial DNA that translocates to the nucleus. Under metabolic stress, it migrates to the nucleus and activates ARE (antioxidant response element) genes — effectively communicating mitochondrial health status to nuclear gene expression machinery.
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AMPK & Insulin Sensitivity
MOTS-c activates AMPK (AMP-activated protein kinase) and downstream PGC-1α, improving insulin sensitivity, reducing hepatic gluconeogenesis, and enhancing skeletal muscle glucose uptake. In diabetic models, it restores mitochondrial respiration and reduces fasting glucose.
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Exercise Mimetic
MOTS-c is secreted by skeletal muscle mitochondria during exercise. It upregulates the same metabolic pathways activated by endurance training — making it one of the few true "exercise mimetics" in the research peptide space. Levels are significantly elevated in marathon runners vs sedentary controls.
Healthspan Extension
Late-life MOTS-c treatment in aged mice (equivalent to ~75-year-old humans) increased physical performance, reduced frailty, and extended healthspan without apparent toxicity. The AMPK/PGC-1α axis is believed to mediate these effects by supporting mitochondrial biogenesis and reducing cellular senescence.
OVERVIEW

Research Overview

MOTS-c was discovered in 2015 by Chang Hee Lee and colleagues at the University of Southern California. Its discovery overturned the established dogma that the mitochondrial genome only encodes for 13 proteins of the respiratory chain — revealing that mitochondria also produce regulatory peptides with systemic metabolic effects.

MOTS-c functions as a retrograde signal from mitochondria to the nucleus and other cells, coordinating metabolic responses to bioenergetic stress. Its plasma levels decline with aging in humans, and are lower in type 2 diabetic patients, suggesting it plays a physiological role in metabolic homeostasis. Exercise increases circulating MOTS-c, and exogenous MOTS-c supplementation produces exercise-like metabolic benefits even in sedentary animals.

Mechanism of Action

// AMPK ACTIVATION

MOTS-c activates AMP-activated protein kinase (AMPK) — the master cellular energy sensor — by modulating the folate cycle in a manner that increases AMP:ATP ratio. AMPK activation drives glucose uptake (via GLUT4 translocation), mitochondrial biogenesis (via PGC-1α), and fatty acid oxidation.

// FOLATE CYCLE & AICAR PRODUCTION

MOTS-c inhibits the folate cycle enzyme MTHFD1L, causing accumulation of AICAR (5-aminoimidazole-4-carboxamide ribonucleotide) — a natural AMPK activator. This is distinct from other AMPK activators and explains MOTS-c's unique metabolic signature.

SEQUENCE

Amino Acid Sequence

Arg-Ala-Ser-Leu-Leu-Gly-Glu-Tyr-His-Gly-Trp-Thr-Gln-Lys-Phe-Thr
DOSAGE

Dosage & Administration

INJECTABLE (SUBCUTANEOUS)
DOSE
5–10 mg, 3×/week
FREQUENCY
3 times per week
NOTES
Most studied route in preclinical models. Reconstitute in bacteriostatic water. Human dosing protocols are empirical — no Phase 2/3 dose-finding trials published. Research context only.

MOTS-c is banned by WADA (2024) as a peptide hormone with potential performance-enhancing effects. Human clinical data is very limited — most evidence from mouse studies. Endogenous MOTS-c levels rise naturally with exercise, particularly endurance training. Marathon runners show significantly higher circulating levels than sedentary controls.

CYCLING

Cycle Duration Guide

ON CYCLE
4–8 weeks on
OFF CYCLE
4 weeks off

Cycle protocols are based on preclinical mouse studies showing longevity and metabolic benefits with intermittent dosing (3×/week). Late-life (23.5 month) mice treated intermittently showed increased physical capacity and healthspan. No established human cycle protocol exists.

WADA-banned substance. Prohibited for use in competitive sports as of 2024. Research context only — not approved for human therapeutic use.

Quick Reference
FORMULAC₁₀₁H₁₅₈N₂₉O₃₁
MOL. WEIGHT2,174.49 Da
LENGTH16 amino acids
ORIGINEndogenous peptide encoded by the mitochondrial 12S rRNA gene
HALF-LIFE~2–4 hours (subcutaneous); exercise increases endogenous production
SOLUBILITYWater soluble
CAS NO.1627580-64-6
STATUSPreclinical
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TAGS
mitochondrialinsulin sensitivityexercise mimeticlongevityanti-agingAMPK