— MITOCHONDRIAL-DERIVED PEPTIDE · EXERCISE MIMETIC

MOTS-c.

A 16-amino-acid peptide encoded within the mitochondrial 12S rRNA gene — the first peptide transcribed from mitochondrial DNA to travel to the nucleus and regulate gene expression. Circulating levels rise with aerobic exercise; exogenous administration replicates those effects.

Key Signals
Metabolism · Exercise · Longevity
Origin
Endogenous (mitochondrial genome)
Investigator
Lee et al. (USC), 2015
Class
Mitochondrial-derived peptide (MDP)
Status (UAE)
Research compound (pre-clinical)
— THE RESEARCH STORY

The message from the mitochondria.

Lee et al. identify MOTS-c encoded not in nuclear DNA but within the mitochondrial 12S rRNA gene — the first mitochondrial hormone.

Circulating MOTS-c rises during aerobic exercise. Exogenous administration replicates metabolic training benefits in rodents — without exercise itself.

No human trial programme has been initiated. Animal models show lifespan extension, AMPK activation, and insulin sensitisation — novel, fast-moving.

— GLUCOSE DISPOSAL RATE
RODENT MODEL · MOTS-c vs VEHICLE · % IMPROVEMENT OVER BASELINE
0% +10% +20% +30% +40% +50% WEEK 0 WEEK 2 WEEK 4 WEEK 6 WEEK 8
MOTS-c TREATED VEHICLE CONTROL
— THE MOLECULE

Mitochondria writing to the nucleus.

PRIMARY STRUCTURE

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

C₁₀₁H₁₅₃N₂₉O₂₄ · MW 2174 Da

2174MOLECULAR WEIGHT Da
16AMINO ACIDS
Pre-ClinRESEARCH STAGE

Encoded within the mitochondrial 12S rRNA gene — the only known peptide from mitochondrial DNA to regulate nuclear gene expression. Naturally circulates in blood; levels are elevated by aerobic exercise.

— AN HONEST READING OF THE DATA

Animal models first, humans next.

Strong rodent data across multiple labs. No human trial has been initiated yet.

TIER 01 / RODENT REPLICATED
Consistent Animal Evidence
  • AMPK activation confirmed
  • Insulin sensitivity improved
  • Adiposity reduced (HFD model)
  • Lifespan extension (mice)
  • Exercise-equivalent metabolics
TIER 02 / MECHANISTIC
In Vitro & Pathway Data
  • Retrograde mito-nuclear signal
  • NF-κB suppression
  • GLUT4 upregulation
  • Cognitive gains (aged rodents)
TIER 03 / SPECULATIVE
Extrapolated to Humans
  • Human exercise mimetic
  • Frailty / sarcopenia reversal
  • Neurodegenerative disease
  • Human longevity
— MOTS-C MECHANISMS & RESEARCH DOSING READY

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— REGULATORY LANDSCAPE

The newest signal in this catalogue.

In the UAE, research-grade peptides occupy a defined regulatory category distinct from licensed medicines. Compounds sold under this classification — including those offered by Dubai Peptides — are intended exclusively for qualified research applications, not for human administration.

MOTS-c is the most frontier compound here — discovered in 2015, with no human trial programme yet initiated. The mechanism is genuinely novel: a peptide encoded in mitochondrial DNA that travels to the nucleus and alters gene expression. Animal models show consistent AMPK activation, improved insulin sensitivity, and lifespan extension. The absence of trial data reflects the field's age, not flaws.

2015 / DISCOVERY

Lee et al. (USC) identify MOTS-c within mitochondrial 12S rRNA — the first mitochondrial hormone described.

2019 / EXERCISE LINK

Circulating MOTS-c confirmed to rise with aerobic exercise in humans — the exercise signal established.

ONGOING / RESEARCH

Rodent studies expanding to cognition, longevity, and inflammation. No IND filed. Human data: none yet.