shelf(0)

No. 026 · Metabolic · Metabolic Peptide

MOTS-c

MOTS-cMitochondrial ORF of the 12S rRNA type-c

C Tier C · Animal data how tiers work →
  • Not FDA approved
  • WADA ✗ S4
Compare Cite
Fingerprint 16 residues
MOTS-c sequence fingerprint
  • Nonpolar 8
  • Polar 3
  • Positive charge 4
  • Negative charge 1

Each dot is a residue placed around the ring from N- to C-terminus; its distance from the centre reflects its chemistry.

01

Evidence

  1. D In vitro
  2. C Animal
  3. B Human pilot
  4. A RCT
  5. S Approved

TIER C — Evidence comes mostly from animal studies.

Interventional evidence is from rodent studies (e.g. Lee et al., Cell Metab 2015); human data are observational measurements of circulating levels, with no published human trial of MOTS-c itself.

Tiers rate the strength of published evidence — not effectiveness, safety, or a recommendation.

02

At a glance

Residues
16 amino acids, N→C
Molecular weight
2,174.6 Da
Formula
C101H152N28O22S2
Discovered
2015 Identified as a peptide encoded in the mitochondrial 12S rRNA gene (Lee et al., Cell Metab 2015).
Routes studied
Subcutaneous, Intramuscular Routes used in published research
FDA
Not approved
WADA
Prohibited · S4 Hormone and metabolic modulators
03

Sequence

N → C · 16 residues · hover, tap, or use arrow keys to inspect

04

Overview

A mitochondrial-derived peptide that regulates metabolic homeostasis and insulin sensitivity. It acts as an exercise mimetic, activating AMPK signaling pathways.

Research status Published human observational studies; preclinical interventional data showing metabolic benefits

05

Mechanism

MOTS-c is a 16-amino-acid peptide encoded by the mitochondrial 12S rRNA gene. It translocates to the nucleus during metabolic stress and activates AMPK signaling, which promotes glucose uptake, fatty acid oxidation, and mitochondrial biogenesis. It also regulates the folate-methionine cycle, affecting cellular methylation and nucleotide synthesis.

06

Effects reported in research

Reported outcomes, not promises. These come mostly from preclinical (cell or animal) research and have not been confirmed in human trials.

  • Improved insulin sensitivity
  • Enhanced mitochondrial function
  • Exercise-mimetic AMPK activation
  • Protection against metabolic stress
07

Safety & unknowns

Endogenous mitochondrial-derived peptide with naturally declining levels during aging. Limited formal human safety data from interventional use. Preclinical studies suggest good tolerability. Not FDA-approved.

Unknowns. No randomized controlled trials in humans have been published, so human safety has not been established in controlled studies.

Informational only — not medical advice. peptidemeta publishes no dosing, protocols, or sourcing. Talk to a qualified clinician about any treatment decision.

08

Studies [1]

  1. Preclinical 2015

    The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance

    Lee C, Zeng J, Drew BG, et al. Cell Metabolism

    Discovery paper identifying MOTS-c as a 16-amino-acid peptide encoded in the mitochondrial 12S rRNA that acts on the folate cycle to activate AMPK; treatment prevented age-dependent and diet-induced insulin resistance and diet-induced obesity in mice.

    [pubmed] [doi]

10

Status sources

Sources behind the tier, regulatory status, sequence and dates on this page.

11

Cite this entry

$ cite --format=apa

peptidemeta. (2026). MOTS-c. In peptidemeta: The peptide library, ranked by evidence. Retrieved November 8, 2026, from https://peptidemeta.com/p/mots-c/

$ cite --format=bibtex 
@misc{peptidemeta-mots-c,
  title = {MOTS-c},
  author = {{peptidemeta}},
  year = {2026},
  howpublished = {\url{https://peptidemeta.com/p/mots-c/}},
  note = {Accessed 2026-11-08}
}

Accessed date reflects when you opened this page. Cite primary studies for scientific claims.

esc
↑↓ navigate ↵ open