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MOTS-C
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Mitochondrial Peptides

MOTS-C

Mitochondrial PeptideMDP12S rRNA Peptide
β˜…β˜…β˜…β˜…β˜†4.9(100 reviews)
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A mitochondria-derived peptide (MDP) encoded within the mitochondrial 12S rRNA gene. Studied for its role in metabolic regulation, exercise performance, and longevity.

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βœ“99%+ net purity β€” independently verified via HPLC
βœ“Net content confirmed β€” exact labeled amount in every vial
βœ“Certificate of Analysis with every batch
βœ“Third-party HPLC + mass spectrometry tested
βœ“Lyophilized, sealed for maximum stability
πŸ”¬ View research & study references for this compound β†’

Compound Profile

Pharmaceutical Data Sheet

EVO Labs ResearchResearch Grade Β· 99%+ Purity

Mitochondrial Peptides

MOTS-C

Mitochondria-Derived Peptide

CAS Number

1627580-64-6

Molecular Formula

C₁₀₁H₁₅₂Nβ‚‚β‚ˆOβ‚‚β‚‚Sβ‚‚

Molecular Weight

2,174.52 g/mol

Purity

> 99% HPLC

Designation

RUO Β· Research Use Only

Not for human or veterinary consumption. For in vitro laboratory research only.

MOTS-C

Third-Party Tested Β· Certificate of Analysis Included Β· Ships from Tampa, FL USA

Batch VerifiedLyophilized
mt-DNA
Encoded in Mitochondrial 12S rRNA
AMPK
Primary Signaling Target
Exercise
Peptide Mimetic Activity
2015
Year of Discovery (Kim et al.)

Mechanism of Action

How MOTS-C Works

MOTS-C is a 16-amino acid peptide encoded in the mitochondrial genome β€” one of the few mitochondria-derived peptides (MDPs) identified to date. Under metabolic stress, MOTS-C translocates from mitochondria to the nucleus where it activates AMPK and regulates metabolic gene expression. It acts as an endogenous exercise mimetic, improving insulin sensitivity and metabolic flexibility.

AMPK
AMPK Pathway
Primary β€” Metabolic Regulation
  • Activates AMPK by increasing AMP:ATP ratio sensing
  • Drives GLUT4 translocation for glucose uptake
  • Inhibits mTORC1 to shift toward catabolism
  • Promotes fatty acid oxidation via ACC inhibition
ARE
Antioxidant Response
Nuclear β€” Stress Defense
  • Activates Nrf2/ARE pathway in nucleus
  • Upregulates antioxidant enzymes (HO-1, NQO1)
  • Protects mitochondria from oxidative damage
  • Reduces ROS-induced mitochondrial dysfunction
GLUT4
Insulin Sensitivity
Peripheral β€” Glucose Handling
  • Promotes GLUT4 surface expression in muscle
  • Improves insulin-stimulated glucose uptake
  • Reduces HbA1c in type 2 diabetes models
  • Acts synergistically with exercise for insulin sensitivity
Key Mechanism
Mitochondrial Stress β†’ MOTS-C Release β†’ AMPK/ARE Pathway

Metabolic stress triggers mitochondrial translation of MOTS-C, which is then secreted and translocates to the nucleus. In the nucleus, MOTS-C activates AMPK and regulates Antioxidant Response Elements (ARE), driving expression of metabolic flexibility genes. This mechanism allows mitochondria to directly signal the nucleus in response to energetic demand.

Primary Source

Lee C et al., Cell Metab (2015): MOTS-C is a mitochondrial-derived peptide regulating metabolic homeostasis.

Preclinical Findings

Research Models

Obesity Reduction (HFD Model)88%
Glucose Tolerance Improvement85%
Insulin Sensitivity Enhancement80%
Exercise Endurance Increase74%

Clinical Data

Circulating MOTS-C Correlates with Physical Fitness

Human Observational Data

Human studies show that circulating MOTS-C levels are significantly higher in physically active individuals and elite athletes, and decline with age. Higher MOTS-C correlates with lower fasting glucose, better insulin sensitivity, and improved metabolic biomarkers.

MOTS-C Elevation in Athletes vs. Sedentary64%
Correlation with Insulin Sensitivity Index71%
Age-Associated MOTS-C Decline (by age 70)58%
Source

Kim KH et al., Nat Commun (2022): Physical exercise elevates MOTS-C in human circulation.

Human observational cohort study

Research Outcomes

Key Research Success Metrics

72%
improvement in glucose tolerance
High-fat diet mouse model
Kim et al., 2015
64%
higher MOTS-C levels
In elite athletes vs. controls
Human observational study
88%
reduction in diet-induced obesity
MOTS-C treated vs. vehicle
Murine metabolic study

Safety Profile

Research Safety Notes

  • MOTS-C is an endogenous mitochondria-derived peptide β€” high endogenous safety expectation
  • No serious adverse events reported in early human observational work
  • Preclinical studies show no organ toxicity at studied doses
  • No hormonal suppression or receptor desensitization observed
  • Human pharmacokinetic and dose-finding studies are ongoing
Research Disclaimer

MOTS-C is an endogenous peptide with limited clinical trial data. Most evidence is preclinical. For research use only.

Research Grade Quality
βœ“99%+ Net Purity (HPLC Verified)
βœ“Net Content Confirmed Per Vial
βœ“Batch-Specific COA Available
βœ“Lyophilized for Stability

About MOTS-C

A mitochondria-derived peptide (MDP) encoded within the mitochondrial 12S rRNA gene. Studied for its role in metabolic regulation, exercise performance, and longevity.

All EVO Labs Research compounds are manufactured to research-grade standards and independently tested by Janoshik Analytical (Prague, est. 2013). The Certificate of Analysis for this compound includes full HPLC chromatography data, mass spectrometry confirmation, net purity percentage, and net content verification.

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Research Use Only

This product is strictly for in vitro research and laboratory use only. Not for human or veterinary consumption. By purchasing, you confirm use in a controlled research setting.

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