MOTS-c | Peptide Reference Material
RESEARCH PEPTIDE

MOTS-c | Peptide Reference Material

Mitochondrial-Derived Peptide (12S rRNA) — Research Peptide
$29.00
16-amino-acid mitochondrial-derived peptide supplied as a lyophilized laboratory reference material for AMPK and mitonuclear-signaling research. Research use only. Not for human or veterinary use.
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Primary Literature Peer-reviewed sources
Research Use Only Laboratory research materials

Scientific Specifications

Reference characteristics for laboratory research materials.

CAS Number
1627580-64-6
Purity
≥98%
Molecular Formula
C101H152N28O22S2
Molecular Weight
2174.34
Appearance
White lyophilized powder
Storage
-20°C
Research Classification
Research Use Only (RUO). Not for human or veterinary use.

SCIENTIFIC OVERVIEW

Scientific background and research classification for this laboratory reference material.

MOTS-c (mitochondrial open reading frame of the 12S rRNA type-c) is a 16-amino-acid mitochondrial-derived peptide encoded within the mitochondrial 12S ribosomal RNA gene (MT-RNR1). It is studied as a regulator of cellular energy metabolism and as a model system for mitochondrial-to-nuclear signaling.

This material is supplied as a lyophilized research peptide for in-vitro and preclinical laboratory investigation only.

Primary Research Category
Metabolic Research
Material Type
Lyophilized Peptide
Intended Use
Laboratory Research
Research Categories
Energy Homeostasis Glucose Metabolism

Mechanism of Action

Molecular interaction profile describing how this research material engages receptor systems and influences downstream biological signaling pathways.

In published preclinical research, MOTS-c activates AMP-activated protein kinase (AMPK), in part by inhibiting the folate cycle and its tethered de-novo purine biosynthesis, which raises AICAR levels. Studies also report involvement of NAD+/SIRT1 signaling.

Under metabolic or oxidative stress, MOTS-c has been reported to translocate to the nucleus in an AMPK-dependent manner and associate with antioxidant-response-element (ARE) programs and the stress-responsive transcription factor NRF2 (NFE2L2), illustrating mitochondrial-encoded regulation of nuclear gene expression.

Molecular Targets
  • AMPK
  • Nuclear Factor Erythroid 2–Related Factor 2 (Nrf2)
Biological Pathways
  • AMPK Signaling Pathway
  • Glucose Uptake
  • Insulin Signaling
Primary Organ Systems
  • Metabolic System

Research Documentation

Laboratory documentation is presented when available for the selected product specification and current lot.

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Scientific References
Peer-Reviewed Literature

Explore published literature, clinical investigations, and foundational scientific research.

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Laboratory Resources
Technical Guidance

Storage guidance, handling recommendations, analytical methods, and laboratory best practices.

Related Research
Companion Materials

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Research Center

Scientific literature, laboratory resources, and related materials curated to support research involving this research material.

Scientific References
Peer-Reviewed Literature

Explore curated publications from peer-reviewed journals including clinical investigations, mechanistic studies, and foundational scientific literature.

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Scientific Dossier
Deeper Technical Treatment

Comprehensive scientific documentation including literature review, mechanism, pharmacology, and study data for this research material.

Laboratory Resources
Technical Guidance

Storage guidance, handling information, analytical standards, research policies, and laboratory support documentation.

Research Library

Curated peer-reviewed literature selected to provide scientific context for this research material.

Pharmacology Study•Cell Metabolism• 2015

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

Foundational study identifying MOTS-c as a 16-amino-acid peptide encoded in the mitochondrial 12S rRNA that targets skeletal muscle and activates AMPK via inhibition of the folate cycle and de-novo purine biosynthesis, improving insulin sensitivity in preclinical models.
Velora Research Insight
Defines the core AMPK-linked mechanism and the skeletal-muscle focus that anchor most subsequent MOTS-c research.
PubMed →DOI →
Pharmacology Study•Cell Metabolism• 2018

The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress

Reports AMPK-dependent nuclear translocation of MOTS-c under metabolic and oxidative stress, where it associates with antioxidant-response-element programs and NRF2, demonstrating mitochondrial-encoded regulation of nuclear gene expression.
Velora Research Insight
Establishes MOTS-c as a mitonuclear signaling factor, a key rationale for its use in cellular stress-response research.
PubMed →DOI →
Pharmacology Study•Nature Communications• 2021

MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis

Shows exercise induces endogenous MOTS-c in human skeletal muscle and circulation, and that MOTS-c administration improves physical capacity across ages in mice via skeletal-muscle metabolic regulation.
Velora Research Insight
Bridges preclinical mechanism to human exercise physiology, supporting MOTS-c as a model for metabolic-adaptation research.
PubMed →DOI →
Pharmacology Study•Physiological Reports• 2019

The mitochondrial-derived peptide MOTS-c is a regulator of plasma metabolites and enhances insulin sensitivity

Uses untargeted metabolomics to show MOTS-c modulates sphingolipid, monoacylglycerol, and dicarboxylate metabolism and enhances beta-oxidation, improving insulin sensitivity in diet-induced obese mice.
Velora Research Insight
Extends the mechanistic map of MOTS-c to defined plasma-metabolite pathways relevant to metabolic-dysfunction research.
PubMed →DOI →
Clinical Trial•Journal of Applied Physiology• 2021

Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans

Randomized human trial reporting that acute endurance exercise increases circulating mitochondrial-derived peptides (humanin, with a MOTS-c trend) alongside modality-specific skeletal-muscle gene-expression changes.
Velora Research Insight
Provides human, exercise-context evidence of endogenous MDP dynamics; publication_type/evidence_level are HALT-AND-MAP candidates.
PubMed →DOI →