≥99% Purity MOTS-c vial

MOTS-c

Mitochondrial Metabolism Studies

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About this compound

MOTS-c is a short peptide, 16 amino acids long. What makes it unusual is where the instructions for it are stored. They sit inside mitochondrial DNA rather than in the cell nucleus. Studies have measured how it activates AMPK, a pathway that senses cellular energy levels, and how it affects glucose use in muscle models. Only a handful of peptides like it have been found, all within the past twenty years.

Mitochondrial-derived 16-amino acid peptide

Formula: C101H152N28O25S2
Molecular weight: 2174.64 g/mol
Form: Lyophilized Powder
Sequence length: 16 residues

Amino Acids

Encoded in mitochondrial 12S rRNA gene

AMPK Activation

Skeletal muscle AMPK phosphorylation increase

Published Studies

Mitochondrial peptide research papers

Research Areas

Insulin Resistance & Obesity · Age-Related Metabolic Decline · Exercise Mimicry & more

How It Works

How MOTS-c works

The pathways MOTS-c acts on — and what each one does. Signalling pathways studied in preclinical models · illustrative.

AMP-Activated Protein Kinase Signaling

AMPK Activation

MOTS-c activates AMP-activated protein kinase (AMPK) in skeletal muscle, adipose tissue, and liver. AMPK is a master metabolic sensor that responds to cellular energy status. MOTS-c–induced AMPK activation in preclinical models was associated with increased glucose uptake, fatty acid oxidation, and mitochondrial biogenesis signaling.

Direct AMPK phosphorylation (Thr172) in skeletal muscle
Downstream activation of PGC-1α and mitochondrial biogenesis
Enhanced GLUT4 translocation and glucose uptake

Mitochondria-to-Nucleus Retrograde Signaling

mtDNA Origin

MOTS-c is encoded within the 12S rRNA gene of the mitochondrial genome — a discovery that established mitochondria as an endocrine organ capable of producing bioactive peptides. Under metabolic stress, MOTS-c translocates from mitochondria to the nucleus where it acts as a transcriptional regulator, modulating antioxidant response element (ARE) gene expression.

Encoded in mitochondrial DNA (12S rRNA gene region)
Nuclear translocation under metabolic stress conditions
Modulates ARE-driven antioxidant gene expression

Metabolic Homeostasis & Exercise Signaling

Exercise Mimetic

MOTS-c levels naturally rise in response to exercise, and exogenous MOTS-c administration in mouse models replicated several exercise-associated metabolic adaptations including improved insulin sensitivity, reduced adiposity, and increased physical endurance — even in sedentary animals. It inhibits the folate cycle and purine synthesis under stress, redirecting metabolic flux.

Endogenous levels increase with aerobic exercise
Improves insulin sensitivity in rodent obesity models
Inhibits AICAR-independent AMPK activation via folate cycle

Uses & applications

What MOTS-c is researched for

The main areas MOTS-c is being studied for — and the study-reported figures behind them.

Metabolic Research

Insulin Resistance & Obesity

MOTS-c administration in high-fat diet mouse models improved insulin sensitivity, reduced fat accumulation, and normalized glucose tolerance — effects mediated primarily through skeletal muscle AMPK activation.

Lee C et al. 2015

Aging Biology

Age-Related Metabolic Decline

Circulating MOTS-c levels decline with age in both humans and rodents. Exogenous MOTS-c restored age-related declines in physical performance and metabolic flexibility in aged mouse models, suggesting its role in mitochondrial-nuclear communication during aging.

Reynolds JC et al. 2021

Exercise Biology

Exercise Mimicry

Circulating MOTS-c increases significantly with aerobic exercise in humans. In sedentary mouse models, exogenous MOTS-c replicated exercise-related improvements in energy metabolism, mitochondrial biogenesis markers, and physical endurance.

Kim SJ et al. 2022

Longevity Research

mtDNA Variation & Longevity

Population studies identified MOTS-c variants (particularly R150Q) enriched in elderly Japanese populations. Genetic variation in MOTS-c sequence correlates with metabolic disease risk, linking mitochondrial peptide biology to human longevity phenotypes.

Zempo H et al. 2016

Study-reported magnitudes

Representative figures from published research. Bars fill as you scroll.

AMPK Phosphorylation Increase (Skeletal Muscle)42%
Fat Mass Reduction (HFD Mouse Models)30%
Exercise Endurance Improvement (Aged Mice)55%
Insulin Sensitivity (HOMA-IR Improvement)38%

Figures are representative of published research findings and shown for reference.

Third-Party Verified

Independently tested. Verifiably pure.

Every batch of MOTS-c is sent to an accredited independent laboratory before it ships. Here is what we screen for.

HPLC Purity AnalysisConfirms the peptide is ≥99% pure
Mass SpectrometryVerifies the exact molecular identity
Heavy Metals ScreeningLead, arsenic, cadmium & mercury — Pass
Endotoxins (LAL)Bacterial endotoxin levels — Pass
Sterility TestingNo microbial contamination — Pass
Net Peptide ContentActual peptide mass per vial verified

Compound Information

Full specification

Full Name	Mitochondrial Open Reading Frame of the 12S rRNA-c
Sequence	MRWQEMGYIFYPRKLR
Amino Acids	16 residues
Molecular Weight	2174.6 Da
Gene Origin	Mitochondrial 12S rRNA (mt-RNR1)
Primary Target	AMPK activation; folate cycle; nuclear ARE pathways
Form	Lyophilized powder (5mg)
Purity	≥99% (HPLC verified)
Testing	Third-party HPLC, Mass Spec, Endotoxin
Storage	-20°C for long-term stability
Solubility	Bacteriostatic water or sterile saline
COA	Included with every order

FAQ

Common questions about MOTS-c

MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA-c) is a 16-amino acid peptide encoded within the mitochondrial genome — specifically in the 12S ribosomal RNA gene. Discovered in 2015 by researchers at USC led by Dr. Changhan David Lee, it was one of the first identified mitochondrial-derived peptides (MDPs). Unlike most mitochondrial proteins, MOTS-c is translated from a small open reading frame within non-coding RNA, establishing a new category of regulatory peptides originating from the organelle long considered only a metabolic powerhouse.

Circulating MOTS-c levels in humans and rodents increase significantly in response to aerobic exercise. MOTS-c activates AMPK — the same master energy sensor activated by exercise — in skeletal muscle and other metabolic tissues. In preclinical studies, exogenous MOTS-c administration in sedentary mice produced metabolic adaptations similar to exercise training: improved insulin sensitivity, enhanced fatty acid oxidation, increased mitochondrial biogenesis markers, and improved physical endurance. This exercise-mimetic profile has made MOTS-c a subject of significant research interest for metabolic biology.

MOTS-c levels decline with age in both humans and rodents, inversely correlating with age-related metabolic dysfunction. Population genetic studies identified a MOTS-c variant (R150Q, also called K14Q in some notation systems) enriched in elderly Japanese men — suggesting that specific MOTS-c sequences may influence longevity phenotypes. In aged mouse models, exogenous MOTS-c administration partially restored physical performance and metabolic flexibility, positioning it as a candidate for aging biology research.

MOTS-c activates AMPK through an indirect mechanism involving the folate cycle. Under metabolic stress, MOTS-c inhibits the enzyme MTHFR (methylenetetrahydrofolate reductase) in the folate-methionine cycle. This disrupts purine nucleotide biosynthesis, causing accumulation of ZMP (5-aminoimidazole-4-carboxamide ribonucleoside monophosphate) — a known AMPK activator. This AICAR-independent pathway for AMPK activation is one of the key mechanistic findings distinguishing MOTS-c from other metabolic peptides.

Human research on MOTS-c primarily consists of observational and correlational studies measuring circulating MOTS-c levels in various populations. These have shown associations between MOTS-c levels and: exercise status, aging, insulin resistance, and cardiovascular disease. Human genetic studies have identified longevity-associated MOTS-c variants. However, no randomized controlled trials of exogenous MOTS-c administration in humans have been completed or published as of 2024.

Store lyophilized MOTS-c at -20°C, protected from light and humidity, and minimize freeze-thaw cycles. MOTS-c is water-soluble, making it suitable for aqueous research systems. For cell culture experiments, filter-sterilize laboratory solutions before use. Always consult published protocols for concentration-specific guidance.

Published Literature

Peer-reviewed literature

Independent published research indexed from PubMed and peer-reviewed journals — not Zorva Lab claims.

[1] PubMedThe mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity2015 · Lee C et al.View source →[2] PubMedMOTS-c is an exercise-induced mitochondrial encoded regulator of age-dependent physical decline2021 · Reynolds JC et al.View source →[3] PubMedMOTS-c: A novel exercise-mimetic mitochondrial signal2022 · Kim SJ et al.View source →[4] PubMedA mitochondrial-encoded peptide in aging and longevity genetic studies2016 · Zempo H et al.View source →

For Research Use Only.

Not for human or veterinary use. For in-vitro laboratory research only. These statements have not been evaluated by the FDA; this product is not intended to diagnose, treat, cure, or prevent any disease. Sold exclusively to qualified researchers and institutions.

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