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Peptide Profile
Mitochondrial ORF of the 12S rRNA type-c
MOTS-c (mitochondrial ORF of the 12S rRNA type-c) is a 16-amino-acid mitochondrial-derived peptide (MDP) encoded within the 12S ribosomal RNA gene of the mitochondrial genome, secreted from mitochondria into the cytoplasm and…
Educational research information — not medical advice. Review primary sources and consult a qualified professional before any decision.
Educational research tools — not medical advice.
Mitochondria-derived peptide that translocates to nucleus under stress; activates AMPK pathway, regulates AICAR and folate-methionine cycle
MOTS-c (mitochondrial ORF of the 12S rRNA type-c) is a 16-amino-acid mitochondrial-derived peptide (MDP) encoded within the 12S ribosomal RNA gene of the mitochondrial genome, secreted from mitochondria into the cytoplasm and circulation in response to metabolic stress and exercise, where it functions as a hormonal signal regulating nuclear gene expression to promote metabolic homeostasis and insulin sensitivity. MOTS-c translocates from mitochondria to the nucleus under metabolic stress conditions, where it activates AMPK-dependent pathways that increase glucose uptake in skeletal muscle and adipose tissue, reduce lipid accumulation, and modulate one-carbon metabolism through the AICAR-AMPK-folate cycle — effects that parallel some metabolic actions of physical exercise and metformin. Foundational research published in Cell Metabolism characterized MOTS-c as a mitochondrially encoded metabolic hormone that promotes metabolic homeostasis, reduces obesity, and improves insulin resistance in preclinical models, and subsequent work has analyzed its broad metabolic regulatory role and clinical potential as an insulin-sensitizing agent. MOTS-c is a research compound with no regulatory approval in any jurisdiction; while circulating MOTS-c levels in humans have been characterized and decline with age, no clinical trials have established safety or efficacy for exogenous MOTS-c administration. MOTS-c dosage protocol: No human clinical trial has established a reference dosing protocol for exogenous MOTS-c administration. Animal research protocols examining MOTS-c metabolic effects have used subcutaneous injection as the primary delivery route, with doses determined by body weight in rodent models. Human circulating MOTS-c levels have been measured in exercise and aging studies — endogenous levels decline with age and rise transiently with aerobic exercise — but these observations do not establish a target dose for supplemental administration. Research interest focuses on MOTS-c as a potential exercise mimetic and insulin sensitizer, with investigation of dosing frequency and timing relative to metabolic challenge or fasted states. MOTS-c is a research compound; there are no approved human dosing guidelines for any indication.
Commonly researched in the context of
Population research notes
These signals reflect research interest areas, not treatment indications.
based on 19 studies · most recent 2026
Mitochondria-derived peptide encoded in 12S rRNA. Regulates metabolism and exercise capacity. No FDA approval, no NDA or IND. Pure research compound; no clinical development program.
Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
19 sources cited · 1 strong · 18 moderate
17 Cohorts · 1 Review · 1 Animal
The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance
Cell Metabolism · 2015
The original discovery paper demonstrated that MOTS-c, a 16-amino-acid mitochondrial-derived peptide encoded in the 12S rRNA, inhibits the folate cycle and de novo purine biosynthesis, activating AMPK signaling; systemic MOTS-c administration prevented age-related and diet-induced insulin resistance and obesity in mouse models, establishing it as a mitochondrial hormone.
LAT1-mediated delivery of engineered R13A-MOTS-c attenuates radiation-induced lung injury via Nrf2 activation and mitochondrial protection.
Redox Biol · 2026
# Summary Research found that an engineered peptide variant called R13A-MOTS-c, which enters cells more efficiently through a specific transport mechanism (LAT1), activated antioxidant signaling pathways and protected mitochondrial function in lung cells exposed to radiation injury. This study demonstrated that the peptide's therapeutic effects depended on both its cellular uptake via LAT1 and activation of the Nrf2 antioxidant pathway, suggesting a potential mechanism for mitigating radiation-induced lung damage.
Circulating mitochondrial-derived microproteins at rest and in response to an acute bout of endurance exercise in individuals with cerebral palsy.
Exp Physiol · 2026
Mitochondrial-derived peptide MOTS-c activates metabolic signaling but blunts reparative function in human mesenchymal stromal cells.
Inflamm Regen · 2026
Mitochondrial peptide MOTS-c suppresses systemic and cardiac inflammasome activation in a diabetic rat model.
Exp Physiol · 2026
# Research Summary This study demonstrated that MOTS-c, a mitochondrial-derived peptide, suppressed inflammasome activation (specifically NLRP3 pathway components) in both systemic circulation and heart tissue of diabetic rats, while simultaneously reducing blood glucose levels and inflammatory markers. Researchers observed that MOTS-c treatment modulated inflammatory cytokine profiles and reduced key components of the inflammasome cascade in cardiac tissue, suggesting a potential mechanism for reducing inflammation-related cardiovascular complications in type 2 diabetes.
Mitochondrial-derived peptide MOTS-c activates metabolic signaling but blunts reparative function in human mesenchymal stromal cells.
Inflamm Regen · 2026
Circulating mitochondrial-derived microproteins at rest and in response to an acute bout of endurance exercise in individuals with cerebral palsy.
Exp Physiol · 2026
Reduced Circulating MOTS-c Levels in Hashimoto's Thyroiditis Reflect Integrated Autoimmune and Metabolic Dysregulation: A Cross-Sectional Study.
J Clin Med · 2026
Mitochondrial peptide MOTS-c suppresses systemic and cardiac inflammasome activation in a diabetic rat model.
Exp Physiol · 2026
Circulating mitochondrial-derived microproteins at rest and in response to an acute bout of endurance exercise in individuals with cerebral palsy.
Exp Physiol · 2026
Mitochondrial peptide MOTS-c suppresses systemic and cardiac inflammasome activation in a diabetic rat model.
Exp Physiol · 2026
Mitochondrial-derived peptide MOTS-c activates metabolic signaling but blunts reparative function in human mesenchymal stromal cells.
Inflamm Regen · 2026
MOTS-c, a mitochondrial-derived peptide, ameliorates lysosomal membrane permeability and improves survival of soft tissue transplantation.
Autophagy · 2026
# Summary Research found that MOTS-c, a mitochondrial-derived peptide, improved survival of transplanted soft tissue by reducing lysosomal membrane damage and enhancing autophagy through inhibition of the PLA2G4A signaling pathway. This study demonstrated that MOTS-c protects ischemic tissue by suppressing a specific cellular damage mechanism (pyroptosis) and restoring cellular homeostasis, suggesting potential therapeutic applications in reconstructive surgery.
Humanin and MOTS-c Attenuate Atrial Fibrillation by Suppressing Fibrosis and Mitochondrial Dysfunction.
Biomedicines · 2026
# Summary Research found that two mitochondrial-derived peptides, humanin and MOTS-c, are significantly reduced in atrial fibrillation patients and their levels inversely correlate with disease severity. This study demonstrated that administering these peptides in mouse models reduced atrial fibrillation inducibility and attenuated fibrosis and mitochondrial dysfunction through anti-inflammatory and antioxidant mechanisms.
MOTS-c attenuates hyperoxia-induced neonatal cardiac injury by inhibiting oxeiptosis via maintaining the KEAP1-PGAM5 interaction.
Life Sci · 2026
# Research Summary This study demonstrated that MOTS-c, a mitochondrial-derived peptide, protects neonatal hearts from hyperoxia-induced damage by inhibiting a form of oxidative stress-triggered cell death called oxeiptosis through its interaction with the KEAP1 protein. Researchers observed that MOTS-c administration reversed cardiac dysfunction, fibrosis, and hypertrophy in hyperoxia-exposed neonatal mice and identified KEAP1 as a critical molecular target of MOTS-c's protective mechanism.
MOTS-c partially protects against skeletal muscle deterioration in C26 cachexia.
Front Med (Lausanne) · 2026
Reduced Circulating MOTS-c Levels in Hashimoto's Thyroiditis Reflect Integrated Autoimmune and Metabolic Dysregulation: A Cross-Sectional Study.
J Clin Med · 2026
MOTS-c partially protects against skeletal muscle deterioration in C26 cachexia.
Front Med (Lausanne) · 2026
MOTS-c: a promising mitochondrial-derived peptide for therapeutic exploitation
Journal of Molecular Medicine · 2019
This review summarizes evidence for MOTS-c as a circulating insulin-sensitizing and exercise-mimetic peptide, discussing its mechanisms in lipid oxidation, glucose homeostasis, and mitochondrial quality control, and its potential as a therapeutic target for metabolic and age-related conditions.
Research-use compound with limited human data. Evidence strength varies — see the Evidence section.
No established clinical contraindications. This is an investigational compound with limited human data and has not been evaluated by the FDA for safety in this context. Consult a qualified clinician.
Consult a qualified healthcare professional before making any health decisions. This information is educational only and does not constitute medical advice.
Compare
VSMOTS-c
Median tested purity
99.1%
Median tested purity of 99.1% across 8 verified third-party lab COAs (interquartile range 99.0%–99.2%), as reported by the independent testing lab below. PeptideBase reports these lab-published figures and does not itself test, endorse, or certify any product.
PeptideBase provides educational research tools and provider discovery. It does not provide medical advice, diagnosis, treatment, prescribing guidance, or dosing instructions. Consult a qualified healthcare professional before making health decisions.
MOTS-C 20mg · Lot Clear Pink Cap · Jul 16, 2026 · View source COA
99.5%
Purity
MOTS-C 20mg · Lot V3312329807 · Jul 2, 2026 · View source COA
99.6%
Purity
MOTS-C - 40mg · Lot MS40-08 · Jun 28, 2026
99.9%
Purity
MOTS-c · Jun 22, 2026 · View source COA
99.2%
Purity
MOTS-c · Lot MTC-LD-01 · Jun 12, 2026
MOTS-c · Jun 10, 2026 · View source COA
99.2%
Purity
MOTS-c · May 28, 2026 · View source COA
99.3%
Purity
MOTS-c · Lot B-7058391-E · May 27, 2026
MOTS-C - 40mg · Lot MTS40-07 · May 23, 2026
99.0%
Purity
Mots-C · Lot 260507MO103 · May 19, 2026
99.8%
Purity
MOTS-c · May 15, 2026 · View source COA
98.7%
Purity
MOTS-C 20mg · Lot Purple Cap · May 9, 2026 · View source COA
99.5%
Purity
MOTS-c · May 4, 2026 · View source COA
99.0%
Purity
MOTS-c · May 4, 2026 · View source COA
99.0%
Purity
MOTS-C · Lot 260413MO203 · Apr 24, 2026
99.8%
Purity
Mots-c 10mg · Jan 26, 2026 · View source COA
99.6%
Purity
MOTS-c · Jan 13, 2026 · View source COA
99.4%
Purity
Mots-C 20mg · Dec 30, 2025 · View source COA
99.6%
Purity
MOTS-c · Nov 21, 2025 · View source COA
99.0%
Purity
MOTS-c · Nov 13, 2025 · View source COA
99.1%
Purity
MOTS-c · Lot FP25-0075 · Jul 4, 2025
99.1%
Purity
PeptideBase reports these lab-published figures and does not itself test, endorse, or certify any product. Verified results come from an independent third-party lab database lookup. Vendor-published results are reported by the vendor itself and have not been independently verified by PeptideBase or a third-party lab.
PeptideBase provides educational research tools and provider discovery. It does not provide medical advice, diagnosis, treatment, prescribing guidance, or dosing instructions. Consult a qualified healthcare professional before making health decisions.
Self-reported, anecdotal experiences aggregated from public Reddit discussions — community sentiment, not clinical evidence or medical advice.
Attribution note: many of these reports describe stacking MOTS-c with other compounds, so outcomes may not be attributable to it alone.
Outcome distribution
Outcomes by goal · improved % · reports
Side effects people mention
Counts are mentions across reports, not incidence rates.
Most reported
What they wish they'd known
Based on 91 community reports · Updated
MOTS-c (mitochondrial ORF of the 12S rRNA type-c) is a 16-amino-acid mitochondrial-derived peptide (MDP) encoded within the 12S ribosomal RNA gene of the mitochondrial genome, secreted from mitochondria into the cytoplasm and circulation in response to metabolic stress and exercise, where it functions as a hormonal signal regulating nuclear gene expression to promote metabolic homeostasis and insulin sensitivity. MOTS-c translocates from mitochondria to the nucleus under metabolic stress conditions, where it activates AMPK-dependent pathways that increase glucose uptake in skeletal muscle and adipose tissue, reduce lipid accumulation, and modulate one-carbon metabolism through the AICAR-AMPK-folate cycle — effects that parallel some metabolic actions of physical exercise and metformin.
metabolic regulation, insulin sensitivity, exercise mimicry, anti-aging.
Research on MOTS-c primarily documents effects related to metabolic regulation and insulin sensitivity and exercise mimicry and anti-aging. These are areas covered in preclinical and clinical literature — individual response varies and effects depend on context of use.
For MOTS-c, its FDA status is Nomination Withdrawn, and it is designated for research use only. Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
146 providers in the directory currently offer MOTS-c.
Across 64 research vendors tracked on PeptideBase, MOTS-c has a median price of about $5.50 per mg, typically ranging $3.60–$8.00 per mg. This reflects research-use vendor pricing, not clinical or prescription costs.
The original discovery paper demonstrated that MOTS-c, a 16-amino-acid mitochondrial-derived peptide encoded in the 12S rRNA, inhibits the folate cycle and de novo purine biosynthesis, activating AMPK signaling; systemic MOTS-c administration prevented age-related and diet-induced insulin resistance and obesity in mouse models, establishing it as a mitochondrial hormone.
MOTS-c is featured in the following research stacks on PeptideBase: MOTS-c + SS-31: Mitochondrial Optimization.
Price per mg varies by quantity, vendor type, and formulation. Research use only.
Data verified July 2026 · MOTS-c price intelligence
AMAVA Regenerative Medicine Peoria-Glendale AZ
Apex Health & Wellness
Avendano Health Medical Wellness & Lab
Body Lounge Park Cities
Center for Advanced Urology
Denver Wellness & Aesthetics Center
Hormone & Peptide Therapy Greenville SC
Mind Body Reset Functional Medicine
Montecito Concierge Medicine
Northeast Medical Aesthetics
Commonly stacked with
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Data last updated July 20, 2026
Free to reference and republish with attribution to PeptideBase. Choose a format:
PeptideBase. (2026). MOTS-c — Per-mg Price Benchmark. Retrieved July 22, 2026, from https://peptidebase.io/peptides/mots-c