MOTS-c
Mitochondrial open reading frame of the 12S rRNA-c. A 16-amino-acid peptide encoded in the mitochondrial genome. Acts as an exercise mimetic by stimulating AMPK phosphorylation, enhancing cellular glucose uptake, and regulating lipid beta-oxidation. Not approved by US FDA; restricted under Category 2 bulk compounding warning; prohibited by WADA under S0/S4.
60-Second Scientific Briefing
MOTS-c is a 16-amino-acid peptide encoded within the mitochondrial genome (12S rRNA). Investigated preclinically for regulating metabolic homeostasis, enhancing insulin sensitivity, and activating AMPK pathways. It is an unapproved research compound prohibited by WADA under Category S0 and S2.
What is MOTS-c?
Pharmacological Classification & Molecular IdentityMitochondrial-derived 16-amino-acid peptide encoded in the 12S ribosomal RNA region of mitochondrial DNA.
Verified Chemical & Regulatory Registry Identifiers
Mechanism of Action & Receptor Targets
Biological Pathway and Target BindingBiological pathway and target receptor binding mechanism.
Receptor Selectivity: Translocates to the nucleus under stress and activates AMPK, downregulating the folate cycle and enhancing cellular glucose uptake in skeletal muscle.
Regulatory & FDA Approval Status
Legal and Regulatory ClassificationsNot approved by the US FDA for any human medical use. Prohibited at all times by WADA under Category S0 and S2.
MOTS-c is not approved for commercial sale, prescription therapy, or compounded medication distribution. It exists strictly within authorized scientific and clinical research frameworks.
Human Evidence & Clinical Trials
Clinical Study Readouts and Evidence SynthesesPrimary published evidence derives from cell culture and rodent metabolic studies; lacks peer-reviewed Phase 2 or Phase 3 human randomized controlled trials.
Clinical Evidence
Primary published evidence derives from cell culture and rodent metabolic studies; lacks peer-reviewed Phase 2 or Phase 3 human randomized controlled trials.
Safety Profile & Clinical Limitations
Documented Adverse Events and Known UncertaintiesSystematic human safety profiles and clinical adverse event incidence remain unestablished due to absence of completed human registration trials.
Effects on human cellular metabolism, potential mitochondrial pathway interference, and long-term toxicity.
Dose Approval Status
Commercial Dosing Status and Policy DirectivesNOT ESTABLISHED. No approved human dose or clinical guideline exists.
Under Egypt Peptides medical governance policies, no personal dosages, titration intervals, cycles, stacking recommendations, or self-injection instructions may be provided for unapproved investigational compounds. Clinical study protocols represent controlled experimental research parameters exclusively.
What is Known vs. What is Unknown
Evidence Comparison and Clinical Evidence Boundaries✓ Confirmed Scientific Evidence
- Mitochondrial-derived 16-amino-acid peptide encoded in the 12S ribosomal RNA region of mitochondrial DNA.
- Targets & Selectivity: Translocates to the nucleus under stress and activates AMPK, downregulating the folate cycle and enhancing cellular glucose uptake in skeletal muscle.
- Primary published evidence derives from cell culture and rodent metabolic studies; lacks peer-reviewed Phase 2 or Phase 3 human randomized controlled trials.
- Safety considerations: Systematic human safety profiles and clinical adverse event incidence remain unestablished due to absence of completed human registration trials.
? Unknown / Under Ongoing Investigation
- Effects on human cellular metabolism, potential mitochondrial pathway interference, and long-term toxicity.
Verified Questions & Answers
10 Verified scientific answers with permanent anchor keysMOTS-c is classified as a Mitochondrial-Derived Peptide (MDP). Molecular structure: Mitochondrial-derived 16-amino-acid peptide encoded in the 12S ribosomal RNA region of mitochondrial DNA..
Pharmacological classification and molecular integrity are documented in verified regulatory and scientific literature.
- The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance (Cell Metabolism, 2015-03-03)
MOTS-c exerts biological activity via Translocates to the nucleus under stress and activates AMPK, downregulating the folate cycle and enhancing cellular glucose uptake in skeletal muscle..
Receptor binding affinity and selectivity dictate the physiological response observed in laboratory and clinical trials.
- MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis (Nature Communications, 2021-01-20)
- The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance (Cell Metabolism, 2015-03-03)
Regulatory status: Not approved by the US FDA for any human medical use. Prohibited at all times by WADA under Category S0 and S2.
Investigational and research-only compounds cannot be legally distributed or marketed as prescription drugs.
- World Anti-Doping Agency (WADA) Prohibited List: Non-Approved Substances (S0) and Peptide Hormones (S2) (World Anti-Doping Agency, 2024-01-01)
Clinical evaluation status: Primary published evidence derives from cell culture and rodent metabolic studies; lacks peer-reviewed Phase 2 or Phase 3 human randomized controlled trials.
Clinical trial readouts and systematic analyses establish the boundary between demonstrated findings and experimental hypotheses.
- MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis (Nature Communications, 2021-01-20)
- The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance (Cell Metabolism, 2015-03-03)
Reported safety profile: Systematic human safety profiles and clinical adverse event incidence remain unestablished due to absence of completed human registration trials.
Adverse reaction monitoring and contraindications are critical parameters in pharmacological risk-benefit evaluation.
- The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance (Cell Metabolism, 2015-03-03)
Key scientific uncertainties: Effects on human cellular metabolism, potential mitochondrial pathway interference, and long-term toxicity.
Egypt Peptides enforces strict transparency regarding scientific limitations and gaps in longitudinal clinical data.
- The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance (Cell Metabolism, 2015-03-03)
NOT ESTABLISHED. No approved human dose or clinical guideline exists.
Under medical governance mandates, clinical study dosages represent strictly controlled experimental parameters and must never be interpreted as individual therapeutic advice.
- World Anti-Doping Agency (WADA) Prohibited List: Non-Approved Substances (S0) and Peptide Hormones (S2) (World Anti-Doping Agency, 2024-01-01)
Storage status: NOT ESTABLISHED for pharmaceutical use. Laboratory storage requires deep freeze (-20°C).
Peptide integrity degrades rapidly when exposed to elevated temperatures, repeated freeze-thaw cycles, or direct UV light exposure.
- The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance (Cell Metabolism, 2015-03-03)
Yes. Unapproved pharmacological substances are strictly prohibited at all times in competitive sports under WADA Category S0 (Non-approved substances) or Category S2.
Athletes subject to drug testing face strict liability and multi-year competition bans upon detection of prohibited peptides or their metabolites.
- World Anti-Doping Agency (WADA) Prohibited List: Non-Approved Substances (S0) and Peptide Hormones (S2) (World Anti-Doping Agency, 2024-01-01)
Egypt Peptides provides peer-reviewed scientific reference monographs for research documentation. We strictly prohibit individual medical consultations, reconstitution guides, stacking recipes, or off-label use instructions.
All scientific claims must link to verified authoritative sources (FDA, PubMed, ClinicalTrials.gov) with zero tolerance for ungrounded marketing claims.
- The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance (Cell Metabolism, 2015-03-03)
Authoritative Sources & Literature Registry
Regulatory dossiers, clinical trial registries, and peer-reviewed studiesWorld Anti-Doping Agency (WADA) Prohibited List: Non-Approved Substances (S0) and Peptide Hormones (S2) ↗
https://www.wada-ama.org/en/prohibited-list
MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis ↗
https://doi.org/10.1038/s41467-020-20790-0
The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance ↗
https://doi.org/10.1016/j.cmet.2015.02.009