MOTS-c
Mitochondrial-Derived Metabolic Signaling Peptide
MOTS-c is a mitochondrial-derived research peptide encoded within mitochondrial DNA, currently cataloged within Alford Molecular Research's Research Compound Library as a signaling molecule for investigation into cellular metabolic adaptation and mitochondrial-to-nuclear communication.
Chemical Class
Mitochondrial-derived 16-amino-acid peptide
Evidence Classification
Preclinical / Preliminary
Primary Research Domain
Mitochondrial & Metabolic Signaling
Primary Research Areas
mitochondrial signaling; metabolic adaptation; AMPK-associated pathways; glucose metabolism; exercise & skeletal-muscle biology; aging & cellular stress
Molecular Data Card
Compound
Aliases / Synonyms
Chemical Class
CAS Number
Molecular Formula
Average Molecular Weight
Sequence
N-Terminal State
C-Terminal State
MOTS-c
Mitochondrial-derived peptide MOTS-c
Mitochondrial-derived 16-amino-acid peptide
1627580-64-6
C101H152N28O22S2
approximately 2174.6 g/mol
Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg
Free amino terminus
Free carboxyl terminus
MOTS-c is a mitochondrial-derived peptide encoded within mitochondrial DNA and studied as a signaling molecule associated with cellular metabolic adaptation. The exact chemical sequence is Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg; notably, the sequence contains two methionine residues and one tryptophan residue, which makes oxidation-state control analytically important for research material integrity.
Molecular Target / Mechanism
The MOTS-c research model is framed around mitochondrial-to-nuclear signaling, metabolic adaptation, and cellular stress-response systems. As a mitochondrial-derived peptide, it is studied for its role in modulating energy metabolism and adaptive bioenergetic responses within the cell. While its effects on metabolic signaling pathways are well documented in preclinical literature, exact direct receptor identities remain under investigation and have not been universally defined in a single-receptor model.
Intracellular Signaling
Experimental studies have investigated MOTS-c-associated changes in cellular energy-sensing and metabolic signaling pathways, including AMPK-related mechanisms. Research models explore how these pathways respond to altered energetic demand and substrate availability at the cellular level.
Note: Current research observes these interactions primarily in experimental frameworks. The signaling pathways listed represent areas of ongoing mechanistic inquiry rather than established clinical endpoints.
Cellular & Tissue-Level Research
Experimental investigations of MOTS-c involve various preclinical models and cell/tissue systems—including metabolic, exercise, stress-response, and aging-related experimental frameworks—to observe cellular-level physiological changes. These studies are strictly nonclinical and do not establish efficacy or safety in human subjects.
Mitochondrial Signaling
Research involving mitochondrial-derived signaling molecules and mitochondrial-to-cellular communication.
Metabolic Adaptation
Experimental investigation of cellular responses to altered energetic demand and substrate availability.
AMPK-Associated Signaling
Research involving cellular energy-sensing pathways associated with AMPK.
Glucose Metabolism
Experimental work examining glucose handling, insulin-related physiology, and metabolic flexibility.
Exercise & Skeletal-Muscle Biology
Research involving metabolic adaptation, muscle energetics, and exercise-associated signaling.
Aging & Cellular Stress
Experimental investigation of age-associated metabolic decline, cellular stress, and mitochondrial signaling.
Translational Chain
MOTS-c
Mitochondrial-Derived Signaling
Cellular Energy-Sensing / AMPK Pathways
Metabolic Cellular Response
Tissue Energy Metabolism
Metabolic Biomarkers
Functional Outcomes
Each downstream step requires independent evidence. A signaling change at the cellular level does not by itself establish a meaningful human metabolic or longevity outcome.
Evidence Assessment
Evidence Classification: Preclinical / Preliminary. Much of the mechanistic evidence derives from cellular and animal models; early translational observations do not establish broad human efficacy. Exercise, metabolic, aging, and longevity claims should be kept distinct; findings in one experimental context should not automatically be extrapolated to another. Route, formulation, exposure, population, and endpoint materially affect interpretation.
Analytical Considerations
Example Analytical Documentation
Alford Molecular Research has reviewed third-party analytical documentation for MOTS-c research material including molecular identity, quantitative content, purity, and related quality-control testing. Analytical results are lot-specific and should not be generalized to other batches.
- Identity by MS
- RP-HPLC or UPLC purity
- Quantitative net peptide content
- Exact sequence confirmation
- N-terminal and C-terminal state
- Counterion / salt state
- Residual solvents
- Water content
- Oxidation products
- Degradation products
- Endotoxin where relevant
- Sterility where relevant
Oxidation-State Control
MOTS-c contains methionine and tryptophan residues that may be susceptible to oxidative modification during synthesis, purification, storage, and handling. Analytical characterization should distinguish intact peptide from oxidized or otherwise modified species where relevant.
Stability & Handling — Scientific Context
Research-material stability is materially affected by environmental exposure factors including moisture, light, ambient temperature, and oxidation. Integrity is further influenced by repeated freeze-thaw cycles and container closure integrity. Chromatographic purity, net peptide content, oxidation state, and molecular identity are analytically distinct quality attributes.
Research / Regulatory Context
Research Context Notice
MOTS-c is an investigational mitochondrial-derived peptide studied in metabolic, exercise, stress-response, and aging-related research. Its inclusion in experimental literature does not establish clinical efficacy or approved therapeutic use. Human evidence remains limited compared with the preclinical literature, and regulatory status varies by jurisdiction. Alford Molecular Research evaluates the compound as a research subject rather than as a therapeutic recommendation. FOR SCIENTIFIC CONTEXT ONLY: The information provided is strictly for academic and research purposes and is not intended for the treatment, diagnosis, or prevention of any condition, nor for human or veterinary administration.