MOTS-c
MOTS-c is a peptide, indexed here under Mitochondrial and longevity-associated peptides.
Identity
| Field | Value |
|---|---|
| Classification | Peptide |
| Primary class | Mitochondrial and longevity-associated peptides |
| CAS registry number | 1627580-64-6[1] |
| PubChem CID | 146675088[1] |
| UniProt accession | Unknown No UniProt query was run in v1. |
| Molecular formula | C101H152N28O22S2[1] |
| Molecular weight | 2174.6 g/mol[1] |
| Amino-acid sequence | Unknown Not reported by the PubChem property set retrieved for this record; no sequence database query was run in v1. |
| Reported half-life | Unknown No pharmacokinetics source was retrieved in v1. PubChem does not carry half-life as a property, so this is recorded as not yet sourced rather than estimated. |
What the cited literature examines
MOTS-c is described in the retrieved literature as a mitochondrial-derived peptide, encoded in mitochondrial rather than nuclear DNA. A 2015 Cell Metabolism paper reports that it promotes metabolic homeostasis, and a 2018 Cell Metabolism paper reports that the mitochondrial-encoded peptide translocates to the nucleus.
A 2021 Nature Communications paper describes it as an exercise-induced mitochondrial-encoded regulator of age-dependent processes, and a 2016 Free Radical Biology and Medicine paper reports regulation of muscle and fat metabolism. A 2015 Aging Cell paper asks whether it is a player in exceptional longevity, and a 2018 International Journal of Cardiology paper reports downregulated circulating levels in patients with coronary endothelial dysfunction.
[3, 4, 5, 6, 7, 8]Reported mechanism
A mitochondrial-encoded peptide; the retrieved records report nuclear translocation and regulation of metabolic homeostasis rather than action at a named surface receptor.
[4, 3]Stated in the titles of the cited 2018 and 2015 Cell Metabolism papers.
Targets named in the cited records: nuclear gene expression, metabolic homeostasis.
FDA application register
A query of the FDA Drugs@FDA application register on 2026-10-09 returned no application records for this compound name. This compound is not approved by the FDA for human use.[2]
Scope statement: this records the result of a single automated query against the openFDA drugsfda endpoint on the stated date. It is not legal advice and is not a jurisdiction-by-jurisdiction legality assessment.
Retrieved 2026-10-09.
Amounts reported in the cited literature
Unknown. No retrieved record in this dataset states an amount, so none is shown. Where an amount is recorded it is what a named study reported administering in its own stated model, in the past tense, and is not a protocol.
No study-reported dose was taken from a source read in v1. Literature-reported values are only recorded where the retrieved citation metadata states the figure.
Adverse effects reported in the cited literature
Unknown. No retrieved record in this dataset reports an adverse effect for this compound, so no row is shown. Absence of a row records the absence of a retrieved report, nothing more.
No adverse-effect row was taken from a source read in v1. Rows are only recorded with the study model named and the reporting citation attached.
Other names
MOTS-c appears under these other names in the cited records or in common usage. Each one resolves to this page rather than to a separate page of its own.
- mitochondrial open reading frame of the 12S rRNA type-c
Where this page sits
Research records
Cited research records for MOTS-c, each with its identifier, the publication type it is indexed as, and the study model stated by its assigned subject headings.
Compounds indexed next to it
- Humanin — Mitochondrial and longevity-associated peptides
- Elamipretide — Mitochondrial and longevity-associated peptides
- Epitalon — Mitochondrial and longevity-associated peptides
Class page: Mitochondrial and longevity-associated peptides. Full index: all indexed compounds.
Questions this page answers
What does the cited literature examine for MOTS-c?
MOTS-c is described in the retrieved literature as a mitochondrial-derived peptide, encoded in mitochondrial rather than nuclear DNA. A 2015 Cell Metabolism paper reports that it promotes metabolic homeostasis, and a 2018 Cell Metabolism paper reports that the mitochondrial-encoded peptide translocates to the nucleus.
Which class is MOTS-c indexed under?
MOTS-c is indexed under Mitochondrial and longevity-associated peptides. This class groups peptides whose retrieved literature concerns mitochondrial function or ageing endpoints.
What does the FDA application register show for MOTS-c?
A query of the FDA Drugs@FDA application register on 2026-10-09 returned no application records for this compound name. This compound is not approved by the FDA for human use.
Sources
- PubChem Compound Summary for CID 146675088, Mots-c. PubChem, National Library of Medicine (2026). pubchem:146675088
- Drugs@FDA application register query for this compound, no application records returned. U.S. Food and Drug Administration, openFDA drugsfda endpoint (2026). fda:mots-c
- The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell metabolism (2015). pmid:25738459
- The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress. Cell metabolism (2018). pmid:29983246
- MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nature communications (2021). pmid:33473109
- MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism. Free radical biology & medicine (2016). pmid:27216708
- The mitochondrial-derived peptide MOTS-c: a player in exceptional longevity?. Aging cell (2015). pmid:26289118
- Downregulation of circulating MOTS-c levels in patients with coronary endothelial dysfunction. International journal of cardiology (2018). pmid:29242099
On each stated value was matched to the record cited for it. That is record matching, not an appraisal of the research. Compiled and checked by: Peptide Monographs editorial desk. No qualified clinical reviewer.