database / mitochondrial
MOTS-c
Skeletal structure drawn from the computed atomic coordinates in PubChem CID 146675088. Carbons are implicit vertices; hydrogens on carbon are suppressed, as in any structural formula. Nothing here is estimated — every atom sits where PubChem placed it.
Research reference only. The observations below are recorded in the cited literature. Nothing here is advice or a recommendation, and no dosing information is published on this site.
Sequence
MRWQEMGYIFYPRKLR
Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg
- hydrophobic
- positive
- negative
- polar
- aromatic
- glycine
- proline
- cysteine
Computed backbone mass 2174.61 Da agrees with PubChem's reported 2174.6 Da (Δ 0.01 Da). Two independent sources agree on the primary structure.
Molecular data
| molecular formula | C101H152N28O22S2 |
|---|---|
| molecular weight | 2174.6 Da (PubChem) |
| computed backbone mass | 2174.61 Da |
| length | 16 residues |
| net charge (pH 7.4) | +3 |
| mean hydropathy | -0.94 |
| half-life | not characterised |
| delivery route | not characterised |
| PubChem CID | 146675088 |
| PDB | not characterised |
| UniProt parent | not characterised |
Mechanism
Mitochondrial-derived peptide encoded in the 12S rRNA region; described as acting through AMPK and folate-cycle metabolism.
Reported targets: AMPK pathway
Experimental structure
No experimental structure of this peptide is deposited in the PDB. Nothing is rendered here — a predicted fold would not be a structure, and this site does not draw one.
Reported effects
Each row is an outcome described in the literature indexed for this peptide. Reported in the cited work — not a claim, not a recommendation.
| reported outcome | where it appears |
|---|---|
| insulin sensitivity in models | MOTS-c is a mitochondrial-encoded interferon-linked host defense peptide eLife 2026 |
| exercise capacity in models | MOTS-c in sepsis-induced cardiomyopathy: Mechanisms and translational potent… European journal of pharmacology 2026 |
| metabolic regulation | MOTS-c attenuates hyperoxia-induced neonatal cardiac injury by inhibiting ox… Life sciences 2026 |
Registered trials
| NCT | title | status | phase |
|---|---|---|---|
| NCT07678073 | Comparison of the Effects of General Anesthesia and Combined Spinal-Epidural Anesthesia on F | RECRUITING | NA |
| NCT07638696 | Mitophagy and Mitochondrial DNA Dynamics During Ramadan Dry Fasting vs 16:8 Time-Restricted | NOT_YET_RECRUITING | — |
| NCT04027712 | Platelet Reactivity, B-amyloid, MOTS-c and Mortality of Type II Diabetics With CAD | UNKNOWN | — |
| NCT06500975 | Long Term Outcomes After Vestibular Implantation | RECRUITING | NA |
| NCT07438002 | Analysis of Effects of High-intensity Physical Exercise in Subjects With Dialyzed Chronic Ki | RECRUITING | NA |
Literature (8)
MOTS-c is a mitochondrial-encoded interferon-linked host defense peptide — eLife 2026
abstract not reproduced — this record is not open-access, so it is linked rather than copied.
publisher record ↗ · PMID 42611943 · DOI 10.7554/elife.87615
MOTS-c in sepsis-induced cardiomyopathy: Mechanisms and translational potential — European journal of pharmacology 2026
abstract not reproduced — this record is not open-access, so it is linked rather than copied.
publisher record ↗ · PMID 42633878 · DOI 10.1016/j.ejphar.2026.179261
MOTS-c attenuates hyperoxia-induced neonatal cardiac injury by inhibiting oxeiptosis via maintaining the KEAP1-PGAM5 interaction — Life sciences 2026
abstract not reproduced — this record is not open-access, so it is linked rather than copied.
publisher record ↗ · PMID 42128272 · DOI 10.1016/j.lfs.2026.124452
MOTS-c: How a secreted mitochondrial microprotein may become a potential treatment for inflammatory lung diseases — Journal of translational medicine 2026
abstract not reproduced — this record is not open-access, so it is linked rather than copied.
publisher record ↗ · PMID 42243958 · DOI 10.1186/s12967-026-08398-2
Are serum MOTS-c levels and MOTS-c m.1382A>C polymorphism related to polycystic ovary syndrome? — Archives of endocrinology and metabolism 2026
ObjectiveMOTS-c is a mitochondria-derived peptide associated with reduced insulin resistance and obesity. The m.1382A>C polymorphism of the MOTS-c gene is linked to an increased risk of type 2 diabetes in men. However, no studies have explored the relationship between this polymorphism and MOTS-c levels in adolescents with polycystic ovary syndrome (PCOS). This study aimed to investigate the differences in MOTS-c levels between adolescents diagnosed with PCOS and those without PCOS, as well as the associations with metabolic parameters. The association between the MOTS-c gene polymorphism and serum MOTS-c levels in adolescents with PCOS was also evaluated.Subjects and methodsAdolescents aged 12-18 diagnosed with PCOS were recruited based on irregular menstrual cycles and clinical/biochemical hyperandrogenism, excluding other conditions. The control group consisted of adolescents with reg…
open access ↗ · PMID 41945630 · DOI 10.20945/2359-4292-2026-0031
MOTS-c partially protects against skeletal muscle deterioration in C26 cachexia — Frontiers in medicine
abstract not reproduced — this record is not open-access, so it is linked rather than copied.
Mitochondrial peptide MOTS-c suppresses systemic and cardiac inflammasome activation in a diabetic rat model — Experimental physiology 2026
abstract not reproduced — this record is not open-access, so it is linked rather than copied.
publisher record ↗ · PMID 42321010 · DOI 10.1113/ep093714
Humanin and MOTS-c Attenuate Atrial Fibrillation by Suppressing Fibrosis and Mitochondrial Dysfunction — Biomedicines 2026
Background: Atrial fibrillation (AF) is a common clinical arrhythmia associated with mitochondrial dysfunction, oxidative stress, and atrial fibrosis. Mitochondrial-derived peptides (MDPs), including humanin (HN) and MOTS-c, exhibit cytoprotective properties, but their role in AF remains largely unknown. Objective: This study aimed to investigate the expression of HN and MOTS-c in AF patients and to evaluate their therapeutic potential and underlying mechanisms in an AngII-induced mouse model and primary cardiac cells. Methods: HN and MOTS-c expression in human atrial tissues was analyzed using public GEO data, immunohistochemistry, and immunofluorescence. Plasma levels were measured in a matched cohort (39 AF patients, 39 sinus rhythm controls). Murine AF models (male C57BL/6J mice, n = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or wit…
open access ↗ · PMID 42193373 · DOI 10.3390/biomedicines14051048