Independent · non-commercial · publishes on a quarterly cycle|Current cycle 2026 Q3
Compound Evidence InstituteEvidence synthesis · established 2023Graded assessments of compounds, trials, methods and supply
Document set current to 30 July 2026
Compound monograph · §2

MOTS-c — pharmacology

Molecular targets, mechanism of action, pharmacokinetics and interactions as characterised in humans.

Document identifier
CEI-MN-043/2
Series
Compound monograph
Version
1.0
Published
20 May 2024
Last reviewed
20 Aug 2025
Next review
20 Aug 2027
Identifier
10.71829/cei.mono.43
Certainty
Very low
Cycle
2024 Q2

§2Pharmacology

§2.1Molecular targets

Table 2. Molecular targets recorded for MOTS-c, with the character of the interaction and the potency where the Institute holds it.

TargetInteractionNote
AMP-activated protein kinase pathwayIndirect activationReported through folate-cycle and 5-aminoimidazole-4-carboxamide ribonucleotide accumulation rather than direct binding
Nuclear gene expressionRetrograde signallingReported translocation to the nucleus with effects on stress-response gene expression

§2.2Mechanism of action

MOTS-c is described as a mitochondrial-encoded regulator of metabolic homeostasis that acts through the folate one-carbon cycle to raise 5-aminoimidazole-4-carboxamide ribonucleotide and thereby activate AMP-activated protein kinase, and separately as a retrograde signal translocating to the nucleus under metabolic stress. In rodent models it improves insulin sensitivity and reduces diet-induced obesity.[1,2]

§2.3Pharmacokinetics

No human pharmacokinetic characterisation of MOTS-c has been identified. In the absence of a half-life, a volume of distribution and a clearance estimate, no dosing interval used in practice can be related to any exposure that produced an effect in any study, and the Institute records this as a first-order gap rather than a detail.

§2.4Interactions

  • Not characterised

References cited on this page

References are numbered in order of first citation in this document. Each superscript in the text links to its entry below.

  1. Lee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, Cohen P. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism 2015;21(3):443–454. doi:10.1016/j.cmet.2015.02.009 · PMID 25738459
  2. D’Hondt M, Bracke N, Taevernier L, Gevaert B, Verbeke F, Wynendaele E, De Spiegeleer B. Related impurities in peptide medicines. Journal of Pharmaceutical and Biomedical Analysis 2014;101:2–30. doi:10.1016/j.jpba.2014.06.012 · PMID 25044089

Identifiers are reproduced only where the Institute holds them. Where a digital object identifier or PubMed identifier is not shown, the Institute has recorded the journal and year and has not constructed an identifier.

Nothing published by the Institute is medical advice, a diagnosis, a prescription, a treatment recommendation or a purchasing recommendation. Compounds supplied for research use are not approved for human or veterinary use in any jurisdiction, and a favourable analytical assessment of a supplier is not a statement that any product is safe or effective. The Institute publishes certainty ratings and never recommendations. No telephone number, messaging handle or ordering channel appears anywhere on this site.