Skip to content
  • Research use only — not for human or veterinary use
  • 55 compound profiles, every source cited
  • 62 research materials listed
  • Prices published, not hidden behind an enquiry
  • Vials and pre-filled pens
  • Dispatched and supported from the UK
  • Every profile states its UK regulatory status

Research profile · Peptide

MOTS-c

Also known as Mitochondrial ORF of the 12S rRNA type-c

Early human — evidence level 3 of 4: Early human evidenceExperimental — UK regulatory status: Experimental — not authorised for human use in the UK

Overview

A 16-amino-acid microprotein encoded within the mitochondrial genome, studied in metabolic and exercise physiology.

Category
Peptide
Highest evidence level identified
Early human evidence
Last scientifically reviewed
19 August 2026
Last regulatory review
19 August 2026

Mechanism under investigation

MOTS-c is a 16-amino-acid microprotein encoded within the mitochondrial genome rather than the nuclear genome, one of a small family of mitochondrial-derived peptides. Its principal described mechanism is inhibition of the folate cycle and tethered purine biosynthesis, raising AICAR and thereby activating AMPK. Under metabolic stress it has also been reported to translocate to the nucleus and interact with stress-response transcription factors. Because it is an endogenous human peptide, its physiological role and its effects when administered are distinct questions.

Research areas

  • Mitochondrial biology
  • Metabolic research

These are fields in which the compound has been investigated. Listing a field is not a statement that anything was demonstrated within it.

Current evidence

In-vitro evidence

Cells, tissues or biochemical systems outside a living organism.

Substantial and internationally distributed. Cell-free and cell-culture work establishes the folate–AICAR–AMPK axis, documents nuclear translocation, and reports direct kinase binding, including reduced binding for a naturally occurring sequence variant.

Animal evidence

Studies in living non-human animals.

Substantial. Administration in mice is reported to prevent age-dependent and diet-induced insulin resistance, to enhance physical performance across age groups, and to attenuate skeletal muscle atrophy. This work is published in high-impact international journals with public funding — a materially different provenance profile from several other compounds in this dataset.

Human observational evidence

Studies observing people without assigning an intervention.

This is the strongest tier. Independent groups across multiple countries report that acute endurance exercise raises circulating mitochondrial-derived peptides in humans, and genetic-epidemiological work on an East Asian-specific variant links it to muscle fibre composition and performance. Circulating-level studies in metabolic disease exist but are inconsistent in direction.

Clinical-trial evidence

Studies assigning an intervention to human participants.

Genuine but immature, with no efficacy results published. One completed phase 1 study tested an analogue rather than the peptide itself; its results were announced by the sponsor but are not posted to the registry and have not been published. A phase 2a of the peptide itself began in February 2026 and is recruiting, with no data.

Study limitations

  • No published efficacy trial of the administered peptide in humans exists. The only completed clinical study tested an analogue, has no registry-posted results and no peer-reviewed publication.
  • Most human data are observational measurements of naturally occurring peptide responding to exercise or disease state. These describe physiology and cannot be read as evidence that administering it produces benefit.
  • Circulating levels are measured by varying, often in-house assays, and the direction of change in metabolic disease is reported inconsistently across studies.
  • Genetic-association work uses a population-restricted variant, so findings from those cohorts do not generalise to a UK population.

UK regulatory context

Experimental — not authorised for human use in the UK

A compound appearing in research literature that holds no UK authorisation for human use in any indication.

Source: The Human Medicines Regulations 2012, regulation 46 — prohibition on sale or supply of an unauthorised medicinal product (opens legislation.gov.uk in a new tab) (legislation.gov.uk)

Regulatory classification is jurisdiction-specific. A compound authorised elsewhere is not thereby authorised in the UK, and a supplier’s description of a substance does not determine how it is classified in law. See safety and regulation for the framework and the authoritative sources.

Safety and interpretation

Because this is an endogenous peptide, its natural presence in the body says nothing about the safety of administering it at pharmacological exposures, and long-term human safety data do not exist. A completed phase 1 study of an analogue reported no serious adverse events according to its sponsor, but no peer-reviewed safety publication exists and no results are posted to the registry. It is also prohibited at all times in sport.

References