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PreclinicalNot FDA-approved

MOTS-c

Mitochondrial-derived 16-amino-acid peptide

Also indexed as: Mitochondrial-derived peptide

What this evidence does not tell us

The linked study shows metabolic findings in cells and mice. Human associations with naturally occurring MOTS-c are not evidence that administration improves outcomes.

Terms on this page

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10 glossary terms used in this profile

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Definitions explain the words—not whether a molecule works or is safe. Research education only, not medical advice.

Overview

MOTS-c is a 16-amino-acid mitochondrial-derived peptide described in metabolic research. Endogenous peptide measurements, experimental administration and clinical treatment are different kinds of evidence.

Mechanism of action

AMPK / mitochondrial metabolism

Preclinical work links changes in folate/purine metabolism with AMPK activation and metabolic stress responses.

A biological pathway describes a proposed or observed interaction—not necessarily a demonstrated health outcome.

Decode the terminology in our glossary

Put the research in context

Simplified educational maps—not a treatment pathway or a prediction of benefit.

Scientific evidence

How strong is the evidence?

Early lab & animal research

  1. Limited evidence
  2. Early researchCurrent category
  3. Human research
  4. Human outcomes

Most support comes from cells or animals. These studies help form questions, but do not prove a treatment works in people.

For this research: The linked study shows metabolic findings in cells and mice. Human associations with naturally occurring MOTS-c are not evidence that administration improves outcomes.

An editorial guide—not a validated score, a percentage, a safety rating or an approval badge. Regulatory status is separate. More research does not mean fewer risks.

Cell studies

Folate/purine pathway effects and AMPK activation were investigated in cellular experiments.

Animal experiments

Mouse models examined diet-induced obesity and insulin resistance; clinical treatment effects in humans are unproven.

Human observational studies

Associations, biomarker studies and anecdotes cannot establish treatment causality; no observational result is used here to infer clinical effectiveness.

Human clinical trials

Reliable, independently replicated human outcome evidence is not established by the selected sources in this edition.

Regulatory evidence

No FDA-approved finished drug for this molecule is identified in this edition. Investigational use, published research or compounding does not establish FDA approval.

Potential research applications

Metabolic stress, insulin sensitivity and skeletal-muscle signaling.

These describe scientific questions, not prescribing recommendations. A research grouping does not establish combination safety or clinical effectiveness.

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Safety considerations

FDA reports no identified human exposure data for nominated MOTS-c drug products and possible immunogenicity and impurity concerns. Endogenous biomarker studies do not establish injection safety.

This is not an exhaustive safety or contraindication list. An absence of reported harm is not proof of safety. Pregnancy, breastfeeding, cancer history, endocrine disease and concurrent medicines can materially change risk. Unregulated preparations add identity, contamination and sterility risks.

Read FDA’s compounding safety information

Regulatory status · United States

Not FDA-approved

No FDA-approved finished drug for this molecule is identified in this edition. Investigational use, published research or compounding does not establish FDA approval.

Regulatory status and evidence strength are different. A nomination for compounding, a clinical-trial registration or a “research use only” label is not approval. International rules vary; consult the current regulator and product label.

Selected literature & source transparency

Cell / animal study· 2015

The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.

Cell metabolism

Matched bibliographic records confirm a publication’s identity, not the validity of every claim. Selected sources are not a systematic literature review.

Continue your own source search

These open search results, not additional verified citations. Trial registration is not evidence that a treatment works.

Three questions worth bringing to your clinician

  1. Which human outcomes—not just biomarkers—support this claim?
  2. What established options address my actual health concern?
  3. What do my medical history and current medicines change about the risks?

Beyond the library

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Education, not a prescription. Research summaries are not medical advice, dosing instructions, or an offer to sell. Mechanistic findings do not establish clinical effectiveness. US regulatory status is product- and indication-specific and may change. Discuss health decisions with a licensed clinician.