Mitochondrial-derived signaling peptide
MOTS-c is a 16-amino-acid peptide encoded within mitochondrial DNA and studied as a signal involved in cellular energy stress. Human studies have mostly measured the body's own MOTS-c rather than administering it. A Phase 2a insulin-sensitivity trial is enrolling, but it has no results yet.
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Depth and confidence summarize the research record—not effectiveness, safety, or a recommendation.
Human administration research is limited to an enrolling Phase 2a trial with no posted results; the completed human record measures endogenous MOTS-c rather than giving the peptide.
Research depth describes how large and mature the overall record is. It does not tell you whether the results were positive.
Metabolic and exercise findings are primarily mouse, cell, or observational biomarker evidence, and native MOTS-c has no completed human efficacy dataset.
Confidence describes how reliable and consistent the conclusions are. It can be high for one outcome and low for another.
The strongest evidence type shows what the best-supported conclusions are actually based on.
Human findings are more directly relevant than animal or laboratory results, but they still apply only to the populations and outcomes studied.
Route-specific record
These are exposures used in cited research for a specific route and population—not a suggested amount.
Half-life describes how long it takes the measured amount in the body to fall by half. It is not a dosing recommendation.
Evidence can change by administration method. Findings from one route should not automatically be applied to another.
Evidence boundary: Registration shows that native MOTS-c is entering human testing; it does not establish benefit, safety, an effective amount, or a public-use protocol. Human CB4211 research belongs to an optimized analog and is not direct native-MOTS-c evidence. Amounts shown describe cited research exposure—not a dosage recommendation.
Practical starting point
Common goals and questions—not recommendations or promises of benefit.
The overview, studies, and source ledger below explain what supports each label—and where the evidence stops.
The short version
MOTS-c is a 16-amino-acid peptide encoded within mitochondrial DNA and studied as a signal involved in cellular energy stress. Human studies have mostly measured the body's own MOTS-c rather than administering it. A Phase 2a insulin-sensitivity trial is enrolling, but it has no results yet.
Includes the enrolling native-MOTS-c Phase 2a trial, human endogenous-biomarker studies, an analog trial kept separate, peer-reviewed preclinical work, FDA's July 2026 review, the July 23 advisory vote, and the 2026 WADA list.
What the evidence says
Human studies show that endogenous MOTS-c changes with exercise and is associated with some metabolic and vascular phenotypes. No completed controlled human efficacy results for administered native MOTS-c were publicly available at the cutoff.
This is the strongest supported conclusion in the current human evidence—not a summary of every claim made about the compound.
Whether administered native MOTS-c improves insulin sensitivity, body composition, physical performance, or meaningful health outcomes in people, and whether repeated exposure is safe.
Keeping the main uncertainty visible prevents an early or promising finding from looking more settled than it is.
The evidence story
Importance shows how much an item changes the evidence story. Quality shows how much confidence the design deserves. A strong negative study can score highly on both.
Importance and quality answer different questions. A rigorous study can be highly important even when it challenges a popular claim.
FDA's 2026 compounding review separated the enrolling native-MOTS-c trial from analog, animal, and endogenous-biomarker evidence and emphasized the absence of completed human effectiveness and adequate safety data.
No results are posted. This trial is designed to test whether native investigational MOTS-c improves insulin sensitivity in people rather than only in animal or cell models.
Pooled results associated lower circulating MOTS-c with diabetes but higher levels with obesity. The directions differed by metabolic condition.
Skeletal-muscle MOTS-c increased about 11.9-fold after exercise, while circulating levels rose more modestly during and shortly after exercise before returning toward baseline.
MOTS-c moved into the nucleus during metabolic stress and influenced adaptive nuclear gene expression in an AMPK-dependent manner.
Administration and handling
The enrolling MOTS-MET trial uses subcutaneous investigational MOTS-c for 12 weeks, but its public registration does not disclose the dose. No completed native-MOTS-c human efficacy results were available. This research design does not establish an approved route, dose, schedule, injection site, or consumer protocol.
No FDA-approved MOTS-c product, regulator-approved consumer reconstitution procedure, or official product-specific storage instructions were located. FDA identified uncertainty around free base versus acetate identity, impurities, aggregation, product formulation, sterility, endotoxins, and immunogenicity. Supplier instructions should not be presented as universal or regulator-approved stability guidance.
Primary-source ledger
2026-07-23
2026-07-23
2026-04-01 · NCT07505745
2026-01-01
2024-08-19 · PMID 39160573 · DOI 10.1186/s13098-024-01451-y
2021-01-20 · PMID 33473109 · DOI 10.1038/s41467-020-20790-0
2019-06-26 · NCT03998514
2018-07-10 · PMID 29983246 · DOI 10.1016/j.cmet.2018.06.008
2018-02-01 · PMID 29242099 · DOI 10.1016/j.ijcard.2017.11.077
2015-03-03 · PMID 25738459 · DOI 10.1016/j.cmet.2015.02.009