Skip to content

Mitochondria · Longevity

MOTS-c

A mitochondrial-derived peptide with genuinely interesting biology and thin translational data.

L2Animal / lab studiesResearch / unapproved supplyPreclinical
How settled this rating is:
very-low confidence in the current evidence rating
Routes studied:
Not established · Subcutaneous injection (marketed but never approved)
Also known as:
mitochondrial ORF of the 12S rRNA type-c
Last reviewed:
2026-09-18
Jump to section

Evidence passport

MOTS-c

A one-screen evidence identity for this compound. These fields describe research maturity, confidence and legal status. They are not a safety guarantee, efficacy percentage or recommendation.

Reviewed 2026-09-18
Evidence level
L2Animal / lab studies
Confidence
Very low confidence in rating
Regulatory status
Research / unapproved supply
Development status
Preclinical

Evidence strength

Human efficacy evidence20 of 100 evidence strength

Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.

Human safety evidence12 of 100 evidence strength

Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number.

The 0-100 values rate the strength and maturity of evidence, not how effective or safe the compound is.

Evidence base
Mostly animal and laboratory research
Furthest established stage
Not established
Human research maturity
Preclinical with early translational human observation
Source curation
Sources fully curated

Routes recorded

SC injection· unapproved

Most of this evidence comes from animals and cells

The supporting research for MOTS-c is predominantly preclinical (Level 1–2). That is a legitimate starting point for science and a poor basis for personal decisions. Human results are not simply a scaled-up version of mouse results.

Overview

Human efficacy evidence strength20 of 100 evidence strength

Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.

Preclinical (animal / lab) evidence strength70 of 100 evidence strength

Higher = more animal, tissue or cell research. Preclinical results are a starting point, not proof of a human benefit.

Human safety evidence strength12 of 100 evidence strength

Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number.

How to read these scores

Every number here rates the evidence, not the compound. They are editorial 0-100 strength ratings, not percentages, and not a rating out of five stars.

  • Human efficacy evidence strength — Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.
  • Preclinical evidence strength — Higher = more animal, tissue or cell research. Preclinical results are a starting point, not proof of a human benefit.
  • Human safety evidence strength — Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number. A score of 80 does not mean “80% safe”.
  • Evidence level (L0-L5) — the strongest type of study behind the compound, from anecdote (L0) to large replicated human trials (L5). It is a description of the study evidence, not a quality, safety or recommendation rating.
  • Confidence — how likely we think it is that this rating changes as new research lands. Low confidence means the picture is unsettled, not that the compound is bad.

None of these ratings is medical advice, a safety guarantee, or a recommendation to use anything. How we grade evidence.

How far human research has progressed: Preclinical with early translational human observation

Routes & formulations

Marketed / research routes — never approved

SC injection· unapproved

No approved formulation exists. Material sold online is typically injectable; route-specific efficacy and safety in humans are unstudied.

Route availability is not evidence of efficacy, and evidence from one route does not transfer to another. The Registry never provides dosing or sourcing information.

Peptide lifecycle

  1. Discovery

  2. Preclinical

  3. Phase I

  4. Phase II

  5. Phase III

  6. Approved

PreclinicalFurthest stage not established in our curated record

Early translational research only; no established clinical development programme.

What it is

A short peptide encoded within mitochondrial DNA that appears to act as a metabolic signalling molecule between mitochondria and the nucleus.

What people claim

  • Reverses age-related metabolic decline
  • Improves insulin sensitivity and exercise capacity
  • Extends healthspan

What the evidence actually says

The biology is genuinely compelling: MOTS-c looks like a real endogenous exercise-and-metabolism signal, and circulating levels associate with metabolic status in human observational work. What is missing is the bit that matters clinically — randomised human trials of administering it. Interesting is not the same as proven.

Useful next reads based on this compound — not recommendations.

Human evidence

  • Observational studies associating circulating MOTS-c with age, fitness and metabolic status.
  • No robust randomised controlled trials of exogenous administration.

Preclinical evidence

  • Rodent studies showing improved insulin sensitivity and exercise capacity.
  • Cell work on AMPK activation and metabolic stress responses.

Animal and cell findings are Level 1–2 evidence.

Mechanism and pathways

  • Activates AMPK, shifting cells toward energy production and glucose uptake.
  • Translocates to the nucleus under metabolic stress to influence gene expression.
  • Interacts with the folate-methionine one-carbon cycle.

Safety and unknowns

  • Essentially no human safety data for administered MOTS-c.
  • Long-term consequences of chronic AMPK-axis manipulation are unknown.

Cancer relevance

This section covers questions raised by how the compound works in the body, plus anything regulators and trial teams keep an eye on. It is not a statement that this compound causes cancer — for most compounds here, no human data exist in either direction.

Theoretical / mechanistic concern only

AMPK signalling has context-dependent roles in cancer biology — sometimes tumour-suppressive, sometimes supportive of stress survival. This is a mechanistic unknown, not a demonstrated risk or benefit in humans.

Regulatory status

Regulatory decisions apply to specific jurisdictions, products, formulations and indications. An approval elsewhere is not automatically an approval in your country.

Check the regulatory note and linked primary sources for jurisdiction-specific details.

Not an approved medicine. Research compound; also prohibited in sport. FDA's Pharmacy Compounding Advisory Committee considered MOTS-c in July 2026 for possible inclusion on the 503A Bulks List. Its recommendations are non-binding: this is a compounding-policy process, not FDA drug approval, validation of efficacy claims or blanket legalisation.

Evidence grade

L2Animal / lab studiesVery low confidence in rating

Documented compound-specific animal or laboratory outcome findings, without qualifying human evidence for the assessed benefit.

What would change our rating?

  • A published Phase 1 human safety and pharmacokinetic study.
  • Randomised trials in metabolic endpoints.

References and sources

Source transparency

A provenance snapshot of this profile. Counts show what kinds of sources are cited, not how much scientific weight each source deserves.

Sources fully curated
Last editorial review
2026-09-18
Recently reviewed · 28 days ago
Linked curated sources
3
Sources still pending
0
External specialist reviews
0
None recorded for this profile
Regulatory / label: 3

Review provenance

Registry editorial review: Colin Jackson-White, creator and editor, who is not a doctor or clinician. External specialist review is credited only when a named reviewer has completed a review of this exact profile.

Literature-discovery and AI tools may help locate or challenge candidate evidence, but they are not counted as evidence sources here. Registry judgements are tied to the underlying papers, trial records, regulator documents and official study records.

Source hierarchy: regulatory documents and trial registries first, peer-reviewed work next, sponsor material flagged as non-independent. We never use supplier or clinic marketing as evidence, and where a verified source has not yet been curated we say so rather than inventing one.

Evidence change history

These entries record changes to our assessment of the published evidence — not changes to the compound itself.

  1. Baseline entry: classified as promising-but-unproven rather than emerging therapy.

    Change 1 of 1
    L2Animal / lab studiesBaseline entry
    Human data are observational. Without a published trial of exogenous administration, therapeutic claims cannot rise above Level 2.

Related claims we’ve checked — in full

Claim verdict

Longevity

Promising but unprovenL2Animal / lab studies

“MOTS-c is a proven longevity therapy.”

This verdict applies to the exact claim above. It is not a verdict on the compound overall, a safety guarantee, or a recommendation to use it.

Registry verdict

Promising but unproven — great biology, missing trials.

Why this verdict

  • Human observational work links circulating MOTS-c with fitness and metabolic status.
  • Rodent studies show metabolic improvements, but no randomised human trial of administration exists.
  • 'Promising' is a compliment about the science, not a recommendation to inject it.