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Peptide Evidence Registry

Mitochondria · Longevity

MA-5 (Mitochonic Acid 5)

A small indole-derived molecule — not a peptide — studied in cells and mice for mitochondrial disease. No human trial evidence in our record.

L2Animal / lab studiesResearch / unapproved supplyPreclinicalSmall molecule — not a peptide
How settled this rating is:
very-low confidence in the current evidence rating
Routes studied:
Not established · Oral (marketed but never approved)
Also known as:
mitochonic acid 5, MA5, 4-(2,4-difluorophenyl)-2-(1H-indol-3-yl)-4-oxobutanoic acid
Last reviewed:
2026-09-21
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Evidence passport

MA-5 (Mitochonic Acid 5)

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 2026-09-21
Evidence level
L2Animal / lab studies
Confidence
Very low confidence in rating
Regulatory status
Research / unapproved supply
Development status
Preclinical

Evidence strength

Human efficacy evidence5 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 evidence5 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
Preclinical
Human research maturity
Preclinical — patient-derived cell work and mouse models of mitochondrial disease
Source curation
Sources fully curated

Routes recorded

Oral· unapproved

Most of this evidence comes from animals and cells

The supporting research for MA-5 (Mitochonic Acid 5) 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 strength5 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 strength55 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 strength5 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 — patient-derived cell work and mouse models of mitochondrial disease

Routes & formulations

Marketed / research routes — never approved

Oral· unapproved

Animal studies administer it systemically. Route detail here describes published experiments, never a human regimen.

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

    Furthest established stage

  3. Phase I

  4. Phase II

  5. Phase III

  6. Approved

Preclinical

A sustained academic programme in Japan spanning renal, cardiac and mitochondrial-disease models. No approval and no adequate human efficacy trial is established in our record.

Last documented development: June 2026 — Scientific Reports paper on MA-5 in a mouse model of mitochondrial disease onset

What it is

A synthetic indole-derived small molecule, chemically 4-(2,4-difluorophenyl)-2-(1H-indol-3-yl)-4-oxobutanoic acid. It is chemically unrelated to peptides and is included here because it circulates in the same mitochondrial-health conversation.

What people claim

  • Restores cellular energy production
  • Longevity and anti-ageing benefit
  • Treats mitochondrial dysfunction and fatigue

What the evidence actually says

The mechanistic work is unusually specific for this field: MA-5 binds mitofilin/Mic60 in the inner mitochondrial membrane and has been reported to promote ATP synthase oligomerisation and ATP production without acting through the electron transport chain. The outcome data are from patient-derived fibroblasts and mouse models, including a 2026 mouse mitochondrial-disease study. No human treatment benefit and no longevity effect is established.

Related evidence

Useful next reads based on this compound — not recommendations.

Human evidence

  • No controlled human trial of MA-5 was identified in our curated record. Cell work using fibroblasts from patients with mitochondrial disease is laboratory evidence, not evidence of patient benefit.

Preclinical evidence

  • A 2017 EBioMedicine paper reports that MA-5 facilitates ATP synthase oligomerisation and supercomplex formation and improves survival of cells from patients with a range of mitochondrial diseases (PMC5478234).
  • Earlier work identified mitofilin at the crista junction as its mitochondrial binding target and reported improved renal and cardiac outcomes in ischaemia-reperfusion and cisplatin nephropathy models, with ATP production raised without changing complex I-IV activity.
  • A June 2026 Scientific Reports study in mito-mice∆, a mouse model of mitochondrial disease onset driven by deleted mitochondrial DNA, reports that MA-5 slowed progression of low body weight and lactic acidosis and protected against mitochondrial respiration defects and renal failure in the kidney, with respiration defects also resolved in the heart.

Animal and cell findings are Level 1–2 evidence.

Mechanism and pathways

  • Binds mitofilin/Mic60, part of the MICOS complex that shapes inner-membrane cristae architecture.
  • Reported to promote ATP synthase oligomerisation and supercomplex formation, increasing ATP production independently of oxidative phosphorylation complex activity.
  • A mechanism explains how an effect could happen. It does not establish that it happens usefully in people.

Safety and unknowns

  • No human safety dataset exists in our curated record.
  • Animal work has not reported the kind of toxicity that halts a programme, but absence of reported harm in mice is not a human safety profile.
  • Anything sold under this name is unregulated material of unverified identity and purity.

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.

No established human signal

Not established. No human data exist, and we make no claim about cancer risk or benefit in either direction.

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. The curated record establishes academic cell and animal research, not a licensed product or an established human trial programme.

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 registered human trial in a defined mitochondrial-disease population.
  • Independent replication outside the originating research group.

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
2026-09-21
Recently reviewed · 25 days ago
Linked curated sources
3
Sources still pending
0
External specialist reviews
0
None recorded for this profile
Peer-reviewed: 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.

No recorded changes yet. Baseline position set on 2026-09-21.