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Peptide Evidence Registry

Mitochondria · Neuro & cognitive

HDAP2

A short mitochondria-targeted research peptide that binds cardiolipin. Evidence is cell and mouse work, including 2026 optic-nerve injury 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:
high-density aromatic peptide 2, Biotin-dArg-Phe-Phe-dArg-amide
Last reviewed:
2026-09-21
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Evidence passport

HDAP2

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 evidence0 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 evidence3 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 — cell studies and mouse retinal and optic-nerve models
Source curation
Sources fully curated

Routes recorded

SC injection· unapproved

Most of this evidence comes from animals and cells

The supporting research for HDAP2 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 strength0 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 strength35 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 strength3 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 — cell studies and mouse retinal and optic-nerve models

Routes & formulations

Marketed / research routes — never approved

SC injection· unapproved

The published animal work gives it systemically to mice. That is an experimental protocol, not a human route.

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

Academic programme with NIH project support (1R16GM149428-01A1). No clinical trial is established in our record.

Last documented development: 2026 — Neuroscience report of systemic HDAP2 in a mouse optic-nerve injury model

What it is

A short synthetic peptide with an unusually high density of aromatic residues, published as Biotin-dArg-Phe-Phe-dArg-amide. It is designed to accumulate in mitochondria and bind cardiolipin, the inner-membrane lipid whose organisation is required for stable respiratory function.

What people claim

  • Neuroprotection and vision preservation
  • Mitochondrial membrane repair
  • Protection against nerve injury

What the evidence actually says

The design rationale is coherent and the animal findings are real: in mouse models, systemic HDAP2 improved retinal ganglion cell survival and reduced mitochondrial loss. This is animal evidence. There is no human study, so it cannot be described as a neuroprotective therapy for people, and nothing here supports use for eye or nerve conditions.

Related evidence

Useful next reads based on this compound — not recommendations.

Human evidence

  • No human study of HDAP2 was identified in our curated record.

Preclinical evidence

  • Published work characterises HDAP2's cardiolipin binding and its effect on mitochondrial membrane stability, with cell studies and mouse glaucoma/retinal models (PMID 41035613, PMC12479369).
  • A 2026 Neuroscience study reports that systemic HDAP2 improved retinal ganglion cell survival and reduced mitochondrial loss after optic-nerve injury in mice (PMID 41633465, DOI 10.1016/j.neuroscience.2026.01.045). Mouse retinal ganglion cells are not a human visual outcome.
  • NIH RePORTER project 1R16GM149428-01A1 provides provenance for the funded research programme, not evidence of efficacy.

Animal and cell findings are Level 1–2 evidence.

Mechanism and pathways

  • Aromatic residues and charge drive accumulation in mitochondria, where the peptide binds cardiolipin.
  • Stabilising cardiolipin organisation is proposed to preserve cristae structure and respiratory function under stress.
  • Stabilising a membrane in a model system is a mechanism, not a treatment effect.

Safety and unknowns

  • No human safety data exist in our curated record.
  • Mouse studies have not reported programme-stopping toxicity, which is not the same as an established safety profile.
  • Material sold under this name is unregulated and unverified.

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 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 and not in human trials in our curated record. It is an academic research peptide supported by published work and NIH-funded projects.

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 Phase 1 human safety study.
  • Independent replication of the retinal ganglion cell findings, and evidence in larger animals.

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: 2Sponsor / official: 1

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.