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Never Tested In Humans

Dihexa

Also known as Dihexa acetate · N-hexanoic-Tyr-Ile-(6) aminohexanoic amide

Summary coverage

At a glance

What it is
Angiotensin IV analogue, never tested in humans, activating a cancer pathway.
Evidence
Preclinical + practitioner useHow the tiers workFDA states it has not identified any human exposure data on drug products containing dihexa administered via any route. Why this tier
Half-life
Not established in available literature
Routes
Oral, Subcutaneous
Category
Cognitive
FDA
Advisory vote planned
As of 3 August 2026. What that means
WADA
We do not state a status

Not schedulable in Claritide. Our sources publish no dosing figure for Dihexa, so there is nothing to build a schedule from.

Evidence

Why this tier

FDA states it has not identified any human exposure data on drug products containing dihexa administered via any route. The preclinical claims are striking: synaptogenesis at picomolar concentrations, reported as around seven orders of magnitude more potent than BDNF in in-vitro spine-formation assays, orally bioavailable and blood-brain-barrier penetrant. They are all in cells and animals. Its related prodrug fosgonimeton is reported to have failed the pivotal LIFT-AD Alzheimer’s trial in September 2024; that report is aggregator-tier and we flag it as unconfirmed. FDA says it will hold an advisory committee meeting on dihexa before the end of February 2027.

Overview

What it is

Dihexa is an angiotensin IV analogue proposed to act as an HGF/c-Met mimetic, reported in preclinical work to promote synaptogenesis at picomolar concentrations. It has never been tested in humans, FDA states it has identified no human exposure data by any route, and its proposed mechanism runs through a pathway with a real cancer caution attached.

Mechanism

How it works

Dihexa is built from Nle-angiotensin IV: the N-terminal valine is replaced with a hexanoyl cap, the Tyr-Ile pharmacophore is retained, and the C-terminal His-Pro-Phe is replaced by a 6-aminohexanoic amide. In cultured hippocampal neurons, dihexa and related angiotensin IV analogues increase dendritic spine density, and that effect is abolished when HGF/c-Met signalling is blocked, which is the basis for calling it an HGF mimetic. The mechanism is contested: the original paper proposing direct HGF binding is reported to have been retracted, and we could not confirm that retraction at primary level, so treat the mechanism as a working hypothesis. What is not in doubt is that c-Met is a growth-factor receptor pathway with well-established oncological significance.

Dosing

Commonly researched ranges

These are figures reported in published literature and practitioner protocols: a commonly researched range, not a recommendation. Claritide does not tell you what to take.

Not established in available literature. Our sources describe Dihexa without publishing a dosing figure, so Claritide does not print one.

Cycle guidance
Not established in available literature
Goals
Cognition
Legal standing

Where this sits with the FDA

Dated, sourced, and separate from whether it works. Removal from a warning list is not permission to compound.
Advisory vote plannedas of 3 August 2026 · US

FDA 503A bulks · nomination withdrawn; FDA says it will hold an advisory committee meeting on it before the end of February 2027

Removal from Category 2 is not permission. FDA says it will hold an advisory committee meeting on dihexa before the end of February 2027, and FDA’s own note on it is that it has identified no human exposure data by any route of administration.

Last change · 22 April 2026 · Dihexa acetate was among the 12 peptides removed from Category 2, announced 15 April 2026 and effective 22 April 2026.

Primary source

How it got here

  1. 15 April 2026

    FDA announced a future Pharmacy Compounding Advisory Committee meeting to discuss dihexa acetate, alongside GHK-Cu, Melanotan II, Cathelicidin LL-37 and PEG-MGF, with its time and place still to be scheduled.

  2. 22 April 2026

    FDA removed 12 peptide bulk substances from Category 2 after the nominators withdrew their nominations. Announced 15 April 2026, effective 22 April 2026.

  3. 28 February 2027

    FDA says its Pharmacy Compounding Advisory Committee will meet before the end of February 2027, on a date not yet set.

An advisory vote is not law. In July 2026 an FDA advisory committee voted in favour of adding several peptides to the 503A bulks list, over the explicit recommendation of FDA’s own scientific reviewers, who recommended against all seven. FDA would still have to write a rule, and it has not proposed one or given a date. None of these compounds is lawfully compoundable today.Note what FDA actually assessed: BPC-157 for ulcerative colitis, TB-500 for wound healing, KPV for wound healing and inflammatory conditions, MOTS-c for obesity and osteoporosis, Epitalon for insomnia, Semax for cerebral ischaemia, migraine and trigeminal neuralgia. Whatever emerges from rulemaking will be scoped to those indications.

Sport

WADA status

The 2026 Prohibited List entered force on 1 January 2026.
We do not state a status

Not named on the 2026 Prohibited List. We could not determine a classification and do not state one.

We looked and could not resolve it. This is not the same as "not prohibited". Treat it as unresolved and check with your federation before competing.

The FDA reclassification has no effect whatsoever on WADA status.

Reconstitution

Mixing recipes our sources document

Concentration (mg/mL) = vial mg ÷ diluent mL. On a U-100 barrel, 1 unit = 0.01 mL.

Not established in available literature. Use the calculator with the figures printed on your own vial.
Open the calculator

Expectations

Week by week

What our material describes people reporting. Individual responses vary widely.

Not established in available literature.

Tolerability

Side effects

Grouped by how often our sources report them. Percentages appear only where a published trial figure exists.

Not established in available literature. Absence from this page does not mean absence of risk. It means our sources publish no side-effect profile for Dihexa.

Safety

Contraindications and interactions

Do not use if

  • Cancer history or active malignancy: dihexa is proposed to act through the HGF/c-Met pathway, which has established oncological significance. This is a real contraindication, not a theoretical one
  • There is no established human dose for dihexa, so there is no dose anyone can justify

Interactions

Not established in available literature.

Absence from this list does NOT mean safety. It means lack of research.

Handling

Storage and cost

Storage
Our sources publish no handling protocol, because there is no human dosing protocol.
Cost
Not established in available literature
Deep dive

Dihexa in full

Limited coverage

Dihexa is an angiotensin IV analogue: the N-terminal valine of Nle-angiotensin IV replaced with a hexanoyl cap, the Tyr-Ile pharmacophore retained, and the C-terminal His-Pro-Phe replaced by a 6-aminohexanoic amide.

FDA states it has not identified any human exposure data on drug products containing dihexa administered via any route of administration. We publish no dose range and a null half-life.

The preclinical claims, and why they are seductive

Synaptogenesis at picomolar concentrations. Reported as around seven orders of magnitude more potent than BDNF in in-vitro spine-formation assays. Orally bioavailable. Blood-brain-barrier penetrant.

That is an extraordinary set of numbers, and every one of them comes from cells and animals. Potency in a dish is not efficacy in a person, and a compound that is very potent at doing something in cultured neurons is also very potent at doing it everywhere else it reaches.

The mechanism is contested

In cultured hippocampal neurons, dihexa and related angiotensin IV analogues increase spine density, and the effect is abolished when HGF/c-Met signalling is blocked. That is the basis for describing it as an HGF mimetic.

The original paper proposing direct HGF binding is reported to have been retracted. We could not confirm that retraction at primary level, so we flag it rather than assert it, but the mechanism is best treated as a working hypothesis either way.

Its related prodrug fosgonimeton is reported to have failed the pivotal LIFT-AD Alzheimer's trial in September 2024. That report is aggregator-tier and unconfirmed against the sponsor's own release.

The cancer caution

The HGF/c-Met pathway is a growth-factor signalling axis with well-established oncological significance. A compound whose proposed mechanism is activating it is a genuine contraindication in anyone with a cancer history, not a boilerplate caution copied from another record.

FDA says it will hold an advisory committee meeting on dihexa before the end of February 2027.

References

Sources

  1. 1
    FDA · Certain bulk drug substances for use in compounding that may present significant safety risks
  2. 2
    FDA · Meeting of the Pharmacy Compounding Advisory Committee, to be held before the end of February 2027, on cathelicidin LL-37, GHK-Cu, dihexa acetate, Melanotan II and PEG-MGF (content current as of 15 April 2026)
  3. 3
    Alzheimer’s Drug Discovery Foundation · Cognitive Vitality report on dihexa (independent assessment, not retrieved)

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