Dihexa

Not FDA-approved Evidence grade D — animal or in-vitro data only Updated 2026-10-20

This page describes published research and public regulatory records. It is not medical advice. SoluneFit does not sell, supply, or recommend any compound. The SoluneFit app includes a private, on-device tracker for people who want a record of what they and their clinician have already decided — the app neither suggests compounds nor doses.

Also known as: PNB-0408, N-hexanoic-Tyr-Ile-(6) aminohexanoic amide, dihexa acetate.

Regulatory status

Not FDA-approved and never tested in humans. Nominated for the 503A bulk list but withdrawn; FDA states it has not identified any human exposure data on dihexa acetate by any route [1]. Not among the seven peptides reviewed at the July 2026 PCAC meeting [6].

What it is

Peptidomimetic angiotensin IV analogue (chemically modified Tyr-Ile dipeptide); proposed HGF/c-Met modulator.

A small modified peptide derived from angiotensin IV, designed at Washington State University to be oral and brain-penetrant, and studied in rodents as a possible dementia treatment. There are no published human studies of any kind.

What the published research shows

Rats and mice only (scopolamine-impaired and aged rats, APP/PS1 Alzheimer's mice, a few small rodent injury models). Zero human data: no published human study and no registered trial on ClinicalTrials.gov. Key papers from the originating lab carry a 2021 expression of concern and two were retracted in 2025.

Published human studies and reports (these describe trial populations, not SoluneFit claims):

Cognition in rats (McCoy et al., J Pharmacol Exp Ther 2013; expression of concern 2021): Oral gavage 2 mg/kg reversed a scopolamine-induced learning deficit in the water maze; aged rats received 2 mg/kg/day orally; IP doses 0.05–0.5 mg/kg in behavioural tests.
Alzheimer's model mice (Sun et al., Brain Sci 2021): In APP/PS1 mice, dihexa at several doses restored water-maze learning and reduced markers of brain inflammation.
Mechanism (Benoist et al., J Pharmacol Exp Ther 2014; RETRACTED 2025): Reported high-affinity binding to HGF and c-Met activation in rat hippocampal neurons; retracted, so not relied on here.

Mechanism, as reported

Proposed to bind hepatocyte growth factor (HGF) and boost signalling through its receptor c-Met, promoting new synapses in the hippocampus. The main paper reporting this mechanism was retracted in 2025, so the mechanism should be treated as unconfirmed.

Practical record

Elimination half-life: 304.0 h (confidence: low). RAT data only: terminal half-life 12.68 days after 10 mg/kg IV (about 8.8 days after IP), from a paper under an expression of concern. Human half-life unknown. The app draws no decay curve for dihexa trackers because of that; enter a value yourself if you accept the rat figure.
Studied routes: oral, intravenous.
Typical supply: No licensed product. Sold as powder or capsules on the research-chemical market (unregulated).

Safety signals on record

Reported adverse events: Unknown in humans: no human exposure has been published. FDA says it lacks important information on any safety issue raised by dihexa.
Contraindications: None established (no label, no human data).
Interactions: None documented.
Notes: HGF/c-Met is a growth pathway also implicated in cancer growth, so a compound designed to amplify it carries a theoretical tumour-promotion concern not addressed in the published animal work. The very long half-life in rats means any effect could persist for weeks. WADA S0 prohibits any substance with no governmental approval for human therapeutic use [5].

Sources

General wellness education, not medical advice. Unapproved compounds have no established dosing, purity standard, or safety profile.

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