Modified two-amino-acid fragment of angiotensin IV, built in a rat lab as a dementia drug; never tested on its own in humans.
Also called PNB-0408, N-hexanoic-Tyr-Ile-(6) aminohexanoic amide, Dihexa acetate, AngIV analog
Dihexa is a lab-made compound from Washington State University: two amino acids from angiotensin IV (tyrosine and isoleucine) with a fatty hexanoic acid cap on one end and an aminohexanoic amide on the other. The caps were added so it would survive digestion and reach the brain when swallowed. In rats it reversed memory loss caused by the drug scopolamine and by old age, and it grew new dendritic spines on neurons in a dish.
The weak spot is the paper trail. Four of the founding lab papers drew expressions of concern in 2021 after a company investigation found a co-author had altered images, and three of them, including the one that named hepatocyte growth factor (HGF) and its receptor c-Met as dihexa's target, were retracted in April 2025. The company that licensed dihexa, Athira Pharma, told the SEC it dropped dihexa itself because it lacked the properties needed for a usable drug.
The closest thing to human data comes from fosgonimeton (ATH-1017), an injectable prodrug that Athira's own SEC filing says breaks down into dihexa in plasma. Fosgonimeton missed its primary endpoint in a 77-person Phase 2 trial in 2022 and in a Phase 2/3 trial in mild-to-moderate Alzheimer's in 2024, whose primary analysis covered 287 people. Nobody has published a human study of dihexa as it is sold online, swallowed or applied to the skin.
What it binds to, and what happens inside the body after that, step by step.
The proposed mechanism is that dihexa binds hepatocyte growth factor and helps it switch on its receptor, c-Met, at HGF levels too low to act alone. c-Met signaling in the hippocampus drives the growth of dendritic spines and new synapses. The paper that made this case was retracted in 2025, so the mechanism is a hypothesis carried forward by Athira's later, independent fosgonimeton work rather than a settled finding.
Human results and animal results are kept apart below. A result in rats tells you a mechanism is plausible. It does not tell you what happens in a person.
Every published efficacy result for dihexa itself comes from rats, mice and cell culture, mostly from one lab, and three of that lab's four flagged papers have been retracted. The only human data are from fosgonimeton, a prodrug that converts to dihexa: it was well tolerated in a Phase 1 study but did not beat placebo on cognition or daily function in two randomized Alzheimer's trials.
287 adults with mild-to-moderate Alzheimer's (primary analysis), 549 dosed overall; fosgonimeton is a prodrug of dihexa
Daily subcutaneous fosgonimeton did not beat placebo at 26 weeks on the primary composite score (difference -0.08, p = 0.70), ADAS-Cog11 or ADCS-ADL23; 14.2% stopped for side effects vs 4.6% on placebo, mostly injection-site reactions.
Read the study77 adults with mild-to-moderate Alzheimer's, 26 weeks of daily subcutaneous ATH-1017 or placebo
Sponsor-reported topline (no peer-reviewed paper): the primary P300 brainwave latency change was not significant, and ADAS-Cog11 and ADCS-ADL23 were not significant at 26 weeks. A cognitive gain appeared only in a post hoc subgroup not taking cholinesterase inhibitors.
Read the study88 people: 48 healthy young men, 29 healthy older adults, 11 people with Alzheimer's
Single doses and 9 days of daily dosing were well tolerated across the tested range; P300 latency moved toward normal in a 7 vs 4 person Alzheimer's subgroup (p = 0.027).
Read the studyRats (scopolamine amnesia and aged models) plus cultured hippocampal neurons
Dihexa, given orally, reversed water-maze deficits and increased synapse formation; the paper carries a 2021 journal expression of concern over possible image manipulation.
Read the studyRats and cultured neurons
Proposed that dihexa works by binding HGF and activating c-Met. RETRACTED by the journal in April 2025; do not rely on it.
Read the studyAPP/PS1 Alzheimer's model mice (independent lab in China)
Oral dihexa improved water-maze performance, lowered IL-1 beta and TNF-alpha and raised IL-10; blocking PI3K reversed the effects.
Read the study40 male Wistar rats, toxin model of Huntington's disease
Dihexa (PNB-0408) did not protect against the weight, memory or motor damage caused by 3-NP.
Read the studyThese are questions the published research has not answered.
No product containing Dihexa is approved as a medicine by the FDA.
No approval anywhere and no registered clinical trial of dihexa itself on ClinicalTrials.gov. Its prodrug fosgonimeton (ATH-1017) reached Phase 2/3 for Alzheimer's disease and failed; Athira paused fosgonimeton after the 2024 readout. Dihexa is not named on the WADA list. Its proposed action, boosting hepatocyte growth factor (HGF) signaling, matches WADA class S2.3, which names HGF and growth factor modulators; if S2.3 did not apply, it would fall under S0 (non-approved substances). Either way it is banned at all times.
No human half-life has been published for Dihexa, so we do not draw a clearance curve. Half-lives quoted online for it are usually estimates from animal data.
No human study or approved label has published a dose for Dihexa, so there is no table to show.
No dose of Dihexa has been tested in a published human study or approved on a label. Numbers that circulate online come from animal studies scaled up by guesswork or from sellers. We do not reproduce them.
Which symptoms are expected and which mean stop and get help: side effects and red flags.
Tap a claim to see what the studies found.
The figure traces back to a cell-culture comparison from the original lab, not a measure of effect in a living brain. That lab's papers drew expressions of concern, and the mechanism paper was retracted in 2025. No human study has compared dihexa to anything.
The reversal was in rats and mice. When a prodrug that turns into dihexa was tested in 287 people with Alzheimer's, it did not beat placebo on cognition or daily function.
FDA says it has found no human exposure data for dihexa acetate. The prodrug was tolerated over 26 weeks in trials, but that is a different molecule given by injection, not oral or topical dihexa.
Athira's own SEC filing describes fosgonimeton as a prodrug that metabolizes rapidly into dihexa in plasma, so the trials did expose people to dihexa. The dose and route differ from what is sold online, so the failure is not a perfect test of oral dihexa, but it is the best human evidence available.
These pairings come up often. Almost none have been tested together in a trial, and the evidence note on each says so plainly.
No published stability data exist for the research-grade powder. Research suppliers generally ship it as a freeze-dried powder and list frozen storage (-20 C), dry and away from light; none of this has been independently verified.
No published stability data exist for a reconstituted solution. The usual lab practice for small peptides is refrigeration at 2-8 C and short use windows, but no study has tested how long this compound stays intact once mixed.
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