The rigorous clinical debunk of the "boost brain growth factors" idea — with a data-fraud scandal attached. Fosgonimeton finishes a story the register started at Dihexa (#44): it targets the same HGF/c-Met pathway, but unlike Dihexa (retracted for fabrication), it was actually taken to Phase 2/3 in
Fosgonimeton (ATH-1017) is a small-molecule positive modulator of the HGF/MET system — the growth-factor pathway that's reduced in the Alzheimer's brain — developed by Athira Pharma as a once-daily injection for Alzheimer's. It matters to this register because it completes the story begun at Dihexa (#44): both target the same HGF/c-Met "brain growth factor" axis, but where Dihexa collapsed under retracted, fabricated data, fosgonimeton was taken all the way to a pivotal Phase 2/3 trial (LIFT-AD) — and honestly failed, missing its primary and key secondary endpoints (cognition and function no better than placebo). That's the rigorous debunk of the "enhance growth-factor signaling to treat neurodegeneration" hypothesis. The drama runs deeper: Athira's founding science was already tainted by a data-manipulation scandal (its CEO ousted over altered images) and an activist proxy fight, and after the failure the company clung to post-hoc subgroups while executives spun the miss as "encouraging." The honest read: a safe, well-tolerated drug for a compelling-sounding mechanism that, tested properly, did not help Alzheimer's patients — a clinical debunk wrapped in a research-integrity cautionary tale. Safety wasn't the problem; efficacy was.
not approved for any indication; its lead Alzheimer's program failed Phase 2/3 (2024). Investigational; the pathway continues only in a separate ALS candidate (ATH-1105).
An honest grade per outcome — drawn from the evidence, not any catalogue. Hype and undemonstrated marketing claims grade low.
A credentialed reviewer (PharmD / PhD / MD) will be named before this entry is finalised. Until then, treat it as a working draft. Last updated July 2026 (Alzheimer's program failed/effectively discontinued; the HGF/MET pathway continues only via oral ATH-1105 in ALS — the remaining test of whether the mechanism helps any neurodegenerative disease).
Grades reflect the published evidence, not our interest. No dosing, reconstitution, or administration is published for research compounds — that restraint is deliberate.
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