Dihexa
PNB-0408 / N-hexanoic-Tyr-Ile-(6) aminohexanoic amide
Estimated 7 million times more potent than BDNF at forming new synaptic connections in animal models. Developed at Washington State University for dementia research. Significant cancer concern via MET oncogene.
Mechanism of action
Activates hepatocyte growth factor HGF and MET receptor system which drives synaptogenesis — the formation of new synaptic connections. Estimated 7 million fold more potent than BDNF in rat models for new synapse formation. Different mechanism from all other cognitive peptides.
Effects in the body
Dihexa emerged from Washington State University research specifically targeting cognitive decline and dementia. The synaptogenesis mechanism — building new neural connections — is mechanistically distinct from neuroprotection or BDNF elevation approaches. The extraordinary potency claim comes from animal data.
Pros & cons (from the literature)
- Potentially revolutionary synaptogenesis mechanism
- More potent than BDNF in animal models
- Oral bioavailability — unique among cognitive peptides
- Active dementia research interest at academic institutions
- Human data extremely limited
- Extraordinary potency means small dosing errors significant
- RUO status not compoundable
- Cancer concern from HGF/MET activation — MET is a known oncogene
- Very new with minimal long-term data
Protocol summary (from published research)
Dosing ranges reproduced from published research literature. Not a prescription, not medical advice.
FDA & regulatory status
Evidence base
McCoy et al. WSU published key animal data. No human trials. Mechanism compelling but significant safety unknowns prevent clinical advancement currently.
Primary research sources
Peer-reviewed literature referenced throughout this profile is drawn from PubMed, Cell Metabolism, and clinical trial registries cited in the evidence base above.