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evidence · mechanism · dose
Experimental/Nootropic / NeurotrophicResearch peptide

Dihexa

aka N-hexanoic-Tyr-Ile-(6) aminohexanoic amide · PNB-0408

Oral angiotensin IV analog with potent synaptogenic effects in preclinical models.

Educational explainer of a research peptide. Profiles in this section deliberately omit clinical-trial citations, dosing protocols, and purchase links. Not FDA-approved as a supplement; not a recommendation to use.

Overview

Dihexa is an orally bioavailable hexapeptide derivative of angiotensin IV designed for blood-brain-barrier penetration and synaptogenic activity.

Source
  • Synthesized in research laboratories
Forms
  • Oral
  • Transdermal (research)

Mechanism of action

Potentiates hepatocyte growth factor (HGF) / c-Met signaling to drive dendritic spine formation and synaptogenesis.

Pathways
  • · HGF/c-Met
  • · Synaptogenesis
  • · Angiotensin IV receptor binding

How it acts on the body

Dihexa was developed at Washington State University specifically to overcome the limitations of angiotensin IV — poor oral availability and rapid breakdown — while keeping the cognitive-enhancing activity seen in models of Alzheimer's disease and stroke.

It is reported to be orders of magnitude more potent than BDNF at promoting dendritic spine formation in cultured neurons, with the c-Met receptor playing the central role. Human data are essentially absent; everything below is preclinical inference.

Hormonal & endocrine impact

How this peptide is reported to shift specific hormones and signaling molecules. Directionality reflects research literature and preclinical models, not clinical prescribing data.

Projected hormonal trajectory
Illustrative curves derived from reported direction of effect. Not measured patient data.

Curves are schematic shapes (sigmoid for increases/decreases, damped oscillation for modulation/stabilization) anchored to a 100% baseline. They communicate direction and tempo of change reported in research literature — not absolute hormone concentrations.

HGF/c-Met signalingIncreases
Potentiates HGF-driven synaptogenesis.
BDNF pathwayModulates
Indirect synergy reported in preclinical work.

Effects on the body

Supports
Synaptogenesis in preclinical models
Supports
Cognitive performance in animal AD models

Organ system effects

Brain & CNS

Hippocampal and cortical synaptic density.

Endocrine

Minimal systemic endocrine effects characterized.

Reported effects

Drawn from preclinical research, anecdote, and small-scale clinical observation. No evidence grades are assigned — most peptides on this page lack rigorous human trials.

  • Oral bioavailability unusual for a peptide
  • Targets a synapse-formation pathway directly

Potential side effects

Common
  • · Limited human data — no profile established
Rare
  • · Headache reported anecdotally
Serious
  • · Theoretical concern: c-Met overactivation in oncology contexts

Drug interactions

No notable interactions reported.

Pairing context

Often combined with
  • Cognitive training
    Activity-dependent synaptic consolidation.
Avoid combining with
  • Active or recent cancer
    c-Met signaling is implicated in several tumor types.
Important. Research peptides described here are not FDA-approved supplements. Supplement Scholar does not endorse, recommend, or link to any source for purchase. Consult a qualified clinician before considering any peptide therapy.