Dihexa
A compound derived from angiotensin IV, reported to be extremely potent at enhancing memory and brain plasticity in animal studies. One of the most discussed nootropic compounds for memory enhancement. Works through a different pathway than typical brain drugs — the HGF/c-Met system rather than traditional neurotransmitter pathways.
Dosage
User-reported: 10-40 mg oral or sublingual daily (no clinical protocol)
Dosages shown are for research reference only. Always consult a qualified healthcare provider.
Administration
Oral, sublingual, or intranasal (no established route)
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Effects
Cognitive Enhancement
Reported 10 million times more potent than BDNF for synaptic connectivity in vitro.
Dendritic Spine Growth
HGF/c-Met pathway activation promotes new synaptic connections.
Mechanism of Action
Dihexa (N-hexanoic-Tyr-Ile-(6) aminohexanoic amide) is a modified hexapeptide derivative of angiotensin IV developed at Washington State University by Dr. Joseph Harding's laboratory. It was designed to mimic the cognitive-enhancing effects of angiotensin IV and its analogue Nle1-AngIV (DIIIA), which had shown procognitive properties but required central administration. Dihexa was engineered with metabolic stability modifications (hexanoic acid modifications at both termini) for oral bioavailability and blood-brain barrier penetration.
Dihexa's mechanism centers on the hepatocyte growth factor (HGF)/c-Met receptor system, which plays a critical role in brain development, neuroplasticity, and neuroprotection. Dihexa acts as an allosteric modulator and potentiator of HGF signaling — it facilitates HGF dimerization and binding to the c-Met receptor tyrosine kinase, amplifying the downstream signaling cascade. Activated c-Met triggers the PI3K/Akt pathway (neuronal survival), the Ras/MAPK/ERK pathway (synaptic plasticity and gene expression), and the Rac1/Cdc42 pathway (cytoskeletal remodeling for dendritic spine formation).
The cognitive effects stem from enhanced dendritic spine formation and synaptic connectivity in the hippocampus — the brain region critical for learning and memory. Dendritic spines are the postsynaptic structures where most excitatory synapses form, and their density and morphology are directly correlated with cognitive function. Dihexa treatment in animal models increased spine density, enhanced long-term potentiation (LTP — the cellular correlate of memory formation), and restored cognitive function in models of dementia. The reported potency — up to 10 million times more potent than BDNF in promoting synaptic connectivity in cell culture assays — is striking but should be interpreted cautiously, as in vitro potency does not always translate to in vivo efficacy. The activation of the HGF/c-Met pathway raises theoretical concerns about tumor promotion, as this pathway is frequently co-opted in cancer for metastasis and angiogenesis, and no human safety data exists to evaluate this risk.
Regulatory Status
Not FDA approved. Research chemical status. No human clinical trials completed. Available through research chemical suppliers. Exercise significant caution.
Risks & Safety
Serious
may promote tumor growth and spread via HGF/c-Met pathway, potential blood pressure effects, no human safety data available.
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Research Papers
3Published: December 31, 2025
AI Summary
A broad review explains how various therapeutic peptides—including dihexa—support tissue repair, inflammation control, and nerve recovery in musculoskeletal care. While animal studies look promising, human clinical trials are still lacking.
Published: March 31, 2024
AI Summary
Researchers investigated Dihexa for Huntington's-like symptoms in rats, given its neuroprotective and procognitive effects in Alzheimer's and Parkinson's models. The compound was tested in animals given a mitochondrial toxin that mimics HD pathology.
Published: April 10, 2022
AI Summary
A method was developed to generate liver cells from human stem cells using small molecules instead of expensive growth factors. The approach could enable cheaper, large-scale production for research and therapy.
Frequently Asked Questions
What is Dihexa?
A compound derived from angiotensin IV, reported to be extremely potent at enhancing memory and brain plasticity in animal studies. One of the most discussed nootropic compounds for memory enhancement. Works through a different pathway than typical brain drugs — the HGF/c-Met system rather than traditional neurotransmitter pathways.
What is Dihexa used for?
A compound derived from angiotensin IV, reported to be extremely potent at enhancing memory and brain plasticity in animal studies. One of the most discussed nootropic compounds for memory enhancement. Works through a different pathway than typical brain drugs — the HGF/c-Met system rather than traditional neurotransmitter pathways.
What is the dosage for Dihexa?
Extremely limited human data. User-reported: 10-40 mg oral or sublingual once daily. Some report effects at lower doses. No established clinical dosing protocol. No human clinical trials completed.
What are the side effects of Dihexa?
Serious: may promote tumor growth and spread via HGF/c-Met pathway, potential blood pressure effects, no human safety data available.
How does Dihexa work?
Dihexa (N-hexanoic-Tyr-Ile-(6) aminohexanoic amide) is a modified hexapeptide derivative of angiotensin IV developed at Washington State University by Dr. Joseph Harding's laboratory. It was designed to mimic the cognitive-enhancing effects of angiotensin IV and its analogue Nle1-AngIV (DIIIA), which had shown procognitive properties but required central administration. Dihexa was engineered with metabolic stability modifications (hexanoic acid modifications at both termini) for oral bioavailability and blood-brain barrier penetration. Dihexa's mechanism centers on the hepatocyte growth factor (HGF)/c-Met receptor system, which plays a critical role in brain development, neuroplasticity, and neuroprotection. Dihexa acts as an allosteric modulator and potentiator of HGF signaling — it facilitates HGF dimerization and binding to the c-Met receptor tyrosine kinase, amplifying the downstream signaling cascade. Activated c-Met triggers the PI3K/Akt pathway (neuronal survival), the Ras/MAPK/ERK pathway (synaptic plasticity and gene expression), and the Rac1/Cdc42 pathway (cytoskeletal remodeling for dendritic spine formation). The cognitive effects stem from enhanced dendritic spine formation and synaptic connectivity in the hippocampus — the brain region critical for learning and memory. Dendritic spines are the postsynaptic structures where most excitatory synapses form, and their density and morphology are directly correlated with cognitive function. Dihexa treatment in animal models increased spine density, enhanced long-term potentiation (LTP — the cellular correlate of memory formation), and restored cognitive function in models of dementia. The reported potency — up to 10 million times more potent than BDNF in promoting synaptic connectivity in cell culture assays — is striking but should be interpreted cautiously, as in vitro potency does not always translate to in vivo efficacy. The activation of the HGF/c-Met pathway raises theoretical concerns about tumor promotion, as this pathway is frequently co-opted in cancer for metastasis and angiogenesis, and no human safety data exists to evaluate this risk.
How is Dihexa administered?
Dihexa is administered via oral, sublingual, or intranasal (no established route).
What is the half-life of Dihexa?
The half-life of Dihexa is Estimated several hours (limited pharmacokinetic data).
Is Dihexa legal?
Not FDA approved. Research chemical status. No human clinical trials completed. Available through research chemical suppliers. Exercise significant caution.
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