Dihexa (N-hexanoic-Tyr-Ile-(6) aminohexanoic amide) is a synthetic peptide derived from angiotensin IV that acts as an extremely potent nootropic compound. Published research from Washington State University demonstrated Dihexa is approximately 10 million times more potent than BDNF at promoting hepatocyte growth factor (HGF) signaling, which drives synaptogenesis (new synapse formation) in the hippocampus. It crosses the blood-brain barrier and enhances cognitive function through HGF/c-Met receptor pathway activation.
Quick Start
Route
SubQ
Start low
0.5-1 mg SubQ
Frequency
Daily
Timing
No data
Morning dosing preferred for cognitive effects during the day. No fasting required. Very potent - start with lowest dose.
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Start here. Every protocol below is ordered lowest-first. Begin at the smallest effective dose, hold about a week to assess tolerance, and step up only if needed.
Tiered Protocols · lowest first
Conservative start
0.5-1 mg · SubQ · Daily
conservative starter
0.5-1 mg
Daily
Expert
Synaptogenic Protocol (Oral capsule)
10-20 mg · Oral · Weekly
animal study · McCoy/Harding et al. 2012 (J Pharmacol Exp Ther 344:141-54)
Long half-life means dosing 1-2x weekly is sufficient. Can be taken orally or applied topically in a DMSO solution. No human trial has been conducted. This dose is extrapolated from animal research and has not been tested for safety or effect in people. This is the ORAL capsule dose and is not an injection dose. Oral peptide absorption is poor, so this figure is far higher than the injectable protocol on purpose. Do not inject this amount.
10-20 mg
Weekly
Reconstitution CalculatorU-100
050100u
Draw to
— units
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01
How it works
Dihexa stabilizes hepatocyte growth factor (HGF) at the c-Met receptor, preventing HGF degradation by hepatocyte growth factor activator inhibitor-1 (HAI-1). This prolongs HGF/c-Met signaling which drives synaptogenesis, dendritic spine formation, and neural connectivity in the hippocampus. The extraordinary potency (10 million times BDNF) comes from this stabilization mechanism rather than direct receptor activation.
02
What to expect
Early
Days 1–7
Days 1-7: Possible subtle cognitive improvements.
Mid
Weeks 2–4
Weeks 2-4: Synaptogenesis effects accumulate.
Later
Weeks 4–12
Weeks 4-8: Full cognitive enhancement.
03
Evidence
HumanNo published trials
AnimalPresent
In-vitroPresent
Each reference below was re-fetched from its PubMed record, and the quoted sentence was
confirmed to appear in that abstract and to support the claim it sits under. Follow any of
them to read the source.
Dihexa binds HGF with high affinity, promotes c-Met phosphorylation with subthreshold HGF, and induces synaptogenesis preclinically.
Here, we demonstrate that dihexa binds with high affinity to hepatocyte growth factor (HGF) and both dihexa and its parent compound Norleucine 1-AngIV (Nle(1)-AngIV) induce c-Met phosphorylation in the presence of subthreshold concentrations of HGF and augment HGF-dependent cell scattering.
Evidence scope. Exact molecule, but preclinical; does not establish human efficacy, the page’s HAI-1 claim, or the 10-million-times-BDNF comparison.
Claims we could not support
No abstract we checked supports these for this molecule at this route. That is not the
same as saying they are false — it marks where the evidence is missing.
Quick-start dose/route: 0.5-1 mg SubQ daily. No checked abstract administered Dihexa subcutaneously in humans; located exact-molecule work used oral animals or in-vitro systems.
Detailed mechanism: prevention of HGF degradation by HAI-1 and 10-million-fold BDNF potency. The selected abstract supports HGF binding/c-Met dependence but not these added claims.
Primary safety: theoretical cancer promotion through c-Met. No abstract directly evaluated Dihexa carcinogenic risk at the regimen. Fosgonimeton PMID 35180125 is a different molecule.
04
The honest take
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10 million times more potent than BDNF
Published research claim. Refers to HGF stabilization potency at c-Met receptor, not direct comparison of nootropic effects. The potency comparison is mechanistic, not clinical.
05
Interactions & stacking
Two different questions: what is documented about running these together, and what is documented about drawing them into the same syringe. A good pharmacological partner can still have to be pinned separately.
Documented together
BPC-157Non-overlapping
SS-31Cognitive + mitochondrial
HumaninCognitive + neuroprotection
P-21Both nootropic, different mechanisms
Keep separate
CJC-1295 with DACDAC maleimide.
Check any specific pair in the Stack & Interaction Checker, which answers both questions separately. Absence of a documented conflict is not evidence of safety.
06
Side effects & safety
Commonly reported
Limited data
Generally reported as well tolerated
Less common & notes
HGF/c-Met pathway is involved in cancer biology (c-Met is a proto-oncogene).
Theoretical concern about promoting cancer cell growth.
Not studied long-term.
Use with caution.
07
Pharmacokinetics
Illustrative plasma concentration · 9 h
Half-life
2h
Peak · Tmax
0.5h
Elimination
10h
Bioavailability
~100%
SubQ
Duration of action
12-24 hours
HGF/c-Met signaling and synaptogenesis effects persist beyond plasma clearance