Dihexa
Cognitive
In short
- An angiotensin IV analogue reported to be extraordinarily potent at promoting synapse formation — figures of seven orders of magnitude above BDNF appear in the original work.
- It acts by potentiating hepatocyte growth factor signalling through the c-Met receptor.
- No human study of any kind has been conducted.
- The c-Met pathway is a well-established oncogenic driver, which makes the mechanism itself the main safety question.
- Research compound only, never trialled in people.
Structure
How it works
Dihexa (N-hexanoic-Tyr-Ile-(6) aminohexanoic amide) is a small angiotensin IV analogue designed for blood-brain barrier penetration and metabolic stability.
Its described mechanism is potentiation of hepatocyte growth factor binding to its receptor c-Met, amplifying HGF/c-Met signalling. Downstream, this promotes dendritic spine formation and synaptogenesis in hippocampal neurons.
The potency claims in the original literature are striking, and the mechanism is plausible. The same pathway is also one of the most studied oncogenic signalling axes in cancer biology.
What the research shows
Rodent studies report reversal of cognitive deficits in scopolamine-induced and lesion models, and improvement in models of Parkinson disease.
Cell culture work supports the synaptogenic mechanism.
No human data exists at all. Reports of cognitive effects in people are anecdotal.
Dosing in the literature
Figures below are quoted from published studies, with the species or population they were measured in. They are records of what was studied, not recommendations.
| Studied in | Amount | Route | Source |
|---|---|---|---|
| Rat — cognitive deficit reversal models | Reported active in the microgram-per-kilogram range orally | oral | PubMed |
Commonly reported ranges
These are amounts people report using. They are not from any study, have not been evaluated for safety, and are reproduced here only because they circulate widely and are better seen alongside the evidence than instead of it.
| Reported by | Amount | Route |
|---|---|---|
| Commonly reported | 5–20 mg daily, usually in short courses | oral or transdermal |
No published human pharmacokinetic study establishes a dose, interval, or duration for this compound. Community figures below have no trial behind them and are reports of practice, not evidence. Community doses are orders of magnitude above the amounts reported active in rodents, which is a substantial and rarely-noted discrepancy for a compound whose selling point is extreme potency.
Handling and storage
Oral or transdermal in community use. The molecule was designed for oral bioavailability and CNS penetration.
Short courses are the usual described pattern, generally reasoned from the c-Met concern rather than from any study.
Side effects
No human safety data exists. No toxicology has been published.
The substantive concern is mechanistic and specific. c-Met is among the best-characterised oncogenic receptor tyrosine kinases; its dysregulation drives proliferation, invasion, and metastasis across many tumour types, and multiple approved cancer drugs exist specifically to INHIBIT it.
A compound whose mechanism is amplifying c-Met signalling is doing the opposite of what those drugs do. Whether that translates into meaningful risk in a healthy person is unknown — but this is a case where the mechanism itself, not a hypothetical impurity, is the reason for caution.
Combinations
No interaction data. Combining with other growth-factor-modulating compounds (IGF-1 analogues in particular) compounds proliferative signalling from multiple directions.
Research status
Developed by Joseph Harding's group at Washington State University, with published preclinical work on angiotensin IV analogues and the HGF/c-Met mechanism.
The science is legitimate and published. No clinical trial has been registered, and no human has been dosed under study.
Legal status
Not approved anywhere. Sold as a research chemical.
WADA status
Not specifically named on the Prohibited List. Falls under WADA class S0, which prohibits any pharmacological substance not currently approved by any governmental regulatory health authority for human therapeutic use. Treat it as prohibited in sport.
Conclusion
Dihexa has some of the most dramatic potency claims in this library and no human data whatsoever.
The honest framing is that its mechanism — amplifying c-Met signalling — is the same pathway oncology spends considerable effort blocking. That does not make it carcinogenic, and it does mean the caution here is mechanistic rather than generic.
Sources
- [1]Dihexa — angiotensin IV analogue and synaptogenesisPubMed
- [2]Dihexa and HGF/c-Met potentiationPubMed
- [3]c-Met signalling in oncogenesisPubMed
- [4]PubChem CID 129010512PubChem
- [5]WADA Prohibited List (current)WADA
Track your own Dihexa protocol
Peppers logs your doses, models your levels from this half-life, tracks your vials and tells you when you will run out. Free on iPhone.
Reference and educational information only. Not medical advice. Nothing here diagnoses, treats, or prescribes, and nothing here is a recommendation to use any compound. The compounds described are research chemicals and are not approved for human consumption. Legal and anti-doping status change — the review date above is when these claims were last checked. Talk to a qualified clinician about anything you intend to take.