Is it really seven orders of magnitude stronger than BDNF?

That is the figure from the original laboratory work, measuring synapse formation in cultured neurons. It is a real measurement of a specific effect in a dish. What it means for a person taking a capsule is entirely unknown, and a number that large is a reason to be careful rather than impressed.

What is the cancer concern?

Dihexa works by potentiating signalling through c-Met, which is one of the better-characterised oncogenic receptors: amplified or mutated in several cancers, and the target of approved inhibitors. Amplifying a receptor that oncology drugs are designed to block is a clear mechanistic concern that no study has quantified.

Has anyone studied it in people?

No. Not a trial, not a published case series, not a pharmacokinetic study. Everything known comes from cells and rodents, from essentially one research group.

Anti-aging & longevity

Dihexa

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

PreclinicalReviewed 16 Aug 2026

Dihexa came out of work on angiotensin IV and its effects on memory. It is a modified tripeptide built to survive in the body and cross into the brain, both things the parent molecule does poorly. In animal studies it restores cognitive function in models of dementia and Parkinson's disease.

The number attached to it in every discussion is that it is around seven orders of magnitude more potent than brain-derived neurotrophic factor at promoting new synapse formation. That figure comes from the original laboratory work and it is genuinely remarkable. It is also the reason the page reads the way it does: something that drives synapse formation that powerfully is not obviously a thing you want circulating in an adult brain without knowing what it does.

There is no human data. Not a trial, not a case series, not a pharmacokinetic study. Nothing published at all. What exists is preclinical work from one research group and a patent, and it is sold on the strength of a potency figure rather than any evidence about what happens in a person.

How it works

Dihexa binds hepatocyte growth factor and potentiates its activity at the c-Met receptor. HGF/c-Met signalling drives synapse formation, neuron survival and dendritic growth in the brain, and dihexa amplifies a signal rather than supplying one.

It was engineered from angiotensin IV specifically to be metabolically stable and lipophilic enough to cross the blood–brain barrier. Both properties are essential to the animal results, and both mean any effect is difficult to reverse once dosed.

The reported potency relative to BDNF comes from assays of synapse formation in cultured neurons. It is a laboratory measurement of a specific effect, and translating a number like that into what a dose in a person would do is exactly the step nobody has taken.

HGF and c-Met are not confined to the brain. c-Met is one of the more studied oncogenic receptors. It is amplified or mutated in several cancers, and it is the target of approved cancer drugs designed to block it. A compound whose mechanism is to potentiate that receptor is doing the reverse of what those drugs do, systemically, in someone with no monitoring.

Quick reference

Commonly described dose: 5 mg–20 mg
How often: Once daily, often in short courses
Route: Oral or Topical
Timing: No timing effect established.
Storage once mixed: Refrigerated, 30 days

These describe what sources report, not what you should do. Full detail and provenance in the dosing section below.

Price index

Per-milligram pricing across vendors arrives with the directory. We are recording prices now so the history exists when the page ships.

Vocabulary on this page

Concentration: How much peptide there is in each millilitre of solution, once the vial has been reconstituted.
Evidence level: The category of human evidence behind a compound, from preclinical through to approved. Stated on every profile here as a category, not an adjective.
Peptide: A short chain of amino acids: the same building blocks as a protein, in a chain short enough to behave differently.

The whole glossary →

Regulatory status — United States

Not approved anywhere, and never studied in a published human trial. Developed in academic research with an associated patent; no clinical development programme has reported results. Sold only as a research chemical.

Last reviewed 16 Aug 2026. Regulatory positions in this category change frequently; we date this line so you can see how current it is.

What it is studied for

Each entry states the evidence behind it. We do not rank indications by effectiveness — for most compounds here, that would be a claim nobody can support.

Cognitive impairment and dementia

Published review

What the animal work addressed.

EvidenceRestored performance in rodent models of dementia and Parkinson's disease. Preclinical only — no human study of any kind has been published.

Cognitive enhancement in healthy people

Community practice

Why it is bought.

EvidenceNever studied, in any species, in a healthy state. The animal work is in models of impairment, where restoring a deficit is a different question from improving intact function.

Identity and clearance

Molecule

Class: Modified tripeptide, angiotensin IV analogue and HGF/c-Met potentiator
Molecular weight: 461.6 Da
Length: 3 amino acids

The hexanoic acid modifications are what make it stable and lipophilic enough to reach the brain. Those are the properties the parent molecule lacks.

Dose protocols reported in sources

Displayed for reference only. Every row says where it came from, and a trial protocol and a community convention are not the same kind of information. None of this is fed into the calculator, and none of it is a recommendation.

Dose protocols reported in sources, with the source of each.
Goal	Dose	Frequency	Route	Units, 5 mg vial	Source	Start this protocol
Commonly described community protocol	5 mg – 20 mg	Once daily, often in short courses	Oral5 to 20 mg daily, taken orally or applied transdermally in a carrier. There is no human pharmacokinetic study, so these figures are not scaled from anything. They are conventions that formed in the absence of data.	from 100 u	Community practice	Start this

Start this copies a row into a protocol of your own, which you can then edit. Where a source gave a dose range or an ambiguous frequency, those fields arrive empty — we will not pick a number on your behalf.

CheckRows marked community practice describe what people commonly do, drawn from public discussion. They are not derived from any trial and are not evidence that a dose is safe or effective.

Safety

Reported effects

EverythingCommunity practice
Unknown — no human data exists
Not a formality. No human has been studied on this compound at any dose by any route, so no adverse effect has ever been systematically recorded.
Headache and irritabilityCommunity practice
Anecdotally reported
Unquantified proliferative risk through c-MetPublished review
Mechanistically expected, unmeasured
c-Met is a well-characterised oncogenic receptor, and approved cancer drugs exist specifically to block it. Potentiating it systemically has an obvious theoretical concern that no study has sized.
Consequences of driving synapse formation in an adult brainPublished review
Unknown
Restoring synapses in a damaged brain and adding them to a healthy one are different interventions. Nothing establishes that the second is beneficial, or reversible.

When to stop

Any new neurological symptom: persistent headache, visual change, unusual mood change, confusion or seizure activity. Seek medical assessment.
Any allergic response: rash, hives, facial swelling or difficulty breathing. Seek urgent care.
Any new lump, unexplained weight loss or unexplained persistent pain.
Skin irritation where a transdermal carrier is applied.

Interactions and situations that need care

Active or previous cancerAvoid
c-Met is a recognised oncogenic driver, amplified in several cancers, and pharmaceutical companies have developed approved drugs to inhibit it. This compound potentiates the same receptor. That is the clearest mechanistic contraindication on this site.
Any neurological or psychiatric conditionAvoid
A compound that drives synapse formation in the brain, with no human data and no way to reverse it once dosed, is not something to add to a brain already behaving unpredictably.
Pregnancy and breastfeedingAvoid
HGF/c-Met signalling is central to development. Amplifying it during pregnancy — with no safety data of any kind — is a foreseeable and serious risk.
Anyone under 25Avoid
The brain is still undergoing synaptic pruning and reorganisation into the mid-twenties. Adding a powerful synaptogenic signal to a process that is meant to be removing connections has unpredictable consequences and no data behind it.
Using DMSO as a carrierUse caution
DMSO carries dissolved substances through the skin indiscriminately, including whatever else is on it: lotions, residues, contaminants in the peptide itself. It amplifies the consequences of an impure product rather than only delivering the intended one.

What to expect

HonestlyThere is no human efficacy data for this compound, so there is no evidence-based timeline to give. Any site publishing a week-by-week schedule of expected effects has invented it.

No human data exists. No trial, no pharmacokinetics, no case series. Nothing published at all.
The potency figure is real and it is a laboratory measurement of synapse formation in cultured neurons. It is a reason for caution as much as for interest.
The animal work is in models of impairment. Restoring a deficit and enhancing intact function are different questions, and only the first has been asked.
It potentiates c-Met, a receptor that approved cancer drugs exist to block. Nobody can currently size what that means.
Dose figures are conventions formed in the absence of data, not scaled from any study.

Storage and handling

Freeze-dried powder: Powder refrigerated at 2–8 °C, protected from light and moisture.
After mixing: In a carrier solution, refrigerated and used within weeks. Stability in DMSO or similar carriers has not been characterised.
Long-term, frozen: Powder is stable at −20 °C or colder.

Printable one-pager How to reconstitute a vial, step by step

Checking your vial

Research chemicals carry no manufacturing standard, so what the vial looks like is often the only quality signal available before you use it. More on assessing quality and COAs.

White to off-white powder
Supplied as a powder rather than a lyophilised cake.
Appearance establishes nothing here
There is no visual check that distinguishes dihexa from any other white powder. Third-party testing is the only meaningful verification, and few buyers obtain it.

Questions

Is it really seven orders of magnitude stronger than BDNF?: That is the figure from the original laboratory work, measuring synapse formation in cultured neurons. It is a real measurement of a specific effect in a dish. What it means for a person taking a capsule is entirely unknown, and a number that large is a reason to be careful rather than impressed.
What is the cancer concern?: Dihexa works by potentiating signalling through c-Met, which is one of the better-characterised oncogenic receptors: amplified or mutated in several cancers, and the target of approved inhibitors. Amplifying a receptor that oncology drugs are designed to block is a clear mechanistic concern that no study has quantified.
Has anyone studied it in people?: No. Not a trial, not a published case series, not a pharmacokinetic study. Everything known comes from cells and rodents, from essentially one research group.

References

Dihexa, an angiotensin IV analogue: synaptogenesis and cognitive restoration in animal models
Neuropharmacology and medicinal chemistry literature, 2013 · Animal studies with supporting in vitro work
Rats and cultured neurons
Restored cognitive performance in rodent models of dementia and Parkinson's disease, with synapse formation in cultured neurons reported at concentrations around seven orders of magnitude below BDNF. Mechanism attributed to potentiation of HGF signalling at c-Met.
c-Met as an oncogenic driver and a therapeutic target
Oncology review literature, 2020 · Review
Humans
Documents c-Met amplification and mutation across several cancers and the development of approved inhibitors targeting it, establishing the receptor as one whose signalling oncology seeks to suppress.
Commonly reported community protocols
Bioalmanac editorial summary of public community sources, 2026 · Not a study
Records oral and transdermal dose patterns described in nootropic discussion. No study in any species supports them, and they carry no evidential weight about safety or effect.

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Keep this page honest

If something here is wrong, out of date, or missing a source, tell us and we will fix it and say that we did.

Suggest a correction

This page is educational. It describes what published research reports, not what you should do. Peptides discussed here are largely not approved for human use, and nothing on Bioalmanac is medical advice. No clinician reviews these pages.

Page last updated 16 Aug 2026