compound
Dihexa
An angiotensin IV analog covered claim by claim: the mouse and rat results that stand, the 2014 mechanism paper that was retracted in 2025, and the 554 participant trial of a drug aimed at the same target.
- Primary sources Registry records and papers are read at the source, not through summaries. Read the methodology
- Every claim graded Each claim about what a compound does carries an evidence tier and a numbered citation. How grades derive
- Sells nothing No cart, no price, and no product page anywhere on this site. Conflict disclosure
- Corrections logged Errors are fixed and recorded in a permanent public log, never edited away. Corrections log
Dihexa is a laboratory molecule that reached the consumer market without passing through a clinic. It was designed at a university from angiotensin IV, a fragment of the hormone system that regulates blood pressure, after that fragment turned out to do something unexpected to memory in rats.
The reason to read carefully here is not that the evidence is thin, though it is. It is that two of the papers underneath it carry publication flags. The 2014 paper that connected the behavioural results to the mechanism dihexa is sold for was retracted in April 2025, and a second paper from the same programme has carried an expression of concern since 2021.
There is also a natural control for the idea. A pharmaceutical company took the same biological target into a 554 participant trial, and that trial has posted its results. What happened there is on this page too, because it is the closest thing to a test of the premise that exists.
| Property | Value | Source |
|---|---|---|
| Category | Synthetic angiotensin IV analog, sold as a research chemical for cognition and memory | PMID 25455861 |
| Also known as | PNB-0408, N-hexanoic-Tyr-Ile-(6) aminohexanoic amide | PMID 23055539 |
| Registered human trials | None. A registry sweep on 23 August 2026 covering the compound name, the code PNB-0408 and the full chemical name returned no record at any phase, in any country | ClinicalTrials.gov, read 23 August 2026 |
| The mechanism paper | Retracted in April 2025, after carrying an expression of concern since September 2021 | Retraction notice, PMID 40312093 |
| The same target, tested properly | Fosgonimeton reached a 554 participant Phase 2/3 in Alzheimer's disease and did not meet its primary endpoint | The fosgonimeton record |
| Approval status | Not an approved drug in any indication. FDA has listed dihexa acetate among bulk substances that may present significant safety risks for compounding, stating it has identified no human exposure data for any route | FDA, read 23 August 2026 |
Not medical advice
This page reports what has been documented about a compound. It is not medical advice, not a diagnosis, not a dosing protocol, and not a recommendation to obtain or use anything described here. Talk to a licensed clinician about anything concerning your health. Read the full disclaimer.
Reviewed against editorial standards Updated
Key takeaways
- A registry sweep covering the compound name, the development code PNB-0408 and the full chemical name returns no registration at any phase, in any country, for any indication. The human record is empty.
- The 2014 paper whose title states that the procognitive and synaptogenic effects depend on the hepatocyte growth factor and c-Met system was retracted in April 2025. It had carried an expression of concern since September 2021. That paper is the published link between the behavioural results and the mechanism the compound is sold for.
- A second paper from the same programme, the 2013 evaluation of the analog series dihexa comes from, still carries an expression of concern as of August 2026.
- What stands after those two are set aside is rodent and cell work. The most cited remaining result is a 2021 study in the APP/PS1 transgenic mouse, which reports recovery of memory through a different pathway from the one in the retracted paper. [Animal] [3]
- The premise has been tested properly by someone else. Fosgonimeton, aimed at the same hepatocyte growth factor and c-Met system, was taken into a 554 participant Phase 2/3 trial in Alzheimer's disease that did not meet its primary endpoint.
- REGISTERED HUMAN TRIALS
- 0
- RETRACTED PAPERS
- 1
- NUMBERED SOURCES
- 12
- EVIDENCE GRADE
- D
Who researches Dihexa?
Two groups arrive here and the record answers them the same way, for different reasons.
The first is reading about cognition or memory, usually after seeing dihexa described as many times more potent than something else. That comparison traces to the analog-evaluation literature from one laboratory, and the publication status of that literature is the first thing this page covers.
The second has already found the mechanism story: angiotensin IV analog, acts on hepatocyte growth factor and c-Met, promotes synapse formation. That story has a specific published foundation, and the section below sets out what happened to it.
What is Dihexa?
Plain-English version: a small synthetic molecule built out of a fragment of a blood-pressure hormone, modified so it survives long enough to reach the brain.
Angiotensin IV is a fragment of the hormone system that regulates blood pressure. In the 1990s that fragment turned out to affect memory in rodents, which is a genuinely surprising result and the reason this line of work started at all.
The problem with angiotensin IV as a starting point is that the body destroys it quickly. A programme at a university built a series of analogs designed to survive longer and to cross into the brain, and dihexa is the one from that series that reached the consumer market [7].
The compound is not a peptide in the ordinary sense of a chain of amino acids of stated length. It is a modified dipeptide with a six-carbon chain at each end, which is what the name describes, and those additions are what make it stable rather than what make it active.
It has never been given to a person in any study on the public record.
N-hexanoic-Tyr-Ile-(6) aminohexanoic amide · Not stated here; the compound is a modified dipeptide rather than a peptide of defined residue count
How strong is the evidence, claim by claim?
Every claim area this compound is discussed for gets a row, including the ones with the weakest support. The tier records what the row rests on, and the last column states what that work can and cannot show. Each tier links to its definition on the methodology page.
| Evidence Area | What Has Been Studied | Evidence Level | What It Can and Cannot Show |
|---|---|---|---|
| Memory and cognition | The claim the compound is sold for. The most cited current result is a 2021 study in the APP/PS1 transgenic mouse, a model engineered to develop amyloid pathology, reporting recovery of memory and implicating PI3K and AKT signalling. Earlier rodent work on the analog series it belongs to reported procognitive effects in rats [3] [8] [11] | [Animal] | Rodent models throughout, and no human has been given the compound in any published study. The APP/PS1 mouse is a model of engineered amyloid pathology rather than of Alzheimer's disease, and a great many compounds have improved memory in it. The pathway that study implicates is not the pathway in the retracted 2014 paper, so the two published accounts of the mechanism do not agree with each other |
| Other neurodegeneration models | A 2024 study of an angiotensin IV analog in rats given 3-nitropropionic acid, a chemical model that produces symptoms resembling Huntington's disease [4] | [Animal] | One rat study in a chemically induced model, and the model is a toxin exposure rather than the genetic disease it stands in for. No registered trial of this compound exists in Huntington's disease or in any other condition |
| Acting through hepatocyte growth factor and c-Met | The mechanism given for the compound almost everywhere it is sold. The published statement of it is a 2014 paper reporting that the procognitive and synaptogenic effects of angiotensin IV-derived peptides depend on activation of the hepatocyte growth factor and c-Met system [1] [2] [9] [10] | [In-vitro] | That paper was retracted in April 2025, after carrying an expression of concern from September 2021. A second paper from the same programme, the 2013 evaluation of the analog series, still carries an expression of concern. What remains for this target is work on other molecules: an unrelated hepatocyte growth factor mimetic protecting hair cells in zebrafish, and laboratory work using the target to drive stem cell differentiation. Neither is evidence about this compound |
Rolled up, that puts Dihexa at evidence grade D Animals and anecdote . No completed human study of this compound for any use. The claim set is animal, in-vitro, and anecdote. A grade describes the quality of the research, not whether something works and not whether anyone should use it. The derivation is published.
How Dihexa is thought to work
Writing a mechanism section for this compound means describing the state of the published account rather than the account itself, because the paper that established it has been withdrawn from the record.
1. Where the molecule comes from, a piece of a blood-pressure hormone that turned out to affect memory in rats (established as the design origin)
Angiotensin IV affects memory in rodents. That observation is old, it is not in dispute, and it is the reason a medicinal chemistry programme existed at all. The analogs were built to keep that property while surviving long enough to be useful.
What the origin does not supply is a mechanism. Knowing that a hormone fragment does something to a rat's memory does not say through what, and the answer offered for these analogs is the part of the record that has changed. [Animal] [2] [7]
2. The mechanism account, and what happened to it, the published explanation for the mechanism was withdrawn from the scientific record (retracted)
The account given wherever this compound is sold is that it acts on the hepatocyte growth factor and c-Met system to promote the formation of new synapses. The published statement of that is a 2014 paper in the Journal of Pharmacology and Experimental Therapeutics whose title is the claim itself.
That paper carried an expression of concern from September 2021 and was retracted in April 2025. The retraction notice is on the record with its own identifier. This site did not obtain the reason given for the retraction: the notice carries no abstract in PubMed and the publisher's page did not return a document, so the reason is not stated here and should not be inferred.
What matters for a reader is narrower than any question about how it happened. A retracted paper is removed from the body of published evidence. The mechanism sentence that appears on every page selling this compound no longer has the published source it was resting on. [In-vitro] [1] [9]
3. The second flagged paper, the study that ranked the analog series also carries a warning notice (under an expression of concern)
The 2013 paper evaluating the metabolically stabilised angiotensin IV analogs is the source for how the members of this series compare with one another, which is where potency comparisons for dihexa come from. It carries an expression of concern published in September 2021 and, as read on 23 August 2026, that notice still stands.
An expression of concern is not a retraction. It is the record saying that a question has been raised and not yet resolved. Both notices are stated here with their dates so a reader can check the current status rather than take this page's word for it. [In-vitro] [2]
What we do not know
Why the retraction was issued. The notice carries no abstract in PubMed and the publisher page did not return a document.
Whether the expression of concern on the 2013 analog evaluation has since been resolved. It still stood on 23 August 2026.
How the compound behaves in a person, at any amount, by any route. Nothing on the public record addresses this.
Whether the pathway reported in the 2021 mouse study and the pathway in the retracted paper describe the same thing. They are different pathways and the literature does not reconcile them.
What this evidence can and cannot show
These results come from Rat and mouse for the behavioural work, cell culture for the target work. in APP/PS1 transgenic mouse, 3-nitropropionic acid rat model, human pluripotent stem cell culture., not from people. An animal model is a deliberate simplification: the injury is created on purpose, the animal is young and healthy, the dose is scaled to body weight in a way that does not translate directly, and the outcome is measured at a fixed point rather than lived with. Cell and tissue work is a further step removed, because the concentrations that produce an effect in a dish are often far above anything a body reaches. Mechanism is a reason to run a trial. It is not a substitute for one, and compounds that looked mechanistically convincing have failed in people many times.
Has Dihexa been tested in humans?
There is nothing in this section, and that is the finding rather than a gap in the research behind this page.
A registry sweep on 23 August 2026 queried the compound name, the development code PNB-0408 and the full chemical name, across both the intervention and free-text fields of ClinicalTrials.gov. It returned no record. The table below lists what a reader is most likely to be shown instead.
| Study | People | What was done | Result | Evidence level |
|---|---|---|---|---|
| Dihexa itself | None | No registered trial at any phase, in any country, for any indication | There is no human record | [Anecdote] |
| Fosgonimeton trials | 554 in the largest | A different molecule aimed at the same hepatocyte growth factor and c-Met system, developed by a company | Covered on its own page. The Phase 2/3 did not meet its primary endpoint | [Human RCT] |
| The rodent literature | None | Rats and mice, including the APP/PS1 model | Reported in the claims table above | [Animal] |
Why we are not calling this proof
A trial belonging to another molecule is not evidence about this one, however closely the two are related. That distinction is the same one that runs through the TB-500 and thymosin beta-4 pages on this site, and it applies here with the direction reversed: there, the parent had the trials and the fragment was sold. Here, the properly developed drug had the trials and the research chemical is sold.
The absence of any registration is worth reading plainly. It does not mean the compound was tested and failed. It means nobody has taken it into a registered study, so nothing is known about what it does in a person.
Benefits: what the research shows
The claims table above holds what is claimed and what sits behind each claim. This section is the shape of the whole record rather than a second pass over the same rows.
The honest bottom line on benefits
Three things have to be held at once. The rodent work is real and some of it is recent. The published mechanism connecting that work to what the compound is sold for has been retracted, and a second paper from the same programme is flagged. And the one properly conducted test of the same biological premise, in a different molecule, did not meet its primary endpoint in 554 people.
None of that establishes that the compound does nothing. It establishes that there is no published basis on which anyone can say what it does in a person, and that the strongest available test of the underlying idea came back negative.
How long Dihexa stays in the body
The analog series this compound belongs to was designed for metabolic stability and brain penetration, and the 2013 paper that evaluated the series on those properties is the one carrying an expression of concern. That is an awkward position for a pharmacokinetics section and it is stated rather than worked around.
No human pharmacokinetic study of this compound has been published, because no human study of any kind has been published. There is no half-life in a person, no exposure figure, and no route comparison, and any such number presented elsewhere did not come from a study of people.
No human pharmacokinetic data exists. [Animal] [2] [7]
What is documented about dosing
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
Commonly cited protocols (extrapolated, not validated)
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
| Study | What was given | Frequency | Duration | Notes |
|---|---|---|---|---|
| Rodent behavioural studies | Amounts stated per kilogram of animal body weight in the source papers | As described in each study | As described in each study | Rats and mice. Two of the papers underpinning this literature carry publication flags, covered on the hub |
| Any human use | Nothing documented | Nothing documented | Nothing documented | No registered or published human study exists for this compound |
Commonly cited protocols (extrapolated, not validated) circulate for this compound in milligram amounts taken by mouth or under the tongue. They do not come from a study. There is no human study of this compound from which a figure could come.
Body-weight scaling from a rodent to a person is unreliable even between two species dosed by the same route with a well characterised drug. Here there is no human route, no human exposure measurement, and no pharmacokinetic bridge of any kind, so there is nothing to scale and nothing to scale it with.
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
Main routes people compare, and what each source class actually reported, are set out on the documented protocols page.
Reported effects and what has been measured
What has been measured
Safety observations for this compound come from rodent studies that were designed to measure behaviour rather than to characterise safety. They report what the animals did over the study period.
There is no human safety data of any kind. No registered trial has been run, so no adverse event reporting exists, no dose-limiting toxicity has been established, and no exposure duration has been assessed. [Animal] [3] [4]
What the target itself raises
The hepatocyte growth factor and c-Met system is used in laboratories to drive cells to divide and to change type, and it is a system with a substantial cancer literature attached to it for that reason.
This page does not assert a risk, because no study of this compound has looked. It records that the target is one where the question of unwanted growth is a standard question to ask, and that nothing on the public record answers it here. [In-vitro] [5] [6]
What has been measured about Dihexa, and what has never been studied
Talk to a licensed clinician about anything concerning your health.
Sourcing and quality
What a credible product should show
Nothing sold under this name has been through the identity work that a developed drug goes through. The compound has no regulatory file, no pharmacopoeial monograph and no approved reference standard, so there is no authority a certificate can be checked against.
The molecule is a modified dipeptide rather than a straightforward peptide chain, which makes identity harder to confirm than for a compound whose sequence can be read off a mass spectrum.
Red flags
The mechanism sentence given without its publication status. The paper stating that the effects depend on hepatocyte growth factor and c-Met was retracted in April 2025.
Potency comparisons within the analog series presented without noting that the 2013 paper they come from carries an expression of concern.
Fosgonimeton's trials cited as though they were this compound's. They belong to a different molecule and the Phase 2/3 did not meet its primary endpoint.
Any dosing figure at all. There is no human study to derive one from.
Will it show on a drug test?
This compound is not named on the WADA 2026 Prohibited List by name. That is not a clearance: the growth-factor class at S2.3 closes with a catch-all covering other growth factors and growth factor modulators affecting regenerative capacity and related processes, and this site has not established how that catch-all applies here.
An athlete should treat the absence of a name on a list as an open question rather than an answer, and take it to the relevant anti-doping authority.
Storage
No storage guidance is given here. Storage conditions belong to a characterised formulation and no characterised formulation of this compound exists.
Regulatory status, as of 23 August 2026
| Body | Position | Date | Document |
|---|---|---|---|
| No agency | Not an approved drug in any indication, anywhere | Read 23 August 2026 | ClinicalTrials.gov and the absence of any regulatory file |
| FDA | Dihexa acetate is listed among bulk drug substances for use in compounding that may present significant safety risks. The agency states it has identified no human exposure data for the substance by any route, and lacks important information regarding any safety issues it raises, including whether it would cause harm if administered to humans | Page content current as of 22 April 2026, read 23 August 2026 | FDA human drug compounding, category 2 list |
| ClinicalTrials.gov | No registration at any phase under the compound name, the code PNB-0408, or the full chemical name | Swept 23 August 2026 | ClinicalTrials.gov v2 API |
| J Pharmacol Exp Ther | Retraction of the 2014 mechanism paper | April 2025 | Retraction notice, PMID 40312093 |
| J Pharmacol Exp Ther | Expression of concern standing on the 2013 analog evaluation | September 2021, still standing 23 August 2026 | J Pharmacol Exp Ther 2021;378(3):313 |
There is one agency position on this compound and it is a statement about missing information. FDA lists dihexa acetate among bulk drug substances for use in compounding that may present significant safety risks, and its stated reasoning is that it has identified no human exposure data on drug products containing it by any route, and that it lacks important information regarding any safety issues raised by it, including whether it would cause harm if administered to humans. Beyond that, the compound has not been submitted for approval and is not the subject of an investigational application on the public record.
The two entries above that are dated and checkable are publication actions rather than regulatory ones. They are listed in this section because they are the formal, dated record of what has happened to the evidence, and because a reader looking for the status of this compound will find nothing else of the kind.
This section is dated and re-checked on review. It records actions and their documents, not evidence about an effect, and carries no evidence tier for that reason.
Dihexa compared with other cognitive peptides
| Compound | Evidence grade | What the human record covers | Read more |
|---|---|---|---|
| Fosgonimeton | Graded on its own page | The same biological target developed as a drug: six registrations, a 554 participant Phase 2/3 that did not meet its primary endpoint, and posted results | /peptides/fosgonimeton/ |
| Angiotensin IV | Not covered as a compound on this site | The hormone fragment this molecule was designed from. Its rodent memory literature is the origin of the whole programme | Described in the mechanism section above |
| Semax and selank | Graded on the cognitive group page | The other compounds sold for cognition covered by this site, with separate and unrelated evidence bases | /peptides/groups/cognitive/ |
The comparison that matters is with fosgonimeton, because it is the only case where the underlying idea has been tested to a standard that could settle anything.
That test is the reason this pair is covered together. A research chemical and a clinical candidate aimed at the same system give a reader something rare: a way to see what happens when the premise is examined properly.
What Dihexa typically costs
Frequently asked questions
Has dihexa been tested in humans?
No. A registry sweep on 23 August 2026 covering the compound name, the development code PNB-0408 and the full chemical name found no registration at any phase, in any country, for any indication.
What happened to the mechanism paper?
The 2014 paper reporting that the procognitive and synaptogenic effects depend on the hepatocyte growth factor and c-Met system was retracted in April 2025. It had carried an expression of concern since September 2021.
Why was it retracted?
This site did not establish the reason. The retraction notice carries no abstract in PubMed and the publisher's page did not return a document, so no reason is stated here and none should be inferred from the fact of the retraction.
Is the retraction the only publication flag?
No. The 2013 paper evaluating the analog series this compound belongs to carries a separate expression of concern published in September 2021, which still stood when this page was reviewed.
Does any evidence for it still stand?
Rodent and cell work does. The most cited current result is a 2021 study in the APP/PS1 transgenic mouse reporting memory recovery, and there is a 2024 rat study in a chemical model of Huntington's disease.
What is fosgonimeton and why is it on this page?
It is a drug developed by a company against the same hepatocyte growth factor and c-Met system. It is here because it is the only case where the underlying idea has been tested at scale: a 554 participant Phase 2/3 in Alzheimer's disease that did not meet its primary endpoint.
Does the fosgonimeton result settle anything about dihexa?
Not directly. The two are different molecules and a trial of one is not a trial of the other. It does mean the strongest properly conducted test of the shared premise came back negative, which is the most relevant evidence that exists.
Is there a dose?
No amount has been established for a person, and there is no human study from which one could be derived.
Is it banned in sport?
It is not named on the WADA 2026 Prohibited List. That is not a clearance, because the growth-factor class closes with a catch-all this site has not established the application of. An athlete should take the question to the relevant anti-doping authority.
Is it legal to buy?
This site does not characterise legality in general terms. What is on the record is that no agency has approved it, no agency has evaluated it, and it is sold as a research chemical rather than as a medicine.
Why does this page exist if the evidence is this thin?
Because the thinness is the finding, and because a reader searching this compound will otherwise find the mechanism sentence without its publication status and the fosgonimeton trials attributed to the wrong molecule.
References
- Benoist CC, Kawas LH, Zhu M, Tyson KA, Stillmaker L, Appleyard SM, Wright JW, Wayman GA, Harding JW. The procognitive and synaptogenic effects of angiotensin IV-derived peptides are dependent on activation of the hepatocyte growth factor/c-met system. J Pharmacol Exp Ther. 2014. PMID 25187433 DOI 10.1124/jpet.114.218735 Retracted April 2025 (retraction notice PMID 40312093); carried an Expression of Concern from September 2021 (J Pharmacol Exp Ther 2021;378(3):311). Cited here as the record of what was claimed and what happened to it, not as evidence.
- McCoy AT, Benoist CC, Wright JW, Kawas LH, Bule-Ghogare JM, Zhu M, Appleyard SM, Wayman GA, Harding JW. Evaluation of metabolically stabilized angiotensin IV analogs as procognitive/antidementia agents. J Pharmacol Exp Ther. 2013. PMID 23055539 DOI 10.1124/jpet.112.199497 Carries an Expression of Concern published September 2021 (J Pharmacol Exp Ther 2021;378(3):313), still standing as read on 23 August 2026.
- Sun X, Deng Y, Fu X, Wang S, Duan R, Zhang Y. AngIV-Analog Dihexa Rescues Cognitive Impairment and Recovers Memory in the APP/PS1 Mouse via the PI3K/AKT Signaling Pathway. Brain Sci. 2021. PMID 34827486
- Wells RG, Azzam AF, Hiller AL, Sardinia MF. Effects of an Angiotensin IV Analog on 3-Nitropropionic Acid-Induced Huntington's Disease-Like Symptoms in Rats. J Huntingtons Dis. 2024. PMID 38489193
- Siller R, Greenhough S, Naumovska E, Sullivan GJ. Small-molecule-driven hepatocyte differentiation of human pluripotent stem cells. Stem Cell Reports. 2015. PMID 25937370
- Mathapati S, Siller R, Impellizzeri AA, Lycke M, Vegheim K, Almaas R, Sullivan GJ. Small-Molecule-Directed Hepatocyte-Like Cell Differentiation of Human Pluripotent Stem Cells. Curr Protoc Stem Cell Biol. 2016. PMID 27532814
- Wright JW, Kawas LH, Harding JW. The development of small molecule angiotensin IV analogs to treat Alzheimer's and Parkinson's diseases. Prog Neurobiol. 2015. PMID 25455861 A review by the originating group.
- Ho JK, Nation DA. Cognitive benefits of angiotensin IV and angiotensin-(1-7): A systematic review of experimental studies. Neurosci Biobehav Rev. 2018. PMID 29733881
- Wright JW, Harding JW. The Brain Hepatocyte Growth Factor/c-Met Receptor System: A New Target for the Treatment of Alzheimer's Disease. J Alzheimers Dis. 2015. PMID 25649658 A review by the originating group.
- Benoist CC, Kawas LH, Zhu M, Tyson KA, Stillmaker L, Appleyard SM, Wright JW, Wayman GA, Harding JW. Retraction notice to "The Procognitive and Synaptogenic Effects of Angiotensin IV-Derived Peptides Are Dependent on Activation of the Hepatocyte Growth Factor/c-Met System" [J Pharmacol Exp Ther 351 (2014) 390-402]. J Pharmacol Exp Ther. 2025. PMID 40312093 DOI 10.1016/j.jpet.2025.103567 Read via PubMed on 23 August 2026; the notice carries no abstract there and the publisher page did not return a document, so the stated reason for the retraction was not obtained.
- ClinicalTrials.gov. Registry sweep for dihexa, PNB-0408 and N-hexanoic-Tyr-Ile-(6) aminohexanoic amide across the intervention and free-text fields, run through the v2 API on 23 August 2026. No record returned at any phase, in any country, for any indication. ClinicalTrials.gov. 2026. ClinicalTrials.gov
- US Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. The category 2 table carries the row Dihexa acetate, reading: FDA has not identified any human exposure data on drug products containing dihexa acetate administered via any route of administration; FDA lacks important information regarding any safety issues raised by dihexa acetate, including whether it would cause harm if administered to humans. Page content current as of 22 April 2026, fetched with a browser user agent and read on 23 August 2026. Appended on 2026-08-23, when this page's regulatory section was corrected: it had stated that no agency had evaluated this compound. FDA human drug compounding. 2026. FDA category 2 list