adamax

two real research compounds welded together and sold. the weld has never been measured in any species.

tier D · focus · 0 studies · any species

verdict

does it work: unknown, which is not the same as no. zero published studies of the molecule in any species, zero registered trials in any registry checked, and one sentence in one regulator's submission is the whole official record.

on whether adamax works — nobody has measured it, and that is a specific finding rather than a shrug. no human study, no rat, no mouse, no cell work, no pharmacokinetics, no toxicology on this molecule. eight pubmed query formulations return no record of the peptide, the exact sequence string returns zero in two separate corpora, and three registries return zero while the same sweep returns 42 registered cerebrolysin trials, so the queries work. the bare term returns 39 records and every one is a machine-learning paper about the adamax optimizer. pairing it with peptide returns one more, a blood-glucose forecasting paper containing no peptide, matched through a MeSH expansion. untested is a different verdict from tested and failed, and this compound is the first.

on whether the semax evidence carries over — semax is a different molecule with a real literature, 230 pubmed records and a russian clinical history, including two small placebo-controlled imaging studies in healthy volunteers. none of it was measured on adamax. and the read-across argument has a documented failure inside its own family: P021, the compound the adamantane cap was borrowed from, restored four deficits in cdkl5 knockout cells at 10 micromolar and then failed on neurogenesis, spine maturation, water maze and passive avoidance in the matching mouse, with only the catalepsy bar test restored and the authors calling it limited behavioural benefit. a molecule that cannot carry its own dish result into its own mouse is a poor vehicle for carrying a parent's result to an untested analogue.

on the adamantane cage and brain entry — that is the entire selling point and it is unmeasured in both molecules. the alzheimer's drug discovery foundation's review of P021 states that no study has directly assayed how much P021 reached the brain in mice, and its own fact table lists blood brain barrier as not documented. the 2021 mouse paper that reports P021 as brain-penetrant did so through a commercial permeability assay, and its authors record that brain P021 levels were never measured. for adamax there is no assay of any kind.

on why this isn't F — F is for compounds that are fake, a scam, or actively harmful beyond reasonable doubt. adamax is a coherent molecule that reconciles exactly on paper, and no study anywhere reports harm from it because no study anywhere reports anything. reading a harm finding out of an absence would be inventing a result. the rodent record on the adamantane parent runs the other way: reviewers report up to 18 months of dosing in rodents without weight loss, tumours or the pain behaviour seen with full-length CNTF, and no detectable immune reaction in rats. that record belongs to a different compound and does not transfer, but it removes the basis for an F.

based on published evidence and the public regulatory record. not medical advice.

why D-tier

D-tier, and the placement is clean because there is nothing to weigh. C means early research, mostly preclinical, pointing one way. Preclinical research on Adamax does not exist: eight PubMed query formulations find no record of the peptide, and the 39 records the bare term returns are machine-learning papers about a gradient-descent optimizer. Awarding C would credit this molecule with its parents' rodent work, which is the specific error a tier board exists to prevent. F requires the compound to be fake, a scam, or actively harmful beyond reasonable doubt. It is none of those: the formula reconciles exactly as acetyl-Semax joined to P021's adamantane unit, both parents are genuine research programmes, and no study anywhere reports harm from it because no study anywhere reports anything. What holds it at D rather than lifting it is that the one property the compound is sold on, easier brain entry from the adamantane cage, is unmeasured in Adamax and also unmeasured in P021, per the Alzheimer's Drug Discovery Foundation's own fact table. D on this board usually means thin or conflicting evidence, and Adamax has neither, because it has none. One thing the efficacy pass changes is the framing rather than the letter: the strongest piece of relevant evidence anyone holds, the CDKL5 in vivo failure, runs against the borrowed mechanism rather than for it, and the parent's one PubMed-tagged randomised trial was negative on its objective endpoints. So D is the generous reading here rather than the harsh one. The tier is a floor rather than a description. One published characterisation of the molecule, a synthesis paper with an analytical profile, a rodent pharmacokinetic run, a single measured brain concentration, would move it.

the core tension

The chemistry is exact and the evidence is absent, and those two facts usually do not sit together. Rebuilt from atomic masses, acetyl-Semax joined to P021's own adamantane unit at one amide bond gives C50H69N11O11S at 1032.23, matching the circulating specification to the decimal, and the same construction reproduces P021 at C27H42N6O8 and 578.667. So this is a coherent, reproducible molecule rather than a fiction. The design rationale is the problem. The whole pitch rests on the adamantane cage easing passage into the brain, and that has never been measured even in P021, the molecule the cage was invented for and which carries a rodent programme running since 2010: the Alzheimer's Drug Discovery Foundation states that no study has directly assayed the level of P021 reaching the brain in mice, and its fact table lists blood brain barrier as not documented. A rational design whose central premise is unmeasured in the parent, sold as a finished product on the strength of that premise, is what the D tier is describing.

what it is

Adamax circulates as a designer analogue of Semax, the Russian ACTH(4-7)-Pro-Gly-Pro heptapeptide, carrying the N-terminal acetyl cap and the adamantane-based C-terminal residue found in P021, a ciliary neurotrophic factor peptide from Khalid Iqbal's group at the New York State Institute for Basic Research. The circulating shorthand is Ac-MEHFPGPAG-NH2. No published paper describes its synthesis or characterises it. The compound reaches the public record through vendor catalogues and through a single New Zealand regulatory submission, and the Wikipedia entry that carries its formula cites exactly one reference: that submission.

what it does

Unknown. No published study has measured this molecule in any species. The proposed mechanism is inherited rather than observed. Semax is documented to degrade mainly to the pentapeptide HFPGP and the tripeptide PGP, with its effect on plasma enkephalinases traced to action on aminopeptidases, which is the enzyme class the acetyl cap is theorised to block. P021 carries an adamantylated glycine at the C-terminus, added to increase blood-brain-barrier permeability. Adamax is those two ideas joined at one amide bond, and nobody has looked at what the joined molecule does.

origin

There is no origin paper, no patent and no named developer. A patent search found no filing anywhere claiming Adamax, the sequence Ac-MEHFPGPAG-NH2, or an adamantylated Semax. The adamantane cap is patented on its own molecule, US 8,796,214, assigned to the Research Foundation for Mental Hygiene. Acetylated and amidated Semax is patented by Phoenix Nest for lysosomal storage disease. The specific fusion sits in none of them. Multiple vendor and content sites state that Adamax was created by Ceretropic, a Mexico-based vendor. Every instance located is uncited and the sites recycle each other. No primary trace was reached, so this entry reports it as a widely repeated but unsourced account rather than as history.

why researchers are interested

The pitch is a better Semax. Semax is degraded by aminopeptidases and its human dosing runs in short repeated courses; the adamantane cage is offered as the fix that keeps more of it intact and moves more of it into the brain. The pitch is internally logical, and both halves come from genuine research programmes. That is why it sells. What the pitch does not have is one datapoint from the combined molecule.

does it work

Unknown, and that is the whole answer. Nobody has looked, and every check run against that finding confirms it. Eight PubMed query formulations return no record of the peptide. ClinicalTrials.gov returns zero. The WHO ICTRP portal returns the literal string no results were found for adamax. The EU Clinical Trials Register returns zero. Those zeros were calibrated against a positive control set in the same queries, which returned 42 registered Cerebrolysin trials, 27 for setmelanotide and 5 for davunetide, so the registries do capture unapproved CNS peptides of this class. Unknown is not a soft version of no. Nothing has been measured, so nothing has failed. The distinction matters because the strongest relevant evidence anyone holds runs against the borrowed mechanism rather than for it: P021 restored four deficits in CDKL5 knockout cells and then failed most endpoints in the matching mouse, restoring only catalepsy. Every human number attached to Adamax in marketing copy was measured on Semax, a different molecule with a different mass. That dossier is thinner than the read-across implies and not empty: its three largest human datasets are Russian-language, carry comparison groups and are not described as randomised or placebo-controlled, while two genuinely placebo-controlled studies exist and are small resting-state fMRI biomarker studies in healthy volunteers.

claims vs the data

• an improved semax that gets more peptide into the brain — unverified — No study has measured brain entry, plasma concentration or anything else for Adamax in any species. The claim is inherited from P021, and the Alzheimer's Drug Discovery Foundation's review of P021 states that no study has directly assayed the level that reached the brain in mice, with blood brain barrier listed as not documented in its fact table. The 2021 mouse paper reporting brain penetration used a commercial permeability assay, and its own authors record that brain P021 levels were never measured.
• backed by the semax clinical research — overreach — Semax is a different molecule with a different mass. Its 230 PubMed records and its Russian clinical history belong to it. The three largest human Semax datasets carry comparison groups but none is described as randomised or placebo-controlled in the indexed record, and all three are Russian-language. Placebo-controlled Semax data does exist and should be stated rather than left implied: two resting-state fMRI studies, 24 and 52 healthy volunteers, reporting default-mode-network and amygdala connectivity differences. They are imaging biomarkers in healthy people, not clinical outcomes, and none of it was measured on Adamax.
• the P021 rodent data supports it — overreach — P021 is also a different molecule, and its own read-across has a documented failure. It restored proliferation, survival, neurite length and phospho-GSK3-beta in CDKL5 knockout human cells at 10 micromolar, then produced no effect on neurogenesis, newborn-cell survival, spine maturation, Morris water maze or passive avoidance in the matching knockout mouse, at two doses and two routes. It was not uniformly null: the catalepsy bar test was restored, open field showed a trend, and the paper's own conclusion is limited behavioural benefit rather than none. The same paper states P021 does not raise BDNF in wild-type mouse hippocampus.
• increases BDNF and sensitises hippocampal TrkB receptors — unverified — This wording comes from a chemical seller's catalogue page carrying no citation of any kind. No published measurement of BDNF, TrkB or any other readout exists for Adamax. BDNF findings do exist for Semax, in stressed rats and in one 110-patient Russian stroke cohort, and for P021 in mice, and none of them was made on this molecule.
• improves athletic endurance by two to three times more than other semax analogues — overreach — The figure appears on a chemical seller's catalogue page, attached to human athletic endurance, with no citation and no study behind it. No human has been reported to receive Adamax in any published or registered study. This is a claim about human performance made by a supplier with nothing supporting it.
• the listed formula and CAS number identify what is in the vial — contradicted — Three formulas circulate under the name and they describe different molecules. C50H69N11O11S at 1032.23 reconciles exactly as acetyl-Semax plus P021's adamantane unit. C44H61N11O13S at 984.10 computes as the plain nine-residue peptide with ordinary alanine, ordinary glycine and a free acid terminus, which is a molecule carrying neither the adamantane cage nor the C-terminal amide. C22H52N16O6, printed alongside a mass of 1032.24, computes to 636.76 and contains no sulfur at all, which is impossible for a methionine-containing peptide of that mass. At least three CAS numbers circulate, one of which is Semax's own.
• a nonapeptide, nine amino acids — contradicted — Against the naming convention of the parent, which writes P021 as Ac-DGGL(A)G-NH2 with the A as a superscript modifier on the glycine, the trailing AG in Ac-MEHFPGPAG-NH2 is one adamantane-based residue rather than alanine plus glycine. That gives eight residues, and it is why the nine-letter string and the octapeptide label are not in conflict. Stated as reasoning from the parent's convention, not as a published characterisation of Adamax, because none exists.
• scheduled or banned in new zealand — contradicted — Medsafe proposed classification of ACTH analogues as prescription medicines in June 2025, naming Adamax as one of two examples. The Medicines Classification Committee deferred the decision on 23 July 2025 pending more information about effects on other industries. A secretariat note records that the cosmetics consultation came back with no issues raised and that Medsafe still recommends classification. No document adopting the entry was located, so deferred is the status on the record reachable here.

key facts

• molecular formula: C50H69N11O11S as listed. vendor catalogues also circulate C44H61N11O13S and C22H52N16O6, neither of which describes the same molecule
• molecular weight: 1032.23 g/mol as listed, and it reconciles exactly. the two vendor alternatives compute to 984.10 and 636.76
• amino acids: 8 as reconstructed: the semax heptapeptide plus one adamantane-based residue. listings variously call it a heptapeptide, an octapeptide and a nonapeptide
• half-life: not characterised. no pharmacokinetic study of this molecule exists in any species
• type: designer semax analogue; acetylated ACTH(4-7)-Pro-Gly-Pro with an adamantane-based C-terminal residue
• CAS: no verified CAS. three numbers circulate. 80714-61-0 is semax's own registry number, 63288-34-0 appears on a listing showing molecular weight zero, and wikipedia gives adamax no CAS at all
• 0 published studies of adamax, in any species
• 0 registered trials, every registry checked
• 39 pubmed hits for 'adamax', all of them software papers
• 230 pubmed records for its parent semax

frequently asked questions

What is Adamax?

Adamax is a designer peptide sold as a modified Semax. It is the Semax heptapeptide, ACTH(4-7)-Pro-Gly-Pro, carrying the N-terminal acetyl cap and the adamantane-based C-terminal residue used in the research compound P021. The circulating shorthand is Ac-MEHFPGPAG-NH2. No published paper describes its synthesis or characterisation, and it has no approval anywhere.

What does Adamax do?

No published study has measured Adamax in any species. There is no animal work, no cell work, no pharmacokinetics and no toxicology on the molecule itself. The mechanism attached to it in marketing copy is inherited from its two parent compounds: Semax is documented to raise BDNF in rodents and in one Russian human cohort, and P021's adamantane cap was added to ease brain entry. Neither finding was made on Adamax.

How is Adamax studied in the published literature?

It is not. Eight PubMed query formulations return no record of the peptide, and the exact sequence string returns zero. A bare search for the word returns 39 records, every one of them a machine-learning paper about the AdaMax optimizer, the infinity-norm variant of Adam. ClinicalTrials.gov, the WHO ICTRP portal and the EU Clinical Trials Register each return zero, calibrated in the same queries against 42 registered Cerebrolysin trials, 27 setmelanotide and 5 davunetide. The literature that does exist belongs to its two parents.

What are the side effects of Adamax?

Uncharacterised, because no study of the compound has been published in any species. There is no toxicology record, no adverse-event record and no exposure data for this molecule. The nearest rodent record belongs to the adamantane parent P021, where reviewers report up to 18 months of dosing without weight loss, tumours or the pain behaviour seen with full-length CNTF, and one rat study reports no detectable immune reaction. Those findings were generated on a different compound. New Zealand's regulator, writing about the ACTH-analogue class rather than about Adamax specifically, states that little is known about the side effects or long-term effects.

Is Adamax FDA approved?

No. There is no registered trial of Adamax in any registry checked and no published study in any species, so there is no development programme that could have produced an approval. This entry did not complete a direct query of the FDA and EMA registers, and reports that as an unchecked gap rather than as a verified negative. What is on the record is one regulator's paperwork: Medsafe proposed in June 2025 that ACTH analogues including Adamax be classified as prescription medicines in New Zealand, and the Medicines Classification Committee deferred that decision on 23 July 2025 pending more information. No document adopting the entry was located, so deferred is the status. Semax, the parent, is a registered prescription drug in Russia and is not FDA approved.

How much does Adamax cost?

There is no clinical retail price, because there is no approved product anywhere. On the research-chemical market it is sold by the milligram like other grey-market nootropic peptides. What the price does not buy is a specification anyone can rely on: the catalogue listings that quote a formula quote three different ones, and at least three different CAS numbers circulate under the name, one of which is Semax's own registry number.

related peptides

• semax — the parent, and the only half of this molecule with human data behind it
• selank — the other russian CNS research peptide, same registry absence, more published work
• dihexa — same shape of problem: real preclinical lineage, no human programme for the compound being sold

reptides grades the research record and cites the literature behind every call. research reference only; not medical advice.