Adamax

A research-market analog of Semax described by its sellers as the Semax heptapeptide acetylated at the N-terminus and capped at the C-terminus with the aminoadamantane unit of Peptide 021; the design has no published synthesis, pharmacology, or human data of its own.

Also appears in: Neuroprotection

What is Adamax?

Adamax is a research-market name for a designed analog of Semax, the Russian intranasal heptapeptide Met-Glu-His-Phe-Pro-Gly-Pro, which is itself the adrenocorticotropic hormone fragment ACTH(4-7) joined to a Pro-Gly-Pro tail. Sellers describe Adamax as Semax carrying the two terminal modifications of P21 (Peptide 021, written P021 in most later papers), a ciliary neurotrophic factor-derived peptide from Khalid Iqbal’s group: an acetyl cap on the N-terminal methionine and, at the C-terminus, the aminoadamantane carboxamide unit that P021’s designers call an adamantylated glycine. The compound is usually written Ac-MEHFPGP(A)G-NH2, a notation in which the “(A)G” stands for that single adamantane-bearing residue, a 3-aminoadamantane-1-carboxamide, rather than for alanine followed by glycine. The one structure drawn in public, on an encyclopedia entry whose own editors flag its chemical data as unverified, works out to C50H69N11O11S and a molecular weight near 1,032 Da, which is consistent with the written design; nothing else about the molecule is documented. There is no CAS number, no PubChem entry under the name, the written sequence, or that drawn structure’s InChIKey, and no paper describing its synthesis or characterization.

The design pairs Semax’s following with the P021 rationale that an N-terminal cap and a lipophilic cage should make a short peptide last longer and reach the brain more easily. Adamax is the combination of those two ideas into a product, sold almost entirely as a nasal spray, without any published test of whether the combination does what the rationale predicts.

How it works

No mechanism has been measured for Adamax. Nothing in the indexed literature reports a receptor-binding, cell, animal, or human experiment on the compound, so every mechanistic statement made about it is borrowed from one of its two parents, and the borrowing runs in both directions:

• From Semax: BDNF, trkB, and a specific brain binding site. Intranasal Semax at 50 µg/kg raised BDNF protein 1.4-fold and trkB tyrosine phosphorylation 1.6-fold in the rat hippocampus (Dolotov et al., Brain Research, 2006, 1117(1):54–60), and tritium-labeled Semax bound rat basal forebrain membranes specifically and reversibly with a dissociation constant of 2.4 ± 1.0 nM (Dolotov et al., Journal of Neurochemistry, 2006, 97 Suppl 1:82–86). Labeled Semax also reaches rat brain within two minutes of intranasal dosing (Shevchenko et al., Bioorganicheskaia Khimiia, 2006, 32(1):64–70). Whether a peptide with a blocked N-terminus and an adamantane cage on its C-terminus still occupies that binding site, or crosses the nasal epithelium the same way, has never been tested.
• From Semax: the degradation routes the modifications are meant to close. In rat blood a bestatin-sensitive aminopeptidase strips Met and then Glu from the N-terminus (Potaman et al., Biochemical and Biophysical Research Communications, 1991, 176(2):741–746), and in basal forebrain cell cultures the peptide loses Met-Glu from one end and Gly-Pro from the other (Zolotarev et al., Amino Acids, 2006, 30(4):403–408). Capping both ends is a coherent response to that data; it has not been shown to work for this sequence.
• From P021: the adamantane rationale. Iqbal’s group trimmed a CNTF-derived 11-mer to the tetrapeptide Ac-DGGL-NH2 and then added an adamantylated glycine specifically to improve blood-brain barrier permeability; the resulting pentamer, P021, enhanced learning and memory and hippocampal neurogenesis in mice after peripheral dosing (Li et al., FEBS Letters, 2010, 584(15):3359–3365; Kazim and Iqbal, Molecular Neurodegeneration, 2016, 11:50). That result belongs to a different peptide acting through a different pathway, the leukemia inhibitory factor and BDNF axis of CNTF signaling, and it says nothing about what the same cage does when attached to an ACTH fragment.
• The one measured effect of acetylating Semax points the other way. The only published biological comparison of capped versus uncapped Semax found that N-terminal acetylation removed the peptide’s protection of SH-SY5Y neuroblastoma cells against copper toxicity, because the free terminal amine is what coordinates the metal (Magrì et al., Journal of Inorganic Biochemistry, 2016, 164:59–69). This is the closest any experiment comes to testing part of the Adamax design, and it recorded a loss rather than a gain.

Research status

Adamax has no research record. A PubMed search for the bare name returns about forty records in November 2026, every one of them about AdaMax, the gradient-descent optimizer introduced alongside Adam in machine learning; the name combined with “peptide” or “semax” returns a single record, another machine-learning paper, and searches pairing Semax or ACTH(4-10) with adamantane, adamantyl, or adamantylated return zero. ClinicalTrials.gov lists no study of Adamax and none of Semax in any form. Google Patents returns no adamantane-modified Semax under English or Russian terms; the one family that surfaces, titled “Adrenocorticotropic hormone peptide compositions and methods of use” (US 2025/0127843 A1; EP 4404912 A1), concerns aqueous compositions of the unmodified heptapeptide and lists a C-terminal adamantane moiety among optional derivatizations without naming Adamax or describing a synthesized compound. The group that created Semax continues to publish on derivatives, but the most recent of that work is a sequence substitution, the heptapeptide Met-Glu-Asp-Arg-Pro-Gly-Pro tested beside Semax in APP/PS1 mice (Radchenko et al., Acta Naturae, 2025, 17(4):110–120), not a terminal modification and not an adamantane conjugate, and no Russian-language paper on such an analog is indexed; unindexed Russian conference abstracts cannot be excluded, but none has been cited by any seller or secondary source. No animal study, no in vitro assay, and no human exposure data for Adamax appear anywhere in the indexed literature.

The one non-commercial document that names the compound is regulatory rather than scientific. In a June 2025 submission to New Zealand’s Medicines Classification Committee, Medsafe proposed classifying ten groups of unscheduled peptides as prescription medicines after 56 parcels containing peptides or selective androgen receptor modulators were intercepted at the border between April 1 and May 19, 2025, and cited Adamax and Semax by name as “two peptide products currently marketed as cognitive enhancers” that a group entry for adrenocorticotropic hormone analogs would capture. At its July 23, 2025 meeting the committee deferred the decision pending information on how classification would affect other sectors such as cosmetics; a secretariat note appended to the minutes records that Medsafe then consulted cosmetics industry bodies, found no objection, and maintained its recommendation. The committee’s November 19, 2025 meeting did not return to the item, and Medsafe’s May 21, 2026 consumer advisory states that under the Medicines Act 1981 many peptide products are prescription medicines without listing which group entries took effect. That record establishes that Adamax is a product in commerce. It is not evidence about the molecule.

The evidence usually attached to Adamax is Semax evidence (see Semax); the main items are an open, non-randomized comparison in 30 acute ischemic stroke patients against 80 conventionally treated controls (Gusev et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 1997, 97(6):26–34) and the rat neurotrophin work above. For its July 23–24, 2026 meeting the FDA evaluated semax free base and semax acetate for the section 503A bulk drug substances list, found no human pharmacokinetic study by any route and insufficient effectiveness evidence for the nominated uses, and concluded that the criteria weighed against inclusion; on July 24, 2026 the Pharmacy Compounding Advisory Committee voted 8–5 to recommend inclusion anyway, a vote that is advisory and has not produced a final determination. The briefing document does not mention Adamax, adamantane, or any Semax analog, so none of that review, favorable or unfavorable, applies to this compound.

Common dosage forms

• Pre-mixed nasal spray bottles, the dominant presentation, sold by research suppliers at small milligram quantities per bottle. The nasal format follows the parent: Semax is registered in Russia as 0.1% and 1% nasal drops, and intranasal is the only route its human literature covers.
• Lyophilized powder in sealed vials, typically at 5 mg and 10 mg fills.

No approved product containing Adamax exists in any country, the compound is not on the FDA’s 503A bulk drug substances list and was not among the substances nominated or evaluated in 2026, and no licensed compounding route exists for it in the United States.

Key considerations

• The Research Market status reflects the absence of any approval, any registered trial, and any development program in any country, with the only regulatory document naming the compound being a New Zealand classification proposal that would make it prescription-only. Semax’s Russian registration does not extend to its analogs, and the FDA’s 2026 evaluation of semax covered the free base and the acetate salt only.
• There is no Adamax evidence, and the parts it is assembled from do not add up to any. Semax’s neurotrophin and binding data were generated with the unmodified peptide; P021’s adamantane benefit was measured on a CNTF-derived tetrapeptide with a different target; and the one experiment touching the design, the acetylation comparison above, recorded a loss. Claims that Adamax is more potent, longer-acting, or more brain-penetrant than Semax have no published measurement behind them.
• Identity is harder to pin down than the name suggests. Beyond the “(A)G” notation ambiguity described above, some listings write a free-acid C-terminus, and at least one gives the native ACTH(4-10) sequence with Arg-Trp, a different peptide altogether; chemical-supplier pages publish molecular formulas that do not agree with each other or with their own stated mass. With no registry entry, only a certificate of analysis giving the structure and an observed mass near 1,032 Da identifies the compound.
• Safety is uncharacterized at every level. No tolerability, pharmacokinetic, or immunogenicity data exist for Adamax, and the parent’s record is thin: the FDA found no human pharmacokinetic study of semax by any route, a single adverse-event report in FAERS, potentiation of amphetamine-induced dopamine release in mice that it treated as an abuse-potential question, and an unresolved bleeding-risk question from reported anticoagulant and antithrombotic activity in rats. The adamantane cage is shared with amantadine and memantine, drugs with their own central nervous system pharmacology, but a cage bound as a peptide C-terminal amide is not those drugs, and no data exist either way.
• The name collides with an unrelated term and sits inside a confusing family. Literature searches for “Adamax” return the machine-learning optimizer, not a peptide. Within the Semax family, Adamax is distinct from semax acetate (the acetate salt of the unmodified peptide, the substance the FDA evaluated), from N-Acetyl Semax (acetylated, free acid), and from N-Acetyl Semax Amidate (acetylated, simple carboxamide); only Adamax carries the adamantane unit, and sellers use these names loosely.