Adamax (DW 1032)

They give no sequence, formula, molecular weight or CAS number, and they do not say what DW 1032 stands for.

No peer-reviewed study of Adamax appears in PubMed under that name or code. This guide sets out what is and is not on record, then summarizes the literature on Semax, the peptide that supplier descriptions of Adamax build on, labeled as Semax data throughout.

PubChem has no compound record for Adamax or DW 1032. One vendor-deposited PubChem substance record (SID 513899171) lists Adamax as a synonym of Ac-Met-Glu-His-Phe-Pro-Gly-Pro-Ala-Gly-OH, an acetylated nine-residue peptide containing the full Semax sequence, without a standardized structure. Supplier listings elsewhere describe an acetylated Semax with an adamantane group at the C-terminus instead. These descriptions disagree and none is peer-reviewed, so this guide assigns Adamax no structure. Identity for a given lot rests on its certificate.

A PubMed search for Adamax returns papers on AdaMax, an unrelated machine-learning method, and none on this peptide, and searches for DW 1032 and for adamantane-modified Semax return nothing relevant. No cell, animal or human study of Adamax is on record. The summaries below cover Semax and two published Semax variants, each with its model and the compound tested. None of them tested Adamax.

Semax, the parent sequence

Semax is the heptapeptide Met-Glu-His-Phe-Pro-Gly-Pro, which joins positions 4 to 7 of adrenocorticotropic hormone to a Pro-Gly-Pro tail that adds resistance to peptidases. Our Semax research guide covers that literature in depth.

Neurotrophin signaling and ischemia (Semax, rat)

Tritium-labeled Semax bound specific, calcium-dependent sites in rat basal forebrain membranes with a dissociation constant of about 2.4 nM, and Semax raised basal forebrain BDNF protein at 3 hours (Dolotov et al., 2006a). In rat hippocampus, one application raised BDNF protein up to 1.4-fold and trkB phosphorylation 1.6-fold (Dolotov et al., 2006b). After permanent middle cerebral artery occlusion in rats, immune-system genes made up more than half of the genes Semax changed at 24 hours (Medvedeva et al., 2014). Compound tested in all three: Semax, not Adamax.

Breakdown and modified Semax peptides

Incubated with nerve cells, Semax was broken down mainly to His-Phe-Pro-Gly-Pro and Pro-Gly-Pro (Zolotarev et al., 2006). Small modifications alter its chemistry. N-terminal acetylation (Ac-Semax) changed the structure and redox behavior of the copper(II) complex and removed the protection against copper toxicity in SH-SY5Y neuroblastoma cells that the authors tied to Semax's free N-terminus (Magrì et al., 2016). In APPswe/PS1dE9 transgenic mice, Semax and a derivative with two substitutions, Met-Glu-Asp-Arg-Pro-Gly-Pro, both raised maze and object recognition scores and reduced amyloid plaque counts (Radchenko et al., 2025). Neither Ac-Semax nor that derivative is Adamax.