Tag: N-acetylated and amidated Semax derivative

NA-Semax Amidate (N-acetyl-Met-Glu-His-Phe-Pro-Gly-Pro-NH2) is a doubly modified variant of Semax (the seven-residue ACTH(4-10) analog Met-Glu-His-Phe-Pro-Gly-Pro) developed at the Russian Academy of Sciences as a long-acting analog. Semax itself is registered in the Russian Federation as an intranasal nootropic and stroke treatment at 0.1 percent and 1 percent solutions, with a published pharmacological signature of BDNF and NGF transcriptional upregulation, neuroprotection in middle cerebral artery occlusion stroke models, and pro-cognitive effects in passive avoidance and operant conditioning paradigms. The parent Semax has a plasma half-life of minutes and a central nervous system exposure window of similarly short duration after intranasal administration. The N-acetyl variant of Semax (NA-Semax) extends plasma half-life by approximately 5-fold by blocking the aminopeptidase cleavage at the methionine N-terminus, and the C-terminal amidation in the Amidate variant additionally blocks the carboxypeptidase cleavage at the proline C-terminus, producing a peptide with the longest exposure in the Semax family. Comparative pharmacology in rodent models reports that NA-Semax Amidate at one-tenth the dose of parent Semax produces equivalent or greater BDNF mRNA elevation in cortex and hippocampus and equivalent neuroprotection in stroke models, with substantially longer duration of effect. Routes studied include subcutaneous, intramuscular, intranasal, and intraperitoneal administration. The compound is research-grade and not approved by any regulatory authority; the principal published record is in Russian-language journals from the Institute of Molecular Genetics RAS. Investigators should treat the extended-PK variant as a research tool for studying long-duration ACTH-derived heptapeptide pharmacology where the brief pulse from intranasal Semax is operationally limiting.