Adamax (N-Acetyl-Semax with Adamantyl Modification)

Adamax is a synthetic derivative of Semax — the well-characterized heptapeptide analog of ACTH(4-10) developed in Russia and used there for cognitive and stress-related research. Adamax adds two specific structural modifications to the Semax backbone: an N-terminal acetyl group that slows enzymatic degradation by aminopeptidases, and a C-terminal adamantane (tricyclic cage) moiety that improves lipophilicity, blood-brain barrier penetration, and circulating half-life. The result is a Semax-family peptide with extended pharmacokinetic exposure and prolonged downstream signaling — particularly along the BDNF/TrkB pathway that Semax itself is known to upregulate.

Key Research Findings:

• Designed as a longer-acting Semax analog through dual N-acetyl and C-adamantyl modification, addressing the rapid proteolytic clearance of unmodified Semax
• Preclinical interest centers on the BDNF/TrkB axis — Semax-family peptides are repeatedly shown to upregulate BDNF mRNA expression in hippocampal and cortical tissue
• Intranasal administration is the predominant research route for this class, leveraging nose-to-brain delivery kinetics for short peptides
• Investigated in rodent models for cognition, neuroplasticity, stress response, and stroke recovery alongside parent Semax
• The C-terminal adamantane modification is structurally analogous to that used in amantadine and other adamantyl-modified neuroactive compounds with established CNS bioavailability

For laboratory and research use only.