A doubly modified analog of Semax featuring N-terminal acetylation and C-terminal amidation, designed to enhance blood-brain barrier penetration and extend the functional half-life from minutes to 4–6 hours. The acetyl group improves lipophilicity for mucosal absorption while amidation prevents carboxypeptidase degradation. Produces stronger BDNF upregulation and dopaminergic activation compared to native Semax.
TargetsBDNF/NGF pathways, melanocortin receptors, dopamine system (enhanced)
Research FocusEnhanced nootropic potency, BDNF dose-response, improved pharmacokinetics vs Semax
ReconstitutionNormal saline (0.9% NaCl) for intranasal delivery
Stability14 days at 2–8°C reconstituted
Key distinction: Double chemical modification (acetylation + amidation) extends functional duration ~10x over native Semax while improving BBB penetration — the most pharmacokinetically optimized Semax variant.
Scientific Evidence
Published Research
[1]
Dolotov OV et al. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression. Brain Res 2006;1117:54-60 — PubMed 16996040
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