Semax Heptapeptide Original Nootropic Synthetic ACTH Fragment Cognitive

(1) Neuroprotection: Exercises neuroprotective effects by inhibiting inflammatory responses and apoptotic processes. In cerebral ischemia models, Semax reduces MMP-9, c-Fos, and active JNK levels while upregulating active CREB expression, compensating for ischemia-induced protein expression dysregulation. It enhances survival rates of basal forebrain cholinergic neurons (approximately 1.5-1.7-fold) and stimulates choline acetyltransferase activity.

(2) Anti-inflammatory and Immunomodulatory Effects: Significantly influences immune-related gene expression; over 50% of Semax-regulated genes 24 hours post-cerebral ischemia are associated with immune responses. It suppresses mRNA expression of proinflammatory mediators IL-1α, IL-1β, IL-6, CCL3, and CXCL2, counteracting ischemia-induced upregulation of inflammatory genes.

(3) Cognitive Enhancement (Nootropic Effects): Enhances learning and memory capacity by modulating the hippocampal BDNF/trkB system. A single dose increases BDNF protein levels by 1.4-fold, trkB tyrosine phosphorylation by 1.6-fold, BDNF exon III mRNA by 3-fold, and trkB mRNA by 2-fold.

(4) Neurotrophic factor regulation: In glial cells derived from the basal forebrain of newborn rats, Semax (10 μM) elevates BDNF and NGF levels, increasing BDNF mRNA by 8-fold and NGF mRNA by 5-fold.

(5) Neurotransmitter Regulation: Modulates the striatal serotonergic system, increasing 5-hydroxyindoleacetic acid (5-HIAA) concentration while enhancing dopamine release and behavioral activity

(6) Anti-Amyloid Aggregation: Inhibits Aβ amyloid fiber formation by interfering with Aβ:Cu²⁺ complex fibrillation, exhibiting anti-aggregation and protective properties in the presence of copper ions