Semax

Semax increases BDNF expression in the rat hippocampus and cortex following chronic intranasal administration^[1]

This rodent study examined BDNF and TrkB gene expression changes in hippocampal and cortical tissue following 10 days of intranasal semax at 50 ug/kg/day. Northern blot and RT-PCR analysis revealed a 1.6- to 2.2-fold upregulation of BDNF mRNA and a corresponding increase in mature BDNF protein in hippocampal CA1 and cortical layer II-III neurons. TrkB receptor expression also increased in a pattern consistent with compensatory upregulation in response to elevated ligand. Morris water maze performance was improved in semax-evaluated aged rats compared to controls, with a correlation between BDNF levels and spatial memory scores observed across individual animals.

Last verified: 2026-04-03

Neuroprotective effects of semax in a rat model of transient focal cerebral ischemia — BDNF pathway involvement^[2]

This study used a middle cerebral artery occlusion (MCAO) rat model to evaluate semax's neuroprotective potential when evaluated in the early reperfusion window. Semax at 50 ug/kg intraperitoneally one hour after MCAO significantly reduced infarct volume by 40% compared to vehicle, as measured by TTC staining at 24 hours. Mechanistic analysis showed semax preserved BDNF signaling in the penumbra region, reduced caspase-3 activation (a marker of apoptotic cell death), and attenuated oxidative stress markers including lipid peroxidation products. The combination of anti-apoptotic and neurotrophic mechanisms was proposed as the basis for the observed neuroprotection.

Last verified: 2026-04-03