Semax is a synthetic heptapeptide derived from the ACTH(4-7) sequence with an added Pro-Gly-Pro tail, studied predominantly in rodent models of cerebral ischemia and in human neuroimaging studies of b...
Semax is a synthetic heptapeptide derived from the ACTH(4-7) sequence with an added Pro-Gly-Pro tail, studied predominantly in rodent models of cerebral ischemia and in human neuroimaging studies of brain connectivity. Proposed mechanisms include modulation of neurotrophic signaling, altered hippocampal calcium dynamics, and immune/vascular gene-expression changes in ischemic brain tissue — distinct from ACTH's classical corticotropic hormone activity, which the sequence used here lacks.
International Journal of Molecular Sciences · 2021
Following transient cerebral artery occlusion, Semax upregulated active CREB in subcortical structures and downregulated inflammatory/damage markers (MMP-9, c-Fos, active JNK) in cortical tissue.
View Source →Doklady Biological Sciences · 2020
Resting-state fMRI study in 52 healthy volunteers randomized to Selank, Semax, or placebo found treatment-specific changes in functional connectivity between the amygdala and temporal/parahippocampal regions.
View Source →BMC Genomics · 2014
Genome-wide transcriptomic analysis after permanent cerebral artery occlusion found Semax predominantly upregulated immune-response genes along with vascular-related gene changes.
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