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Key effects documented in rodent models include: Altered expression of major GABA-A receptor subunit genes, including GABRB3, GABRE, and GABRQ Regulation of ion channels involved in GABA transport Modulation of dopamine receptor subtypes (DRD3, DRD5) and serotonin receptor genes simultaneously Changes in HCRT (hypocretin/orexin) gene expression, which may explain the absence of sedative effects observed with classical benzodiazepines Enkephalin Degradation Inhibition Selank, along with the closely related peptide Semax, has been found to inhibit aminopeptidase N (APN) and dipeptidyl peptidase IV (DPP-IV), enzymes responsible for the degradation of enkephalins and other endogenous regulatory peptides[3]