Selank’s anxiolytic mechanism involves multiple neurotransmitter systems. It modulates the GABAergic system by increasing the expression of GABA-A receptor subunits, enhancing inhibitory neurotransmission without directly binding to benzodiazepine sites (which explains the absence of tolerance and dependence). It also influences serotonin metabolism by inhibiting enkephalin-degrading enzymes, increasing the availability of endogenous opioid peptides that modulate anxiety. Selank increases BDNF (brain-derived neurotrophic factor) expression in the hippocampus and prefrontal cortex, supporting neuroplasticity and cognitive function. Its tuftsin-like structure confers immunomodulatory effects: it activates T-lymphocytes and NK cells through tuftsin receptors on immune cells, and has demonstrated antiviral properties in influenza models. Intranasal administration provides rapid CNS delivery through olfactory nerve pathways.