Binds delta and mu opioid receptors with peripheral preference due to limited CNS penetration. Reduces gastric acid secretion, promotes mucosal blood flow, and inhibits ulcer formation via prostaglandin-mediated pathways.

Selank is believed to modulate the expression of GABA-A receptor subunits and increase BDNF levels, contributing to its anxiolytic and neuroprotective profile. It appears to regulate serotonin transporter gene expression and influence dopaminergic signalling. Unlike classical anxiolytics, it does not appear to produce tolerance or physical dependence in animal models.