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Mechanism of Action# Selank's anxiolytic mechanism involves multiple neurotransmitter systems: GABAergic enhancement: Modulates GABA-A receptor signaling, enhancing inhibitory neurotransmission without the direct benzodiazepine-site binding that causes sedation and dependence Serotonin metabolism: Influences serotonin metabolism and the expression of serotonin-related genes in the brain Enkephalin stabilization: Inhibits enkephalinase, the enzyme that degrades endogenous opioid peptides (enkephalins), thereby prolonging the activity of the body's natural anxiolytic system Anti-inflammatory: Reduces neuroinflammation through modulation of IL-6, TNF-alpha, and other cytokines -- relevant because neuroinflammation is increasingly recognized as a contributor to depression and anxiety BDNF expression: Increases brain-derived neurotrophic factor expression, supporting neuroplasticity Research Findings# Anxiolytic efficacy: Clinical studies in Russia showed anxiolytic effects comparable to low-dose benzodiazepines, without the sedation, cognitive impairment, or dependence risk Unpredictable chronic stress model: Selank enhanced the effects of diazepam in reducing anxiety behaviors in chronically stressed rats, suggesting complementary mechanisms Cognitive preservation: Unlike benzodiazepines, selank does not impair memory or cognitive function -- it may actually enhance them No dependence: No evidence of tolerance, physical dependence, or withdrawal effects in clinical use Rapid onset: Anxiolytic effects observed within minutes of intranasal administration Administration# Route: Intranasal spray (0.15% solution) Dose: 75-450 mcg per administration, typically 2-3 times daily Duration: 14-day courses, repeated as needed Important Considerations# Western-standard RCTs for selank are limited