Selank GABAergic and Enkephalin Mechanism Summary — VialBase Research
Selank allosterically modulates GABA-A receptors for anxiolytic effect
- Selank allosterically modulates GABA-A receptors for anxiolytic effect
- Inhibits enkephalinase, extending endogenous enkephalin half-life
- Influences expression of 36 genes in inflammation, immunity, neurotransmission
- Increases serotonin metabolism in cortex, stabilizes dopamine
- Anxiolytic efficacy comparable to medazepam without sedation or dependence
Selank Core Mechanism: GABA + Enkephalin + Gene Expression
GABA-A Modulation
Selank acts as an allosteric modulator at GABA-A receptors, enhancing inhibitory neurotransmission. Unlike benzodiazepines (which bind at the benzodiazepine site), Selank’s modulation does not produce sedation, tolerance, or dependence.
Enkephalin Stabilization
Selank inhibits enkephalinase enzymes (aminopeptidase N and other peptidases), extending the biological half-life of endogenous met-enkephalin and leu-enkephalin. These endogenous opioid peptides provide natural anxiolysis and pain modulation without the dependency profile of exogenous opioids.
Transcriptomic Effects
Russian transcriptomic studies identified 36 genes whose expression is altered by Selank, spanning:
- Chemokine signaling (CCL2, CXCL1)
- Cytokine production (IL-6 modulation)
- Neurotransmitter metabolism (serotonin, dopamine)
- Inflammation regulation
Clinical Comparison
Head-to-head studies vs medazepam (benzodiazepine) showed comparable anxiolytic efficacy with:
- No sedation
- No cognitive impairment (actually improved cognition)
- No psychomotor impairment
- No dependence or withdrawal