|Jmol 3D model||Interactive image|
|Molar mass||230.26 g·mol−1|
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
|what is ?)(|
Kavain has anticonvulsive properties, attenuating vascular smooth muscle contraction through interactions with voltage-dependent Na+ and Ca2+ channels. How this effect is mediated and to what extent this mechanism is involved in the anxiolytic and analgesic effects of kavalactones on the central nervous system is unknown. Kavain's pharmacological activities have not been sufficiently investigated and neither its effect as a serotonin reuptake inhibitor nor its monoamine (norepinephrine) uptake inhibitions and activation of NMDA receptors have been confirmed.
The mechanism behind the psychotropic, sedative and anxiolytic actions of kavain and related kavalactones is still debated. Direct binding to the benzodiazepine/flumazenil binding site of the GABAA receptor does not occur with kavain enantiomers. Many studies involved kava extracts from different plant parts and are therefore not applicable to kavain itself. In 2016 kavain was shown to bind at the α4β2δ GABAA receptor and potentiate GABA efficacy.
A comparative review of in-vivo studies with kavain (and related kavapyrones) to commonly used antiepileptic drugs and mood stabilizers affecting ion fluxes indicates that the kavapyrones are weakly Na+ antagonistic and therefore antiepileptic. They also have pronounced L- type Ca2+ channel antagonistic properties and act as a positive modulator of the early K+ outward current, which contribute to mood stabilizing properties similar to lamotrigine.
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