|Jmol-3D images||Image 1|
|Molar mass||230.26 g mol−1|
| (what is: / ?) |
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
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 acting as a serotonin reuptake inhibitor has not been confirmed but monoamine (norepinephrine) uptake inhibitions and activation of NMDA receptors has been noted.
The mechanism behind the psychotropic, sedative and anxiolytic actions of kavain and related kavalactones is still debated. Direct binding to the GABAA receptor (benzodiazepine-receptor) does not occur with kavain enantiomers. Many studies involved kava extracts from different plant parts and are therefore not applicable to kavain itself.
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.