Kavain
 | |
 | |
| Names | |
|---|---|
| IUPAC name
4-methoxy-2-[(E)-2-phenylethenyl]-2,3-dihydropyran-6-one | |
| Other names
Kawain | |
| Identifiers | |
500-64-1  | |
| ChemSpider | 4520267  |
| Jmol interactive 3D | Image |
| KEGG | D08096 |
| PubChem | 5369129 |
| UNII | W1ES06373M |
| |
| |
| Properties | |
| C14H14O3 | |
| 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). | |
| verify (what is ?) | |
| Infobox references | |
Kavain is the main kavalactone found mostly in the roots of the kava plant.
Pharmacology
Kavain has anticonvulsive properties, attenuating vascular smooth muscle contraction through interactions with voltage-dependent Na+ and Ca2+ channels.[1] 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 GABAA receptor (benzodiazepine-receptor) does not occur with kavain enantiomers.[2] 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.[3]
Kavain and analogs remain interesting for drug discovery against a variety of cellular targets, including P-glycoprotein (Pgp), cytochrome P450 and cyclo-oxygenase (COX) enzymes, among others.[4]
See also
References
- ↑ Bradić, I; Pasini, M (1975). "Hirschsprung's disease -- therapy and results". Acta chirurgica Iugoslavica 22 (2): 183–95. PMID 1235738.
- ↑ Boonen, Georg; Häberlein, Hans (2007). "Influence of Genuine Kavapyrone Enantiomers on the GABAABinding Site". Planta Medica 64 (6): 504–6. doi:10.1055/s-2006-957502. PMID 9776662.
- ↑ Grunze, Heinz; Langosch, Jens; Schirrmacher, Karin; Bingmann, Dieter; Von Wegerer, Jörg; Walden, Jörg (2001). "Kava pyrones exert effects on neuronal transmission and transmembraneous cation currents similar to established mood stabilizers - a review". Progress in Neuro-Psychopharmacology and Biological Psychiatry 25 (8): 1555–70. doi:10.1016/S0278-5846(01)00208-1. PMID 11642654.
- ↑ Rowe, A.; Narlawar, R.; w. Groundwater, P.; Ramzan, I. (2011). "Kavalactone Pharmacophores for Major Cellular Drug Targets". Mini Reviews in Medicinal Chemistry 11 (1): 79–83. doi:10.2174/138955711793564088. PMID 21034404.
| ||||||||||||||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
This article is issued from Wikipedia - version of the Sunday, February 21, 2016. The text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for the media files.