Carbenoxolone disodium, derived from Glycyrrhizic acid, acts as an inhibitor of both human 11β-HSD and bacterial 3α, 20β-HSD enzymes[1]. Carbenoxolone disodium also serves as an uncoupling agent for gap junctions and effectively inhibits the replication of Vaccinia virus[2].
体内研究
In animal models, Carbenoxolone administered via intraperitoneal injection (100, 200, and 300 mg/kg; at 30, 60, and 60 minutes before Diazepam) does not exhibit muscle relaxant activity compared to normal saline, and it even surpasses diazepam in effectiveness in the traction test[3].
Additionally, when given before Pentylenetetrazole (PTZ), Carbenoxolone significantly prolongs sleep time and reduces latency in a dose-dependent manner in a PTZ seizure model, with an effective dose (ED50) of 83.3 mg/kg (95% confidence limit: 556.29)[3].
体外研究
In cellular studies, pre-treatment with Carbenoxolone disodium (6-150 μM; 1 hour) in HaCaT cells inhibits Vaccinia virus (VACV) replication independently of gap junction interaction, showing toxic effects on VACV-A5L-EGFP infected cells after 48 hours[2].
Moreover, Carbenoxolone at 30 μM does not increase PP2A expression but does induce the expression of the late protein A27 in HaCaT cells when administered one hour prior to observation[2].
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