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Overview
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Background
CH 223191 is a potent aryl hydrocarbon receptor (AhR) antagonist with an IC50 value of 30 nM [1].
The aryl hydrocarbon receptor (AhR) is a cytosolic ligand-activated basic helix-loop-helix transcription factor. The toxicities of 2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD) are mostly mediated by binding and activating AhR, which causes nuclear signal transduction and adverse effects.
CH 223191 inhibits TCDD-induced AhR-dependent transcription in vitro. By the HepG2-DER-luc-cell-based assay, CH 223191 showed the most potent inhibitory (IC50=0.03±0.005 mΜ). CH 223191 had no agonist-like effect (at concentrations up to 100 μM) compared with known AhR antagonists such as resveratrol and α-naphthoflavone. Besides, CH 223191 had no effect on estrogen receptor-mediated luciferase activity while flavone potentiated that in MCF-7 breast cancer cells [1].
Male mice were administrated with vehicle or CH 223191 (10mg/kg) orally once a day for 25 days and treated with TCDD (100μg/kg) once after the first week of CH 223191 administration. Expression of cytochrome P450 1A1protein from extracts of the liver was quantitated, which showed significant suppression by treatment of CH 223191 (10 mg/kg). By measuring plasma AST and ALT levels, the level of TCDD-induced toxicity was decreased apparently by CH 223191. By measuring body weights, the drug significantly avoided the symptoms of severe wasting caused by TCDD [1].
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