Anthraflavic acid

Anthraflavic acid specifically inhibits the activity of cytochrome P-448 without affecting phenobarbital-induced cytochrome P-450 or NADPH-dependent cytochrome c reduction. Anthraflavic acid inhibits cytosolic metabolic pathways, blocks the microsomal and cytosolic activation of IQ, and reduces the metabolic activation level of Glu-P-I. Anthraflavic acid may exert anticancer activity by inhibiting the metabolic activation of chemical carcinogens. Anthraflavic acid is applicable to cancer-related research^[1][2][3]. In Vitro:Anthraflavic acid (5×10⁻⁷-5×10⁻⁵ M; 20 min) potently inhibits S9-mediated mutagenicity of IQ in Salmonella typhimurium strain TA98 in a concentration-dependent manner, with complete inhibition observed at 5×10⁻⁵ M^[1].
Anthraflavic acid (1×10⁻⁷-5×10⁻⁵ M; 20 min post-microsomal reaction termination) inhibits cytosol-mediated potentiation of microsome-generated IQ mutagenicity in Salmonella typhimurium strain TA98, with a pronounced effect at 5×10⁻⁵ M^[1].
Anthraflavic acid (5×10⁻⁷-5×10⁻⁵ M) potently and concentration-dependently reduces cytochrome P-448-dependent Glu-P-1 mutagenicity in the Ames test with Salmonella typhimurium strain TA 98 and an Arochlor-1254-induced rat hepatic S9 activation system, and shows no mutagenic activity itself^[2].
Anthraflavic acid (5×10⁻⁷-5×10⁻⁵ M) does not inhibit NADPH-dependent cytochrome c reductase activity in Arochlor-1254-induced rat hepatic microsomes, even at concentrations up to 5×10⁻⁵ M, showing it does not interfere with electron flow to cytochrome P-450^[2]. In Vivo:Anthraflavic acid (100 mg/kg; i.p.; daily; 5 days) is a specific inducer of rat hepatic cytochrome P-450 I proteins, significantly increasing activities of ethoxycoumarin and ethoxyresorufin O-deethylases and enhancing the metabolic activation of the carcinogens Glu-P-1 and IQ to mutagenic intermediates^[3].