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- W2053770173 abstract "1. ML-236A and ML-236B, potent inhibitors of 3-hydroxy-3-methylglutaryl-CoA reductase, were readily absorbed into the liver, the major site of cholesterogenesis, after oral administration in mice; peak concentration of these inhibitors in the liver, which were attained within 60 min after administration, were 4% of the dose for ML-236A and 10% for ML-236B, respectively. 2. ML-236B reduced sterol synthesis from both [14C]acetate and [14C]octanoate in rat liver slices to 50% of control at a concentration of 0.05 μg/ml (0.12 μM) but not that from [14C]mevalonate at higher concentrations up to 1.25 μg/ml. Inhibition of sterol synthesis was also observed in liver slices obtained from rats which had previously received this compound. 3. ML-236B was also inhibitory in vivo to cholesterol synthesis in various tissues of rats in which [14C]acetate was intraperitoneally injected to the animals and labeled digitonin-precipitable sterols synthesized were isolated and determined. Sterol synthesis in the liver was far more strongly inhibited (over 90 % at 4h after oral administration of 50 mg/kg of ML-236B) than that in other organs tested including kidney, lung, adrenal, spleen, and testis. 4. These findings strongly suggest that hypocholesterolemic activity of ML-236A and ML-236B is owing largely to specific inhibition of hepatic cholesterol synthesis." @default.
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- W2053770173 date "1977-07-01" @default.
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- W2053770173 title "Inhibition of Cholesterol Synthesis in vitro and in vivo by ML-236A and ML-236B, Competitive Inhibitors of 3-Hydroxy-3-methylglutaryl-Coenzyme A Reductase" @default.
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- W2053770173 doi "https://doi.org/10.1111/j.1432-1033.1977.tb11637.x" @default.
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