Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Bachmann, K.A. et al.

Dispositional and pharmacodynamic characteristics of brodifacoum in warfarin-sensitive rats.

A dose-response curve for the hypoprothrombinemic effect of brodifacoum 3-[-3(4'-bromobiphenyl-4-yl) 1,2,3,4-tetrahydronaphth-1-yl] -4-hydroxycoumarin, was constructed using doses ranging from 0.1 to 0.33 mg/kg. Brodifacoum exhibited a remarkably steep dose-response curve. Brodifacoum failed to exhibit a dose-dependent effect on the degradation rate constant (kdeg) for prothrombin complex activity (PCA) after a PCA-synthesis-blocking dose of warfarin. Both phenobarbital pretreatment and SKF525A treatment altered to anticoagulant response to brodifacoum. Phenobarbital decreased the anticoagulant effect, whereas SKF525A increased it, suggesting that a substantial portion of brodifacoum-induced hypoprothrombinemia is mediated by brodifacoum itself rather than by metabolites. Finally, rats dosed orally with brodifacoum (0.2 mg/kg p.o.) were sacrificed in groups of 3-5 at various times up to 120 h after the dose. Brodifacoum was assayed in serum, small intestine, and liver by an HPLC method. Brodifacoum disappeared slowly from serum with a half-life of 156 h. Disappearance from small intestine was rapid, for 24 h, but intestinal levels began increasing from 24 to 72 h after the dose. Concentrations in liver were rapidly established, and exceeded serum concentrations by 20-fold. Brodifacoum levels in liver remained relatively constant for 96 h. Sustained liver concentrations after a single dose may partially account for brodifacoum's apparent potency relative to warfarin.[1]

References

Dispositional and pharmacodynamic characteristics of brodifacoum in warfarin-sensitive rats. Bachmann, K.A., Sullivan, T.J. Pharmacology (1983) [Pubmed]

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