Rivaroxaban (BAY 59-7939) is being developed as an oral, direct inhibitor of Factor Xa (FXa) for the prevention and treatment of both arterial and venous thrombosis. It competitively inhibits human FXa with a Ki of 0.4 nM, demonstrating over 10,000 times greater selectivity over other serine proteases and inhibits prothrombinase activity with an IC50 of 2.1 nM. In human and rabbit plasma, Rivaroxaban more potently inhibits endogenous FXa (IC50 21 nM) compared to rat plasma (IC50 290 nM). It effectively doubles prothrombin time and activates partial thromboplastin time at concentrations of 0.23 μM and 0.69 μM, respectively, indicating its anticoagulant effects[2].
体内研究
Rivaroxaban (BAY 59-7939) is a highly potent and selective FXa inhibitor that exhibits excellent in vivo activity and favorable oral bioavailability[1].
Administered intravenously before thrombus induction, Rivaroxaban significantly reduces thrombus formation with an ED50 of 0.1 mg/kg, dose-dependently inhibits FXa, and prolongs prothrombin time. At the ED50, PT is modestly increased (1.8-fold) and FXa activity is inhibited by 32%. At a dose of 0.3 mg/kg, which nearly completely prevents thrombus formation, Rivaroxaban prolongs PT by 3.2±0.5-fold and inhibits 65±3% of FXa activity[2].
体外研究
Rivaroxaban (BAY 59-7939) is being developed as an oral, direct inhibitor of Factor Xa (FXa) for the prevention and treatment of both arterial and venous thrombosis. It competitively inhibits human FXa with a Ki of 0.4 nM, demonstrating over 10,000 times greater selectivity over other serine proteases and inhibits prothrombinase activity with an IC50 of 2.1 nM. In human and rabbit plasma, Rivaroxaban more potently inhibits endogenous FXa (IC50 21 nM) compared to rat plasma (IC50 290 nM). It effectively doubles prothrombin time and activates partial thromboplastin time at concentrations of 0.23 μM and 0.69 μM, respectively, indicating its anticoagulant effects[2].
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