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Idarucizumab mechanism of action
Idarucizumab mechanism of action








idarucizumab mechanism of action

Regular monitoring of coagulation parameters is not required → improved patient compliance.Easily manageable (similar to heparins) when administered orally.For more information about other drugs from this class, see direct thrombin inhibitors under parenteral anticoagulation.Not suited for acute therapy of pulmonary embolism or deep vein thrombosis.Broad range of interactions (see “ Warfarin interactions” below).Requires periprocedural bridging anticoagulation.

idarucizumab mechanism of action

  • Regular monitoring of the PT / INR required (as vitamin K antagonists affect the extrinsic coagulation pathway).
  • Indirect/ delayed reversal by increasing production of coagulation factors (e.g., with vitamin K substitution).
  • Direct reversal by replacement (e.g., with prothrombin complex concentrate, FFP ).
  • idarucizumab mechanism of action

    Mutations and polymorphisms in gene VKORC1 alter the effect of vitamin K antagonists.Inhibit hepatic vitamin K epoxide reductase → ↓ hepatic synthesis (recycling) of the active, reduced form of vitamin K → ↓ γ- carboxylation of glutamate residues on coagulation factors II, VII, IX, and X as well as protein C and protein S.Overview of commonly used oral anticoagulants For all substances, it is important to consider the dose-dependent risk of bleeding, especially when combining different substances that affect hemostasis (e.g., aspirin, clopidogrel, ticagrelor). Because of their comparatively short half-life and fewer interactions, NOACs are easier to control and administer than warfarin and do not require regular monitoring to ensure their efficacy and safety. NOACs act selectively via inhibition of thrombin ( dabigatran) or factor Xa ( rivaroxaban, apixaban, edoxaban). Vitamin K antagonists are also metabolized by C-P450 ( CYP) enzymes and therefore interact with a broad range of foods and drugs. This effect can last for several days, which complicates exact dosing and makes regular monitoring necessary. Vitamin K antagonists inhibit the enzyme vitamin K epoxide reductase, thereby blocking hepatic synthesis of the active, reduced form of vitamin K (needed for carboxylation of coagulation factors II, VII, IX, and X, protein C, protein S). Non- vitamin K antagonist oral anticoagulants ( NOACs) like dabigatran and rivaroxaban have also gained popularity in recent years. The most common oral anticoagulatory agents are vitamin K antagonists such as warfarin and phenprocoumon. Anticoagulants are used for treating and preventing embolic events.










    Idarucizumab mechanism of action