Idarucizumab is used to reverse dabigatran anticoagulation in emergencies. Its mechanism compared to andexanet alfa (which reverses factor Xa inhibitors) is:

• A Idarucizumab is a humanized monoclonal antibody Fab fragment with 350× higher affinity for dabigatran than dabigatran has for thrombin; it sequesters free dabigatran molecules in plasma by direct binding ✓
• B Idarucizumab competitively inhibits dabigatran binding at the thrombin active site by blocking the fibrinogen cleft
• C Andexanet alfa acts similarly to idarucizumab — both are antibody Fab fragments against their respective DOACs
• D Idarucizumab activates thrombomodulin to generate activated protein C, neutralizing dabigatran's anticoagulant effect indirectly

Explanation

Idarucizumab (Praxbind) is a humanized Fab fragment derived from a monoclonal antibody raised against dabigatran. Its binding affinity for dabigatran is approximately 350× higher than dabigatran's affinity for its target thrombin (IIa), enabling near-complete sequestration of both free and thrombin-bound dabigatran within minutes. It does not affect clotting factors and has no intrinsic anticoagulant or procoagulant effect. Andexanet alfa is structurally distinct — it is a modified recombinant inactive Factor Xa decoy that acts as a 'trap' for factor Xa inhibitors (rivaroxaban, apixaban, edoxaban), not an antibody. Neither mechanism involves thrombomodulin or protein C.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.