Dabigatran is a direct oral anticoagulant (DOAC) that does not require therapeutic monitoring. Its mechanism differs from warfarin because:
- A Dabigatran inhibits factor Xa directly in both free and fibrin-bound forms
- B Dabigatran directly and reversibly inhibits thrombin (factor IIa) without requiring antithrombin as a cofactor ✓
- C Dabigatran inhibits vitamin K epoxide reductase, depleting active vitamin K
- D Dabigatran inhibits the prothrombinase complex (factors Xa + Va)
Explanation
Dabigatran (a direct thrombin inhibitor/DTI) binds directly and reversibly to the active site of thrombin (factor IIa), inhibiting both free and fibrin-bound thrombin without requiring antithrombin as a cofactor, unlike heparins. Warfarin inhibits vitamin K-dependent coagulation factor synthesis (II, VII, IX, X). Dabigatran's reversal agent is idarucizumab, a specific antibody fragment. Factor Xa inhibitors (rivaroxaban, apixaban) correspond to option A.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.