Dabigatran (a direct thrombin inhibitor) differs from warfarin in that it:
- A Requires antithrombin III as a cofactor to exert its anticoagulant effect
- B Inhibits vitamin K epoxide reductase, depleting all vitamin K-dependent clotting factors over several days
- C Is reversed exclusively by protamine sulfate in cases of major bleeding
- D Directly and reversibly inhibits both free and clot-bound thrombin without requiring any cofactor, with predictable pharmacokinetics not requiring routine INR monitoring ✓
Explanation
Dabigatran etexilate is a prodrug converted to dabigatran, a direct thrombin (FIIa) inhibitor that binds reversibly to both free circulating and fibrin-bound thrombin without requiring antithrombin III as a cofactor (unlike heparin). Its predictable pharmacokinetics allow fixed dosing without routine INR monitoring. It is reversed by idarucizumab, a specific monoclonal antibody. Antithrombin III-dependence characterises heparin. Vitamin K epoxide reductase inhibition is warfarin's mechanism. Protamine reverses heparin, not dabigatran.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.