Direct factor Xa inhibitors
Thrombin · detail · Rivaroxaban Apixaban Andexanet
Rivaroxaban, apixaban and edoxaban bind the active site of factor Xa directly, inhibiting both free Xa and Xa already assembled in prothrombinase, without needing antithrombin as an intermediary. They give predictable anticoagulation without routine monitoring.
Traced from the start
- Tissue factor and the extrinsic triggerVitamin K cycle and gamma-carboxylation
- Contact activation system (factor XII, prekallikrein, high-molecular-weight kininogen)
- Subendothelial collagen and von Willebrand factor
- Tissue factor-factor VIIa complex (extrinsic tenase)Factor IXaFactor VIIIa and its von Willebrand factor carrierActivated platelet phospholipid surface
- Factor Xa
- Direct factor Xa inhibitors
Detail
- Drugs
- Rivaroxaban, apixaban, edoxaban (the -xabans)
- Uses
- Non-valvular atrial fibrillation, and treatment and prevention of venous thromboembolism
- Not for
- Mechanical heart valves and moderate-to-severe rheumatic mitral stenosis, where warfarin remains mandatory; caution in severe renal impairment
- Monitoring
- None routinely; a drug-calibrated anti-Xa assay if a level is genuinely needed. PT and APTT are unreliable and a normal result does not exclude drug effect
- Reversal
- Andexanet alfa, a decoy factor Xa; prothrombin complex concentrate where andexanet is unavailable
When it goes wrong
Triple-positive antiphospholipid syndrome anticoagulated with rivaroxaban
Higher rate of arterial thrombotic events than with warfarin — vitamin K antagonists remain the standard of care in this group
Practise this structure
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