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Table. Characteristics of oral anticoagulants.

Warfarin Apixaban Dabigatran Rivaroxaban
Brand Coumadin, Marevan Eliquis Pradaxa Xarelto
Licensed indications AF, VTE, valvular heart disease AF, VTE AF AF, VTE
Dosing frequency daily twice daily twice daily Daily
Oral bioavailability 100% 50% 7% >80% §
Excretion unchanged in urine 0% 34% 80% 36%
Major metabolic/transport pathways CYP2C9 CYP3A4, P-glycoprotein P-glycoprotein # CYP3A4, P-glycoprotein
Drug half-life
healthy young individuals 40 hours 10 hours 14 hours 7 hours
chronic kidney disease
          moderate not reported not reported 19 hours 9 hours
          severe 28 hours 10 hours
chronic liver disease
          moderate not reported not reported 12 hours 10 hours
          severe not reported not reported
Effect of chronic disease on anticoagulant concentrations **
chronic kidney disease
          moderate not reported 30% increase 210% increase 50% increase
          severe 40% increase 530% increase 60% increase
chronic liver disease
          moderate not reported 9% increase 6% decrease 120% increase
          severe not reported not reported not reported
Effect of concomitant drugs on anticoagulant concentrations †† Amiodarone increases anticoagulant Erythromycin increases anticoagulant Verapamil increases anticoagulant Erythromycin increases anticoagulant
Rifampicin decreases anticoagulant Rifampicin decreases anticoagulant Rifampicin decreases anticoagulant Rifampicin decreases anticoagulant

AF atrial fibrillation

VTE venous thromboembolism

CYP cytochrome P450

All values are means.

† Initial dosing in normal renal function is twice daily, maintenance dose is once daily.

‡ Values in healthy young individuals.

§ When administered with food (when fasting, the oral bioavailability of rivaroxaban 20 mg is 66%).

# Dabigatran etexilate, the prodrug of dabigatran, but not dabigatran itself, is a P-glycoprotein substrate.

Kidney and liver disease usually reduce drug clearance and thus increase drug half-lives.

** For example, 100% increase indicates that concentrations were double that of the reference healthy group.

†† See Australian Medicines Handbook interaction tables for more examples of drugs that inhibit or induce metabolic or transport pathways.

Source: References 1, 2