Apixaban is an oral, direct factor Xa inhibitor that inhibits both free and clot-bound factor Xa, and has been approved for
clinical use in several thromboembolic disorders, including reduction of stroke risk in non-valvular atrial fibrillation, thromboprophylaxis
following hip or knee replacement surgery, the treatment of deep vein thrombosis or pulmonary embolism,
and prevention of recurrent deep vein thrombosis and pulmonary embolism. The absolute oral bioavailability of apixaban
is ~ 50%. Food does not have a clinically meaningful impact on the bioavailability. Apixaban exposure increases dose proportionally
for oral doses up to 10 mg. Apixaban is rapidly absorbed, with maximum concentration occurring 3–4 h after
oral administration, and has a half-life of approximately 12 h. Elimination occurs via multiple pathways including metabolism,
biliary excretion, and direct intestinal excretion, with approximately 27% of total apixaban clearance occurring via
renal excretion. The pharmacokinetics of apixaban are consistent across a broad range of patients, and apixaban has limited
clinically relevant interactions with most commonly prescribed medications, allowing for fixed dosages without the need
for therapeutic drug monitoring. The pharmacodynamic effect of apixaban is closely correlated with apixaban plasma concentration.
This review provides a summary of the pharmacokinetic, pharmacodynamic, biopharmaceutical, and drug–drug
interaction profiles of apixaban. Additionally, the population-pharmacokinetic analyses of apixaban in both healthy subjects
and in the target patient populations are discussed