Blog Date 29 March, 2023



Apixaban, a pyrazole derivative, is chemically described as 1-(4-methoxyphenyl)-7-oxo-6-[4-(2-oxopiperidin-1-yl) phenyl]-4,5,6,7-tetrahydro-1H-pyrazolo[3,4c] pyridine-3-carboxamide.Its molecular formula is C25H25N5O4, and its molecular weight is 459. 

Apixaban is a novel oral anticoagulant (NOAC) approved by the US Food and Drug Administration (FDA) in 2012 for use in patients with non-valvular atrial fibrillation to reduce the risk of stroke and blood clots. In 2014, it was approved to treat deep venous thrombosis (DVT) and pulmonary embolism (PE). 

Apixaban is used to treat or prevent blood clots, including deep vein thrombosis, which can lead to pulmonary embolism. It can also prevent stroke in patients with non-valvular atrial fibrillation. It is often given to patients after hip or knee replacement surgery to prevent clotting during recovery. It is administered orally and is safer and more convenient than warfarin, the medication previously used for these purposes.

Apixaban’s mode of action is factor Xa inhibition. Factor Xa is activated by the hydrolysis of factor X, an enzyme that is a component of the coagulation (clotting) cascade. Factor Xa, in turn, catalyses the conversion of prothrombin to thrombin, the enzyme that promotes the formation of fibrin clots.

Mechanism of Action:

The clotting cascade is a complex process involving multiple factors acting in three defined phases: initiation, propagation, and fibrin formation.

Initiation: This step occurs when the vascular endothelium and the clotting factors are disturbed.

Propagation: This step involves the production of large amounts of thrombin at the site of injury.

Fibrin Formation: Thrombin acts on fibrinogen to form fibrin. 

 The coagulation proteins form the basic components of the coagulation system. They lead to a complex interplay of reactions resulting in converting plasma-soluble fibrinogen to insoluble fibrin strands. There are two main pathways to the clotting cascade: the intrinsic and extrinsic pathways. External trauma activates the extrinsic pathway and causes blood loss from the vascular system, and it is faster than the intrinsic pathway and involves factor VII. Trauma inside the vascular system activates platelets via exposed endothelium, chemicals, or collagen, which can initiate the intrinsic pathway. It involves factors XII, XI, IX, and VIII. Both pathways share a common ending where they activate factor X to Xa, which activates prothrombin (II) to thrombin (IIa), thereby forming a stable clot.

Apixaban is a highly selective direct factor Xa inhibitor, blocking the propagation phase of the coagulation cascade. It exerts its effect on both free and clot-bound factor Xa. For antithrombotic activity, it does not need antithrombin III. Factor Xa is a catalyst for the conversion of prothrombin to thrombin, which is the final step in the coagulation cascade leading to fibrin and clot formation.[9] Other direct factor Xa inhibitors include rivaroxaban and edoxaban.

Apixaban exerts no effect on platelet aggregation.

Some of the impurities of Apixaban are tabulated below:


CatLog Number

Product Name

Cas No.





Apixaban Formyl Impurity



Apixaban Chloro impurity



Apixaban N-Oxide Dimer Impurity



Apixaban Impurity D



Apixaban Methyl Impurity






4,5-Dehydro Apixaban


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