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Apixaban CAS 503612-47-3 BMS-562247 

Payment Terms: T/T,L/C,WU 
Place of Origin: Shandong, China (Mainland) 
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Product Detail

Model No.: C25H25N5O4
Production Capacity: 1000 KG / month
Delivery Date: within 7 days
Molecular Formula: C25H25N5O4
Specification: CP/USP/EP
Density: 1.421g/cm3
Boiling point: 770.468°C at 760 mmHg
Vapour pressure: 0mmHg at 25°C
Means of Transport: Ocean,Land,Air
Packing: As per request of clients
Molecular Weight: 459.50
Content: 98%min
CAS: 503612-47-3
Flashing point: 419.764°C

Apixaban is an anticoagulant for the prevention of venous thromboembolism and the prevention of stroke in atrial fibrillation.

Apixaban ( CAS: 503612-47-3 )



Molecular Formula


Molecular Weight






Apixaban (INN, trade name Eliquis) is an anticoagulant for the prevention of venous thromboembolism and the prevention of stroke in atrial fibrillation. It is a direct factor Xa inhibitor. Apixaban has been available in Europe since May 2011. The drug was developed in a joint venture by Pfizer and Bristol-Myers Squibb. 


Overdose of apixaban may result in a higher risk of bleeding. In the event of haemorrhagic complications, treatment must be discontinued. There is no established way to reverse the anticoagulant effect of apixaban, which can be expected to persist for about 24 hours after the last dose (i.e., about two half-lives). A specific antidote is not available.  Although treatment with apixaban does not require routine monitoring of exposure, the Rotachrom® anti-FXa assay may be useful in exceptional situations where knowledge of apixaban exposure may help to inform clinical decisions, e.g., overdose and emergency surgery.


There is increased risk of (mainly ischemic) stroke with discontinuation of apixaban. Discontinuing apixaban in the absence of adequate alternative anticoagulation increases the risk of thrombotic events. An increased rate of stroke was observed during the transition from apixaban to warfarin in clinical trials in patients with nonvalvular atrial fibrillation within the first 30 days of transition. This resumption of events was probably related to inadequate control of anticoagulation, but induction of a hypercoagulable state by long-term treatment with the NOAC has not been ruled out. If apixaban must be discontinued for a reason other than pathological bleeding, consider coverage with another anticoagulant.

Drug interactions

Strong dual Inhibitors of CYP3A4 and P-gp (e.g., ketoconazole (Nizoral), itraconazole (Sporanox), ritonavir, or clarithromycin) increase the exposure to apixaban and increase the risk of bleeding . These medicinal products may increase apixaban exposure by 2-fold. Less potent inhibitors of CYP3A4 and/or P-gp as diltiazem and naproxen led to a 1.4-fold and 1,5 fold increase in mean apixaban concentration.

Strong dual inducers of CYP3A4 and P-gp decrease exposure to apixaban and increase the risk of stroke. Avoid concomitant use of apixaban with rifampin, carbamazepine (Tegretol), phenytoin and St. John's wort, because such medicine may lead to a ~50% reduction in apixaban exposure.

Coadministration of antiplatelet agents, fibrinolytics, heparin, aspirin, and chronic NSAID increases the risk of bleeding.

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