Rivaroxaban

Rivaroxaban is an orally bioavailable oxazolidinone derivative and direct inhibitor of the coagulation factor Xa with anticoagulant activity. Upon oral administration, rivaroxaban selectively binds to both free factor Xa and factor Xa bound in the prothrombinase complex. This interferes with the conversion of prothrombin (factor II) to thrombin and eventually prevents the formation of cross-linked fibrin clots. Rivaroxaban does not affect existing thrombin levels.

Rivaroxaban is indicated for the prevention of venous thromboembolic events (VTE) in patients who have undergone total hips replacement and total knee replacement surgery; prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation; treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE); to reduce risk of recurrent DVT and/or PE. Rivaroxaban is also indicated, in combination with aspirin, for reducing the risk of major cardiovascular events in patients with chronic coronary artery disease or peripheral artery disease.

Therapy Area: Stroke
Form: Tablet
Packaging: 1x 10, 1x 15 & 1x 10 Tablets

COMPOSITION:

Rivaroxaban 10 mg, 15mg & 20mg

MODE OF ACTION:

Rivaroxaban is a novel oral anticoagulant (NOAC) drug. Rivaroxaban – the first orally dosed, direct Factor Xa inhibitor – is a small-molecule oxazolidinone derivative. It binds directly and reversibly to Factor Xa via the S1 and S4 pockets. Rivaroxaban competitively inhibits Factor Xa, demonstrating more than 10,000-fold selectivity for Factor Xa than other related serine proteases, and it does not require any cofactors (such as antithrombin) to exert its anticoagulant effect. This activity prevents the progression of the coagulation cascade through the final common pathway, preventing thrombin generation. The factor Xa is active in circulating and clot-bound forms. Unlike indirect Factor Xa inhibitors like fondaparinux or heparin, rivaroxaban inhibits both free and clot-bound Factor Xa, as well as prothrombinase activity, thereby prolonging clotting times.

Metabolism of this drug occurs in the liver via oxidative degradation catalyzed by CYP3A4/5 and CYP2J2 mechanism.

Excretion occurs mostly via Urine 66% and party via feces 28%

INDICATIONS

  • Stroke prophylaxis
  • Venous Thromboembolism Event
  • Deep Vein Thrombosis
  • Pulmonary Embolism

Dosage

Non-valvular Atrial Fibrillation & Stroke prophylaxis: 20 mg once daily with the evening meal

Acute VTE (or DVT) & PE treatment: 15 mg twice daily with food for three weeks; then 20 mg once daily with food

VTE (or DVT) & PE primary prevention: 10 mg once daily, with or without food

Disclaimer:

This information is for registered medical practitioner only. Anyone other than medical practitioner should consult medical practitioner before using this product.

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