Dabigatran and its acyl glucuronides are competitive, direct thrombin inhibitors. Because thrombin (serine protease) enables the conversion of fibrinogen into fibrin during the coagulation cascade, its inhibition prevents the development of a thrombus. Both free and clot-bound thrombin and thrombin-induced platelet aggregation are inhibited by the active moieties.

PRADAXA is a direct thrombin inhibitor indicated to reduce the risk of stroke and systemic embolism in patients with non-valvular atrial fibrillation.

For patients with CrCl >30 mL/min: 150 mg orally, twice daily
• For patients with CrCl 15-30 mL/min: 75 mg orally, twice daily.
• Instruct patients not to chew, break, or open capsules.
• Review recommendations for converting to or from other oral or parenteral anticoagulants.
• Temporarily discontinue PRADAXA before invasive or surgical procedures when possible, then restart promptly.

The most common adverse reactions (>15%) are gastritis-like symptoms and bleeding.

• Active pathological bleeding.
• History of serious hypersensitivity reaction to PRADAXA.

Risk of bleeding: PRADAXA can cause serious and, sometimes, fatal bleeding. Promptly evaluate signs and symptoms of blood loss.
• Temporary discontinuation: Avoid lapses in therapy to minimize the risk of stroke.
• P-gp inducers and inhibitors: Effects on dabigatran exposure.