Abagat

Dabigatran acts through competitive and reversible inhibition of both free and fibrin-bound thrombin activity.‍​‍‍‍​‍‍‍‍‍‍‍‍​‍ By inhibiting thrombin, it blocks the conversion of fibrinogen into fibrin, which forms the clot. Additionally, it inhibits the activity of factor XIII, which is responsible for clot stabilization (fibrin does not assume its cross-linked stabilized form). As a result of the drug's action, thrombin-induced platelet aggregation is inhibited. Dabigatran is rapidly absorbed from the gastrointestinal tract, but its bioavailability is low, ranging from 3–7%. Peak plasma concentration is reached 0.5–2 hours after oral administration. Reduced absorption and prolonged time to peak concentration (approximately 6 hours) have been observed in postoperative patients (particularly on the first day after surgery). Co-administration with food also delays peak concentration by approximately 2 hours. Administration of the drug without the HPMC capsule shell increases bioavailability by approximately 75%; therefore, proper administration must be observed (the capsule must be swallowed whole). Dabigatran is 34–35% bound to plasma proteins. The drug, in the form of dabigatran etexilate, is a prodrug that undergoes conversion to pharmacologically active dabigatran. The principal metabolic reaction of dabigatran is esterase-mediated hydrolysis. Cytochrome P450 is not involved in the drug's metabolism. Dabigatran is excreted 85% unchanged in the urine, while the remaining portion of the dose is excreted in bile via feces as glucuronide conjugates. The elimination half-life after repeated dosing is 12–14 hours.