Drug breakdown: dabigatran

Day 1: As the first new/non-vitamin K oral anti-coagulant (NOAC) in class and the first warfarin alternative for 50 years, #dabigatran was licensed in the USA/UK in 2010–11 for the treatment and prevention of DVT/PE, and prevention CVA/embolism in atrial fibrillation, if there is one or more risk factor

Day 2: #dabigatran is a direct thrombin inhibitor for adults, usually taken as 150 mg capsule twice daily, unless dose reduction is needed eg elderly >75 years, or in moderate renal impairment when dose 110–150 mg twice daily (not exhaustive)

Day 3: Kinetics; #dabigatran is a prodrug; post oral absorption, plasma + liver hydrolases convert it to the active form. Food delays time to peak plasma concentration. There is some conjugation converting to active metabolites, but most of the drug is excreted unchanged, t ½ 12–14 hrs. NOTE t½ is increased in renal impairment

Day 4: #dabigatran attaches to thrombin, as it looks like a peptide normally hydrolysed by thrombin as part of the coagulation cascade. Once bound, thrombin cannot perform its roles, such as converting fibrinogen to fibrin and catalysis of many other coagulation cascade reactions