Do you share some concern that the transient elevation in D-dimer and prothrombin fragment 1+2 occurring after the administration of andexanet, and also the overshoot of endogenous thrombin potential as depicted in Figure 2, might reflect a net prothrombotic tendency, not showing up clinically in healthy volunteers where risk of thrombosis is low, but potentially affecting patients treated with a FXa inhibitor because of their prothrombotic condition?
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