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Tissue factor mediated generation of thrombin in prothrombin complexes is inhibited by anti‐Xa based parenteral and oral agents but not by parenteral and oral antithrombin agents. Results from proteomic profiling using protein chip arrays

This study investigated the effects of direct factor Xa and thrombin inhibitors on tissue factor (TF) mediated activation of prothrombin complexes. Calcified Thromboplastin C and Innovin were used to activate buffered prothrombin complexes that were supplemented with graded concentrations of Xa inhibitors (Apixiban, Rivaroxiban, Otamaxiban) or thrombin inhibitors (Argatroban, Refludan, Hirudin, Melagatran). These mixtures were analyzed using a surface enhanced laser desorption ionization method over a molecular range of 0–150 kDa. Each of the prothrombin complexes provided a unique molecular spectrum with distinct peaks in 71–72 kDa range representing prothrombin. Upon activation, the prothrombin peak was diminished with the appearance of a 36–37 kDa peak representing thrombin. The factor Xa inhibitors produced a concentration dependent inhibition of the generation of thrombin whereas the thrombin inhibitors did not. As tissue factor plays an important role in the pathogenesis of thrombotic stroke and acute coronary syndrome, this data suggests that the anti‐Xa drugs may be more effective in the management of these syndromes. Furthermore, the observed myocardial infarcation signal with the oral thrombin inhibitors Dabigatran and Ximelagatran may be due to residual tissue factor activation of thrombin in patients treated with these drugs.