Dear Editor, The severe coronavirus disease 2019 (COVID-19) is associated with coagulopathy. Anticoagulants, such as low-molecular-weight heparin, warfarin, thrombin inhibitors, and factor Xa (FXa) inhibitors, are thus recommended by the… Click to show full abstract
Dear Editor, The severe coronavirus disease 2019 (COVID-19) is associated with coagulopathy. Anticoagulants, such as low-molecular-weight heparin, warfarin, thrombin inhibitors, and factor Xa (FXa) inhibitors, are thus recommended by the American Society of Hematology and National Institutes of Health for COVID-19 patients (Wenzler et al., 2020; Adam et al., 2021). Clinical trials with anticoagulants have shown the increased survival of critically ill COVID-19 patients under non-invasive and invasive ventilatory assistance (Wenzler et al., 2020; Adam et al., 2021), along with decreased consumption of platelets and clotting factors and a reduced risk of hemorrhage (Adam et al., 2021). Among the anti-clotting agents, early use of orally available FXa and thrombin inhibitors (Chowdhury et al., 2020; Rentsch et al., 2021) prevented high levels of D-dimer, which is the final product from the clotting/fibrinolysis cascade and is directly implicated with severe COVID-19 (Rentsch et al., 2021). Curiously, the active binding pockets of FXa, thrombin, and the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) main protease (Mpro) share a considerable similarity, as judged by the superimposition of their 3D structures (Supplementary Figure S1; Biembengut and De Souza, 2020). Although structural similarities between FXa and thrombin with Mpro have been
               
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