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Coagulation factor XI is a human blood protein and serine protease zymogen essential for the intrinsic pathway of the coagulation cascade. Synthesized primarily in the liver, it is activated to its enzymatic form, factor XIa, by either thrombin or activated factor XII. Once activated, it plays a key role in amplifying thrombin generation by activating downstream factors such as IX and X, consolidating clot formation and increasing resistance to fibrinolysis. While crucial for stabilizing clots—especially in areas with high fibrinolytic activity—factor XI is less important for initial hemostasis than other factors. Deficiency leads to mild bleeding disorders (hemophilia C), while pharmacological inhibition of FXI/FXIa is being explored as an anticoagulant strategy that may reduce pathologic thrombosis risk with less bleeding compared to traditional anticoagulants[1][3][4][5][6][8].
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