Figure 1.

Central role of FXI(a) in the coagulation system. Inflamed or damaged endothelial layer results in exposure of tissue factor and activation of platelets and neutrophils leading to activation of the extrinsic pathway (via FVII) or contact pathway (via FXII), respectively. FXI activated by either by FXIIa or the feedback loop of thrombin will result in further thrombin generation though the intrinsic pathway. Attenuation of FXI activity inhibiting either FXI or FXIa leads to reduced thrombin formation and venous thromboemblism (light arrows), while the extrinsic pathway and the contact pathway remain unaffected (dark arrows).