 According to this model, the procoagulant reaction occurs in three distinct steps, initiation, amplification and propagation. Initiation of coagulation takes place on tissue factor-bearing cells e.g., activated monocytes, macrophages, and endothelial cells. Coagulation factor VIIa, which forms a complex with tissue factor, catalyzes the activation of coagulation factors IX FIX and X FX, which in turn generates a small amount of thrombin from prothrombin. In the amplification phase also referred to as the priming phase, the small amount of thrombin generated in the initiation phase activates coagulation factors V, VIII, and XI and also activates platelets, which supplies a surface upon which further procoagulant reactions occur. In vivo, the small amounts of thrombin generated during the amplification phase are not sufficient to convert fibrinogen to fibrin, due to the presence of endogenous thrombin inhibitors termed serpins, such as anti-thrombin III, -2-macroglobulin and heparin cofactor II. The final phase of the procoagulant reaction, propagation, occurs exclusively on the surface of activated platelets. During propagation, significant amounts of FIXa are generated by the FXIa-catalyzed activation of FIX. FIXa forms a complex with its requisite cofactor FVIIIa, which activates FX. Subsequently, FXa forms a complex with its requisite cofactor FVa. The FXa-FVa complex activates prothrombin, which leads to a burst of thrombin generation and fibrin deposition. The end result is the formation of a stable clot. 