Sepsis is a potentially fatal medical condition in which the blood is overwhelmed by the presence of bacteria; activating the immune response and potentially causing organ dysfunction due to disruption of homeostasis, tissue perfusion and limited oxygen supply. Systemic inflammatory response syndrome may be a key to disease recognition. This condition can be treated with intravenous antibiotics or by draining the infected fluid. However, treating the infection with appropriate antimicrobial drugs does not always cure the disease. Understanding the activation of inflammation, coagulation, and fibrinolysis in the pathophysiology of sepsis has enabled further research and development of therapeutic agents in its clinical treatment (Della, 2012). In response to pathogens infecting the body, leukocytes release cytokines, some examples are interleukin -1, 6 and tumor necrosis factor α (Bernard, 2001). These can cause extensive activation of coagulation and decreased fibrinolysis; the balance of the organism normally regulated by homeostasis is thus altered (van Deventer, 1990). Coagulation is activated by stimulating factors that lead to the generation of thrombin. Thrombin can stimulate inflammatory pathways, thereby further reducing fibrinolysis. However, activation is reduced in sepsis. An anticoagulant system that regulates thrombin formation is protein C; which is converted to its activated form by thrombin. Therefore, activated protein C (APC) alters the coagulation system and, in turn, prevents thrombosis and promotes fibrinolysis (Esmon, 1989). Protein C is a natural anticoagulant with key pathways beneficial in the treatment of sepsis; such as cytoprotective mechanisms that include ant... middle of paper...... of recombinant human activated protein C in a sheep model of septic shock. Critical Care Med. ;35(11):2594-600.van Deventer SJH, Bluller HR, ten Cate JW, Aarden LA, Hack CE, Sturk A. (1990) Experimental endotoxemia in humans: analysis of cytokine release and coagulation, fibrinolytic pathways and complement. Blood. ;76:2520–2528Hancock WW, Bach FH. (1997) Immunobiology and therapeutic applications of protein C/protein S/thrombomodulin in human and experimental allografts and xenografts. Trends Cardiovasc Med. ;7:174–183. Neyrinck AP, Liu KD, Howard JP, Matthay MA. (2009) Protective mechanisms of activated protein C in severe inflammatory disorders. Br. J Pharmacol. ;158(4): 1034–1047 Bernard GR, Vincent JL, Laterre PF, et al. (2001) Efficacy and safety of recombinant human activated protein C for severe sepsis. N English J Med. ;344:699–709.