Endogenous (or Natural) Protein C
And Endogenous Activated Protein C

Severe sepsis is a leading cause of death in the United States, claiming 215,000 lives each year - more than breast, colon/rectal, pancreatic, and prostate cancer combined. This syndrome, characterized by an overwhelming systemic response to infection, strikes hard and can rapidly lead to organ dysfunction and death.

Sepsis is so complex that a treatment that specifically attacks the syndrome has remained elusive for decades. Now many scientists believe a regulatory system called the Protein C pathway may be a key to the management of sepsis.

In people with sepsis, coagulation, the formation of blood clots, is increased; fibrinolysis, the body's clot-busting system, is decreased; and the Protein C pathway, a regulatory system that inhibits coagulation, supports fibrinolysis, and controls inflammation, is suppressed. The body no longer is able to regulate inflammation and coagulation, which may lead to tissue damage, organ failure, and death.

The Protein C molecule, which occurs naturally and is found in the bloodstream, has no biological effect by itself. But in the presence of coagulation, the molecule goes through four complex chemical modifications to form endogenous (or naturally occurring) Activated Protein C, a biologically active molecule that has multiple properties, including anti-thrombolytic, anti-inflammatory, and pro-fibrinolytic effects.

Evidence suggests that sepsis impairs this activation process. As a result, patients with sepsis have a deficient amount of endogenous Activated Protein C to help control inflammation, coagulation and fibrinolyis.