Lipopolysaccharide (LPS), the major outer wall component of Gram-negative bacteria, plays a critical role in the pathogenesis of sepsis and are known to contribute to the development of disseminated intravascular coagulation (DIC) syndrome. Since LPS aggregates are negatively charged, we hypothesized that LPS may directly interact with and activate the contact pathway coagulation factor (F) XII as part of the pathogenesis of DIC. This project aims to investigate the mechanisms of interaction and activation of FXII by LPS chemotypes.