Modulating the cellular inflammatory response to prevent thrombosis and PTS. Most venous thrombi originate in the valve pockets when endothelial cells activated by stasis and resultant hypoxia express adhesion molecules, such as P- and E-selectin, on their surface. Leukocytes express PSGL-1 on their surface, which tethers them to the P- or E-selectin on activated endothelial cells. Tethered leukocytes express tissue factor, which initiates coagulation, and release proinflammatory cytokines. Together, these factors promote thrombosis and inflammation, which can lead to PTS. SelK2 and GMI-1271 have the potential to block this process by inhibiting PSGL-1 and E-selectin, respectively.