The classic model of blood coagulation proposes a series of cascading reactions that result in clot formation. Thrombin is a key regulatory point in pathways that lead to blood coagulation, as well as those that reverse this process. The proteolytic actions of thrombin are inhibited by interaction with plasma serine proteinase inhibitors(“serpins”), such as heparin cofactor II. Novel HCII mutants with hyperactive thrombin inhibitory activity have been developed demonstrating improved blood coagulation inhibition, wound healing, and tissue repair properties.

File Number: 98-0045 

Other Information:

State of Development
pre-clinical