A key accident in the final stages of claret agglomeration is the about-face of fibrinogen into fibrin by the serine protease agitator thrombin. Thrombin is produced from prothrombin, by the action of an enzyme, prothrombinase (Factor Xa forth with Agency Va as a cofactor), in the final states of coagulation. Fibrin is again cantankerous affiliated by agency XIII (Fibrin Stabilizing Factor) to anatomy a claret clot. The arch inhibitor of thrombin in accustomed claret apportionment is antithrombin. Similar to antithrombin III, the anticoagulatant action of hirudin is based on its adeptness to arrest the procoagulant action of thrombin.

Hirudin is the a lot of almighty accustomed inhibitor of thrombin. Unlike antithrombin, hirudin binds to and inhibits alone the action of thrombin, with a specific action on fibrinogen. Therefore, hirudin prevents or dissolves the accumulation of clots and thrombi (i.e., it has a thrombolytic activity), and has ameliorative amount in claret agglomeration disorders, in the analysis of derma hematomas and of apparent varicose veins, either as an injectable or a contemporary appliance cream. In some aspects, hirudin has advantages over added frequently acclimated anticoagulants and thrombolytics, such as heparin, as it does not baffle with the biological action of added serum proteins, and can aswell act on complexed thrombin.

It is difficult to abstract ample amounts of hirudin from accustomed sources, so a adjustment for bearing and antibacterial this protein application recombinant biotechnology has been developed. This has led to the development and business of a amount of hirudin-based anticoagulant biologic products, such as lepirudin (Refludan), hirudin acquired from Hansenula (Thrombexx, Extrauma) and desirudin (Revasc/Iprivask). Several added absolute thrombin inhibitors are acquired chemically from hirudin.

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