Hirudin is a naturally occurring peptide in the salivary glands of blood-sucking leeches that has a blood anticoagulant property.
Recombinant techniques can be used to produce homogeneous preparations of hirudin.
The anticoagulant activity of hirudin is based on its ability to inhibit the procoagulant activity of thrombin.
In the final stages of blood coagulation the conversion of fibrinogen into fibrin by a serine protease enzyme.
Thrombin is produced from prothrombin, by the action of an enzyme, prothrombinase (Factor Xa along with Factor Va as a cofactor), in the final states of coagulation.
Fibrin is then cross linked by factor XIII (Fibrin Stabilizing Factor) to form a blood clot.
The principal inhibitor of thrombin in normal blood circulation is antithrombin.
Similar to antithrombin, the anticoagulant activity of hirudin is based on its ability to inhibit the procoagulant activity of thrombin.
Hirudin is the most potent natural inhibitor of thrombin.
Unlike antithrombin, hirudin binds to and inhibits only the activated thrombin, with a specific activity on fibrinogen.
Hirudin prevents or dissolves the formation of clots and thrombi with thrombolytic activity and has therapeutic value in blood coagulation disorders, in the treatment of skin hematomas and of superficial varicose veins, either as an injectable or a topical application cream.
It has advantages over more commonly used anticoagulants and thrombolytics, such as heparin, as it does not interfere with the biological activity of other serum proteins, and can also act on complexed thrombin.
Hirudin-based anticoagulant pharmaceutical products, such as lepirudin (Refludan), hirudin derived from Hansenula (Thrombexx, Extrauma) and desirudin (Revasc/Iprivask), and
other direct thrombin inhibitors are derived chemically from hirudin.