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Ancrod is a defibrinogenating agent and anticoagulant derived from the venom of the Malayan pit viper (Calloselasma rhodostoma). It acts as a serine protease that specifically cleaves the alpha chain of fibrinogen, resulting in rapid reduction of circulating plasma fibrinogen levels. This leads to decreased blood viscosity and impaired clot formation, producing small, unstable fibrin polymers that are readily degraded by plasmin and removed from circulation. Ancrod does not activate plasminogen or degrade preformed cross-linked thrombin fibrin. Its primary mechanism is inhibition of clot propagation through depletion of fibrinogen and facilitation of endogenous fibrinolysis. Ancrod has been investigated for acute ischemic stroke, peripheral vascular disorders, heparin-induced thrombocytopenia with thrombosis syndrome (HITTS), thromboembolism, and sensorineural hearing loss. It was granted orphan drug status for HITTS but is not currently approved or marketed in any country due to inconsistent clinical trial results[1][2][3][5][7].
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