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The name hirudin is derived from Hirudo medicinalis, the medicinal leech used since antiquity in the practice of blood-letting, or phlebotomy. As the leech fastens onto the patient's skin, its salivary glands secrete a powerful anticoagulant that prevents the blood clotting that would deprive the leech of its meal.
 In 1884, John Haycraft, who was working in a pharmacology laboratory in Strasbourg, was able to demonstrate that leeches contained a substance with anticoagulant properties. Until the discovery of heparin, this substance was the only means physicians had to prevent blood from clotting.5
Finally, in the late 1950s, attempts to isolate the anticoagulant agent in leech saliva were successful, and hirudin was named and classified as a thrombin inhibitor. In 1976, the primary chemical structure of hirudin was established. A number of difficulties arose, however, in isolating hirudin from medicinal leeches. A limited number of leeches was available due to the failure of breeding trials, and leeches were placed on the endangered species list.5
Because of the shortage of leeches—and the potential value of hirudin for therapeutic purposes—hirudin was an appropriate candidate for production using genetic engineering. The development of recombinant technology has enabled production of large amounts or r-hirudin—now called lepirudin—which has many physicochemical characteristics and biochemical properties identical to those of the natural product.5
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![REFLUDAN [lepirudin (rDNA) for injection]: the first direct thrombin inhibitor FDA-approved for heparin induced thrombocytopenia (HIT)](../images/common/logo.gif){kind=logo}
