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| |  Alexion C5 Inhibitor Protects Blood Vessel Cells From Damage BOSTON, Nov. 11, 1996 -- At the 69th Scientific Sessions of the American Heart Association, Alexion Pharmaceuticals Inc.'s (Nasdaq: ALXN) C5 Inhibitor (5G1.1-SC) was reported to block the damage to blood vessel cells induced by hypoxia and reoxygenation in a study by Dr. Gregory Stahl, Assistant Professor of Anesthesia at Harvard Medical School and Associate Physiologist in the Center for Experimental Therapeutics and Reperfusion Injury at Brigham and Women's Hospital. In a model of tissue injury designed to simulate the damage that occurs with occlusion of a blood vessel leading to a heart attack, blood vessel endothelial cells were starved of oxygen and subsequently replenished with normal amounts of oxygen. The report demonstrates that oxygen starved endothelial cells activate a cascade of inflammatory complement proteins that then damage the endothelial cells upon reoxygenation. The presented work farther demonstrates that administration of Alexion's recombinant C5 Complement Inhibitor, 5G1.1-SC, completely blocked the complement activation and subsequent endothelial damage. "These experiments are the first to demonstrate that during oxygen starvation endothelial cells directly activate the complement cascade of inflammation and that the activated terminal complement proteins are responsible for directly damaging the same endothelial cells during reoxygenation," said Dr. Stahl. "Further, blockade of the complement cascade selectively at C5 with Alexion's 5G1.1-SC completely prevents production of the harmful components of complement responsible for hypoxia-induced endothelial cell damage." Alexion's C5 Inhibitors are specific and potent recombinant drugs which are designed to intervene in the complement cascade, The Company believes that these proprietary C5 Inhibitors intervene at an optimal point which generally preserves the normal disease-preventing functions of complement proteins while generally inhibiting the disease-causing actions. 5G1.1-SC is a novel compound, specifically designed to rapidly penetrate tissue and limit inflammation. In preclinical studies, Alexion's C5 Inhibitors substantially prevent the activation of complement, platelets, and neutrophils and the subsequent inflammatory process that occurs during cardiopulmonary bypass (CPB) and reduce myocardial infarction (MI) associated with ischemia and reperfusion. Alexion completed a Phase I safety trial with 5G1.1-SC in September and 5G1.1-SC is currently being tested in a Phase I/II clinical trial in patients undergoing CPB. According to the most recent statistics available from the American Heart Association, there are approximately 450,000 CPB surgical procedures performed and approximately 1,000,000 patients suffer an MI in the U.S. each year. "Dr. Stahl's work describes on a cellular level the critical contribution of the complement system to causing acute cardiovascular inflammation," said Dr. Leonard Bell, President and Chief Executive Officer of Alexion. "These fundamental studies support the scientific rationale for the development of 5G1.1-SC targeting several significant cardiovascular disorders including CPB-associated inflammation, myocardial infarction and stroke." Alexion Pharmaceuticals Inc. was founded in 1992 and is engaged in the development of selective immunotherapeutic drugs that generally are designed to inhibit the disease-causing segments of the inumme system while preserving the disease-preventing aspects of the immune system. The Company is developing three technology platforms: C5 Complement Inhibitors and Apogen T-Cell Therapeutics which together target severe cardiovascular and autoimmune disorders; and xenografts for organ transplantation. This news release contains forward looking statements. Such statements are subject to certain factors which may cause the Company's plans to differ or results to vary from those expected including unexpected preclinical or clinical results, delays in manufacturing, access to capital, development of commercial relationships and a variety of risks set forth from time to time in the Company's filings with the securities and Exchange Commission, including but not limited to the Company's Annual Report and 10-K for the year ended July 31, 1996. The Company undertakes no obligation to publicly release results of any of these forward-looking statements which may be made to reflect events or circumstances after the date hereof or to reflect the occurrence of unanticipated events.
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