Complement’s Role in Cardiovascular Disease – Brief Article

Researchers from Alexion Pharmaceuticals, Inc. (25 Science Park, New Haven, CT 06511; Tel: 203/776-1790, Fax: 203/772-3655) and Brigham and Women’s Hospital have described a new pathway for complement-mediated inflammation in cardiovascular disease in a paper published in the May 3 issue of the American Journal of Pathology.

The paper is entitled “Complement Activation After Oxidative Stress: Role of the Lectin Complement Pathway” and includes studies from the laboratories of Greg Stahl, staff physiologist at Brigham and Women’s Hospital and associate professor of anesthesiology at Harvard Medical School, and Scott Rollins, senior director of drug development and project management at Alexion.

The studies by Stahl and Rollins demonstrate that the damage associated with oxidative stress to endothelial cells is initiated by the binding of a specific protein, known as MBL, to endothelial cells and subsequent complement activation via the Lectin Pathway. A family of MBL-specific monoclonal antibodies that block inflammation is also described in the manuscript.

“Our results indicate that MBL may play a dominant role in the activation of complement on the surface of injured endothelial cells,” Stahl says.

“In addition to the multiple novel therapeutics that may emerge from this technology, we have already identified a lead antibody product candidate,” states Leonard Bell, president and CEO of Alexion. “Further development will allow us to evaluate its potential utility for the treatment of patients with both acute and chronic cardiovascular diseases.”

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COPYRIGHT 2003 Gale Group

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