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Type 1 diabetes safely arrested with short-term use of new drug

ost. In the mid-1980s, protracted therapy with the immunosuppressive drugs cyclosporine and azathioprine were shown to preserve remaining beta cell function in newly diagnosed patients. But because patients in these trials generally suffered serious side effects from the drugs, such as increased infection risk, kidney disease and certain types of cancer, most of these studies were abandoned.

The new drug, a humanized monoclonal antibody known as hOKT3g1 (ala-ala), acts far more selectively and requires only a short treatment period compared with the earlier immunosuppressive drugs. The selectivity and shorter use are intended to minimize toxicity, and hOKT3g1 (ala-ala) caused few side effects, the study showed.

The drug was designed to prevent activation of T cells that have already identified their target in this case, the insulin producing beta cells in the pancreas. In effect, hOKT3g1 (ala-ala) disarms the T cells once they are poised to attack their target, says UCSFs Jeffrey Bluestone.

Dr. Bluestone developed the monoclonal antibody drug in the late 1980s in collaboration with Johnson & Johnson. He designed it to target activated T cells. In addition, the monoclonal antibody was humanized to avoid provoking an immune response in the host against the drug.

Diabetes, with its many long-term complications, ranks fourth among diseases in its cost to society. One million people in the U.S. have Type 1 diabetes, also known as juvenile diabetes, in which the immune system destroys the bodys natural insulin-secreting islet cells. Another 15 million people have Type 2 diabetes in which obesity, inactivity and other conditions interfere with the bodys insulin control.

The two-week administration of the new drug is not expected to forestall Type 1 diabetes indefinitely, but it significantly extends the period during which patients continue to produce their own insulin, which is likely to reduce complications and improve their ov
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Contact: Annie Bayne
as862@columbia.edu
212-305-3900
Columbia University Medical Center
29-May-2002


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