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Tolerx Initiates Dosing of Otelixizumab, a Novel Type 1 Diabetes Agent, in DEFEND, a Phase 3 Clinical Trial
Date:8/6/2008

gnosed autoimmune type 1 diabetes," said Dr. Douglas J. Ringler, President and Chief Executive Officer of Tolerx.

For additional information about DEFEND, please visit http://www.DefendAgainstDiabetes.com.

About Type 1 Diabetes

Diabetes (medically known as diabetes mellitus) is the name given to disorders in which the body has difficulty regulating its blood glucose (sugar) level. There are two major types of diabetes: type 1 and type 2. Type 1, previously known as juvenile diabetes or insulin-dependent diabetes, is a disorder of the body's immune system. In type 1 diabetes, the immune system attacks and destroys the insulin-producing beta cells in the pancreas. The decrease in endogenous (natural) insulin production means that patients must monitor their glucose levels frequently and take insulin regularly to control their blood glucose levels.

About Otelixizumab

Otelixizumab is a monoclonal antibody that binds to CD3, a T lymphocyte receptor involved in normal cell signaling. Otelixizumab is thought to work by blocking the function of effector T cells that attack the body's tissues and cause autoimmune disease while inducing a subset of T cells known as regulatory T cells. It is thought that the regulatory T cells may protect against effector T cell damage well after the antibody has been eliminated from the body. In addition to DEFEND, Tolerx is also continuing to evaluate otelixizumab in subjects with type 1 diabetes in its ongoing Phase 2 study, TTEDD (TRX4 Therapeutic Evaluation of Different Dosing Regimens). A principal purpose of TTEDD is to evaluate different dosing regimens in an effort to reduce side effects and to acquire additional information about otelixizumab's clinical activity. Tolerx has conducted dose optimization studies in type 1 diabetes and has identified a dosing regimen that thus far has significantly reduced side effects while maintaining im
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SOURCE Tolerx, Inc.
Copyright©2008 PR Newswire.
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