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MedImmune and Micromet Publish Data on Novel Anti-Cancer BiTE,Molecule

- New Compound Targeting Receptor Tyrosine Kinase EphA2 Shows Tumor Destruction at Low Dose Levels in Preclinical Models -

GAITHERSBURG, Md. and CARLSBAD, Calif., April 19, 2007 /PRNewswire-FirstCall/ -- MedImmune, Inc. and Micromet, Inc. today announced that published proof-of-concept data with a new BiTE(R) molecule (bscEphA2xCD3) show that the compound killed tumor cells at dose levels considerably below those required by classical monoclonal antibody-based therapies. The in vitro and in vivo data, collected from cell culture experiments conducted under the companies' BiTE(R) technology research collaboration, were published in the April 15, 2007 issue of Cancer Research.

BiTE molecules represent a novel class of drugs that function as bi- specific T-cell engagers. They are unique in their ability to enable the body's killer T cells to recognize and attack tumor and target cells, leaving normal cells unharmed. bscEphA2xCD3 is a BiTE molecule targeting the tyrosine kinase receptor EphA2, which is frequently overexpressed on a wide variety of solid tumors.

"The results of this study show that a receptor tyrosine kinase may be an appropriate target for a BiTE molecule," said Patrick Baeuerle, Ph.D., Micromet's Chief Scientific Officer. "This highlights the breadth of the BiTE technology for creating molecules that target different kinds of antigens. Recognition of selected sites on a target antigen may provide a means to widen the therapeutic window for this highly potent therapeutic approach."

In the preclinical study, tumor cell destruction approached 100 percent even at low ratios of effector T cells to target cells. In animal models, the BiTE compound redirected unstimulated human T cells to inhibit outgrowth of transplanted human tumor cells. Time-lapsed videomicroscopy showed that bscEphA2xCD3 triggered T cells to destruct tumor cells overexpressing EphA2, but spared normal cells wher
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