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Micromet Data Presented at the International AACR-NCI-EORTC Conference Support the Development of Adecatumumab (MT201) in Earlier Stage Cancer Disease Settings
Date:10/23/2007

observed as patients treated with the higher dose of adecatumumab showed less new lesions compared to patients treated with low doses (10.0% versus 25.0% in very high EpCAM expressing patients, and 30.8% versus 62.5% in low EpCAM expressors, respectively).

"Adecatumumab treatment appears to decrease in a dose dependent fashion the formation and outgrowth of new metastatic lesions in the patient population with very high EpCAM expressing tumors. This phenomenon fits the expected mode of action of a targeted therapy very well," stated Prof. Christian Dittrich, former President of the Central European Society for Anticancer Drug Research (CESAR), and a lead investigator of the MT201-202 study, who presented the new data at the conference. "This observation is highly encouraging and, together with the overall good tolerability of adecatumumab, should support the investigation of adecatumumab in earlier stage disease settings, including adjuvant treatment."

Early and potentially prolonged treatment with adecatumumab is further supported by data on the lack of immunogenicity of this fully human antibody. Abstract B49 reports on the analysis of a total of 169 patients treated with adecatumumab in the two phase 2 studies in breast and prostate cancer. Only one patient has developed a detectable antibody response to adecatumumab, which was not neutralizing. Potential reasons discussed for this very low immunogenicity were closeness to germline, low tendency to aggregate and high stability of adecatumumab.

In addition to these clinical findings, results were presented by Olivier Gires, Ph.D. from the University Clinic of Munich in Grosshadern, Germany, who discovered that EpCAM signals into the cell nucleus via elements of both the notch and wnt pathways (abstract C175). These data not only establish EpCAM as a signal transducer of cancer cells, but could explain how the protein induces cell proliferation and oncogene expression, and support a critical role
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SOURCE Micromet, Inc.
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