Micromet Data Presented at the International AACR-NCI-EORTC Conference Support the Development of Adecatumumab (MT201) in Earlier Stage Cancer Disease Settings
BETHESDA, Md., October 23, 2007 /PRNewswire-FirstCall/ -- Micromet, Inc. , a biopharmaceutical company focusing on the development of novel, proprietary antibody-based products for the treatment of cancer, inflammation and autoimmune diseases, today announced that new data from two previously reported phase 2 studies were presented at the joint international meeting of the American Association for Cancer Research (AACR), National Cancer Institute (NCI) and European Organization for Research and Treatment of Cancer (EORTC) being held in San Francisco, CA, from October 22-26.
Abstract A71 reports on a further analysis of data from the phase 2 trial investigating adecatumumab as single agent in metastatic breast cancer (MBC). Previously, longer time to tumor progression (TTP) has been shown for patients receiving higher doses of adecatumumab and expressing high levels of EpCAM (HR = 0.433 for the comparison of high dose/high EpCAM versus low dose/low EpCAM; p=0.0057). All data have now been re-evaluated in order to investigate the reasons for progression. Whereas no obvious differences were detected for the progression of pre-existing target lesions, a significantly lower incidence of new metastases was observed in patients with very high EpCAM expression (only 3 out of 18 patients with new lesions at week 6; 16.7%) as compared to those with low EpCAM (14 out of 29 patients; 48.3%; p= 0.034). A dose-dependency of this effect was 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 of EpCAM in cancer stem cell regulation.
"All of these new findings correlate well together and highlight the prospects of EpCAM-directed immunotherapies," commented Carsten Reinhardt, M.D., Chief Medical Officer of Micromet. "While the findings from our collaborators in Munich may finally explain the well-known negative prognostic potential of EpCAM, the clinical data on adecatumumabÂ´s potential inhibitory effect on new metastases provide a clear rationale for moving forward into early-stage cancer settings where the goal is prevention of disease re- occurrence rather than palliative shrinkage of large tumor bulk."
All of the above cited abstracts can be viewed on the AACR website at www.aacr.org.
About Micromet, Inc. (www.micromet-inc.com)
Micromet, Inc. is a biopharmaceutical company focusing on the development of novel, proprietary antibodies for the treatment of cancer, inflammation and autoimmune diseases. Three of its antibodies are in clinical development. MT103 (MEDI-538), the first antibody developed using the BiTE(R) technology platform to be clinically validated in Micromet's product pipeline, is being evaluated in a phase 1 clinical trial for the treatment of patients with non- Hodgkin's lymphoma. BiTE antibodies represent a new class of antibodies that activate a patient's own cytotoxic T cells to eliminate cancer cells. Micromet is developing MT103 in collaboration with MedImmune, a subsidiary of AstraZeneca plc. The second clinical stage antibody is adecatumumab (MT201), a human monoclonal antibody targeting EpCAM expressing tumors. Adecatumumab is being developed by Micromet in collaboration with Merck Serono, a division of Merck KGaA in Darmstadt, Germany, in a phase 1b clinical trial evaluating MT201 in combination with docetaxel for the treatment of patients with metastatic breast cancer. The third clinical stage antibody is MT293 (formerly D93), also known as TRC093, a first-in-class humanized monoclonal antibody that inhibits angiogenesis and tumor cell growth by binding cleaved collagen. MT293 is licensed to TRACON Pharmaceuticals, Inc. and is being developed in a phase 1 clinical trial for the treatment of patients with cancer and age- related macular degeneration. In addition, Micromet has established a collaboration with Nycomed for the development and commercialization of MT203, Micromet's human antibody neutralizing the activity of GM-CSF, which has potential applications in the treatment of inflammatory diseases, such as rheumatoid arthritis, as well as autoimmune diseases.
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Posted: October 2007