( BETHESDA Md. June 26 2007 /PRNewswi...)Publication Confirms that EpCAM, the Target for Two of Micromet's,Product Candidates, Is Overexpressed on Cancer Stem Cells of,Certain Cancers,Health

BETHESDA, Md., June 26, 2007 /PRNewswire-FirstCall/ -- Micromet, Inc. , a biopharmaceutical company focusing on the development of novel, proprietary antibody-based products for cancer, inflammatory and autoimmune diseases, announced that a study published recently in the Proceedings of the National Academy of Sciences (1) supports the findings of several other studies that EpCAM (CD326), which is used as the target for Micromet's product candidates adecatumumab (MT201) and MT110, may be suitable as a target for eradication of so called "cancer stem cells" (CSCs). The other studies showed that CSCs from colon (2), breast (3), pancreatic (4) and prostate (5) cancers all express high levels of EpCAM, which, according to these studies, makes these cells particularly capable of causing tumors.

CSCs constitute a small percentage of tumor cells that have the potential to self-renew and to permanently repopulate a tumor with new cancer cells. CSCs appear to be resistant to various chemotherapies, which may be one of the key reasons why most current therapies cannot cure cancer through elimination of all tumor cells (6). Micromet scientists believe that the findings of EpCAM expression by CSCs in many cancers and of EpCAM being a frequently and highly expressed tumor-associated antigen (7, 8), supports Micromet's use of EpCAM for targeted therapeutics.

EpCAM is the target for Micromet's clinical-stage product candidate adecatumumab (MT201), a fully human monoclonal antibody being co-developed with Merck Serono. In addition, Micromet's BiTE(R) product candidate MT110, an anti-EpCAM/CD3-bispecific antibody construct, is currently in late preclinical development. Both product candidates are designed to recognize EpCAM- expressing cancer cells and to instruct cytotoxic cells of the immune system to eliminate such cancer cells.

"The 'seek and destroy' mechanism of our EpCAM-directed therapeutic drug can
'"/>