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EntreMed Presents Mechanism Data for Its Three Lead Oncology,Compounds

Multiple Mechanisms for Panzem NCD, MKC-1, and ENMD-1198 Highlighted at Oncology Drug Discovery Conference

ROCKVILLE, Md., March 26, 2007 /PRNewswire-FirstCall/ -- EntreMed, Inc., a clinical-stage pharmaceutical company developing therapeutics for the treatment of cancer and inflammatory diseases, today announced the presentation of comparative mechanism of action data for its three lead clinical stage compounds Panzem(R), MKC-1 and ENMD-1198. These data were presented by Dr. Theresa M. LaVallee, EntreMed's Senior Director, Cell Biology in an oral podium session during the Apoptosis in Drug Discovery Conference, March 22-23, 2007 in San Diego, CA.

Panzem(R), MKC-1 and ENMD-1198 are three orally available agents that exhibit antiproliferative activity through G2/M arrest, apoptosis and antiangiogenesis. In preclinical models, these compounds are not sensitive to multi-drug resistance pumps and show activity in both vinca and taxane resistant tumor cell lines. While these three agents all bind to the colchicine-binding site of tubulin, they have distinct mechanisms of action. Panzem(R) has a well tolerated safety profile that lends itself to combination therapy with many other chemotherapeutic agents. In addition to binding tubulin, MKC-1 binds to importin-beta and inhibits signaling through the PI3K- Akt-mTor pathway. The PI3K-Akt-mTor pathway is frequently activated in cancer and has been shown to promote tumorigenesis. In an orthotopic animal model of human breast cancer, ENMD-1198 led to the disruption of microtubules within tumor cells and a substantial decrease in tumor cell proliferation and angiogenesis. The mechanisms of action of these three tubulin agents was compared and contrasted during the presentation.

Microtubules are key components of the cell structure and are essential for maintenance of cell shape, cellular functions and cell division (growth). These highly dynamic filaments are
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