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EntreMed's Aurora Kinase Inhibitor Induces Tumor Regression in,Preclinical Models

ROCKVILLE, Md., June 01, 2007 /PRNewswire-FirstCall/ -- EntreMed, Inc. , a clinical-stage pharmaceutical company developing therapeutics for the treatment of cancer and inflammatory diseases, announced the presentation of preclinical results for its Aurora kinase - angiogenesis inhibitor, ENMD-981693. The data were presented during oral and poster presentations by EntreMed scientists at the 2nd Protein Kinases in Drug Discovery Conference being held May 31 - June 1, 2007 in Boston, Massachusetts.

ENMD-981693 is an oral, dual-acting kinase inhibitor with a unique kinase selectivity profile and multiple mechanisms of action. In preclinical studies, ENMD-981693 has been shown to inhibit a unique profile of angiogenic tyrosine kinase targets in addition to the Aurora kinases. Aurora kinases are key regulators of mitosis (cell division), and are often over-expressed in human cancers. ENMD-981693 is selective for the Aurora A isoform in comparison to Aurora B.

Results from in vitro studies demonstrate ENMD-981693's potent activity against oncogenic receptor tyrosine kinases, including FLT3, c-Kit and CSF1R, which are involved in the pathology of hematological cancers. Additionally, ENMD-981693 demonstrated potent inhibition of a spectrum of targets linked to angiogenesis, including KDR (VEGFR2) and FGFR1. The compound was also shown to induce apoptosis and cell cycle arrest in a broad range of cell lines.

ENMD-981693 exhibited antiangiogenic activity in in vivo animal models by preventing the formation of new blood vessels and inducing regression of formed vessels at well-tolerated doses. Orally-administered ENMD-981693 induced tumor regression with minimal toxicity in a preclinical xenograft model of human leukemia. This activity is consistent with tumor regression induced by ENMD-981693 in preclinical models of human tumors derived from colon, leukemia, and breast cancer cell lines.

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