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Millennium Presents New Data on Investigational Drugs for Novel Cancer Targets at EORTC-NCI-AACR Symposium
Date:10/22/2008

CAMBRIDGE, Mass., Oct. 22 /PRNewswire/ -- Millennium: The Takeda Oncology Company today announced new data from early non-clinical studies of Millennium/Takeda-discovered pipeline molecules highlighting novel therapeutic pathways in oncology. MLN4924 data build on the growing body of evidence supporting the importance of the Millennium-discovered Nedd8 Activating Enzyme (NAE) in tumor growth and survival. It is a first-in-class small molecule inhibitor of NAE. Both clinical and non-clinical studies of MLN8237 confirm the importance of inhibiting Aurora A kinase, which is required for cells to proceed through cell division.

(Logo: http://www.newscom.com/cgi-bin/prnh/20080827/NEW076LOGO )

TAK-285 and TAK-593 are receptor tyrosine kinase inhibitors. Non-clinical data suggest their efficacy in affecting the Epidermal Growth Factor Receptor / Human Epidermal Growth Factor Receptor (EGFR/HER) and Vascular Endothelial Growth Factor/Platelet Derived Growth Factor (VEGF/PDGF) pathways, respectively. The data from 21 Millennium abstracts were presented at the 20th EORTC-NCI-AACR* Symposium on "Molecular Targets and Cancer Therapeutics" held October 21 to 24 in Geneva, Switzerland.

"These new data demonstrate the potential of novel pathways and innovative approaches to existing pathways that will further oncology research," said Nancy Simonian, M.D., Chief Medical Officer, Millennium. "Early results such as these demonstrate our oncology expertise in advancing both the current Millennium oncology molecules and those we are integrating into our pipeline from Takeda."

MLN4924

MLN4924 is a first-in-class small molecule inhibitor of NAE, a new target discovered by Millennium scientists. Data from two non-clinical studies showcased at EORTC highlight its potent activity in inducing apoptosis, or programmed cell death, in cultured human tumor cells and human
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SOURCE Millennium: The Takeda Oncology Company
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