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Myogen extends drug discovery collaboration with Novartis
Denver, Colorado | Saturday, May 28, 2005, 08:00 Hrs  [IST]

Myogen, Inc. has extended its heart muscle disease drug discovery collaboration with Novartis.

The collaboration has been expanded to include Myogen's histone deacetylase inhibitor (HDACi) programme. Myogen has also achieved three development milestones under the parties' existing research collaboration for the discovery and development of novel drugs for the treatment of cardiovascular disease.

The expansion of the collaboration extends research funding for a minimum of three years and includes undisclosed signing fees, milestone payments and royalty payments on sales of products that are successfully commercialized. Upon the completion of Phase 2 clinical trials of certain HDACi product candidates Novartis has licensed under the collaboration, Myogen has an option to enter into a co-promotion and profit sharing agreement in certain markets, subject to the Company reimbursing Novartis for certain costs incurred through the completion of Phase 2 trials as well as a commensurate portion of future development and marketing costs and the elimination of the associated royalty.

J. William Freytag, president and CEO of Myogen, Inc says, "We believe the HDACi programme has significant potential therapeutic value. Through this partnership, we have an exciting opportunity to advance the discovery and development of novel small molecule compounds that selectively inhibit HDACs for treatment of cardiac diseases."

"Novartis has focused on developing a deep understanding of diseases of the heart. Our collaboration with Myogen is an important part of our efforts to explore innovative and potentially important targets for drug discovery", said Dr. Jeremy Levin, Global Head of Strategic Alliances of Novartis.

Recent research at Myogen suggests that HDAC inhibitors represent a valid approach to the development of novel, disease-modifying cardiac therapeutics. In work published recently, Myogen scientists have shown that HDAC inhibitors block pathological cardiomyocyte hypertrophy and up-regulate the expression of alpha myosin heavy chain while decreasing beta myosin isoform expression.

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