ARIA / congestive heart failure
CAMBRIDGE, Mass.--(BUSINESS WIRE)--May 16, 2003-- ARIAD Pharmaceuticals, Inc. (Nasdaq: ARIA - News) today announced results of a newly published study demonstrating, for the first time, the cause of human congestive heart failure using a newly developed animal model of heart failure created using ARIAD's cell-signaling regulation technology. The development of clinically effective drugs to treat congestive heart failure has been impeded by the lack of predictive animal models - a limitation that may be overcome with this novel technique.
A team of scientists led by Richard N. Kitsis, M.D., director of molecular cardiology at the Albert Einstein College of Medicine, used the ARGENT(TM) cell-signaling regulation technology to create transgenic animals in which the death of heart-muscle cells can be selectively activated and the extent of killing regulated by administering varying amounts of one of ARIAD's small-molecule compounds.
Their study showed that a low level of heart-muscle cell death, comparable or even lower than that observed in human heart failure, was sufficient to cause irreversible heart damage and expansion of the heart's chambers. Furthermore, experimental drugs that specifically blocked heart-muscle cell death largely prevented these hallmarks of congestive heart failure, potentially offering new therapeutic options for the treatment of this life-threatening disease.
The importance of this breakthrough research is highlighted in the accompanying editorial commentary by Professor Bernardo Nadal-Ginard, M.D., Ph.D. and his colleagues at New York Medical College: the paper provides "conclusive proof that myocyte dropout (heart-muscle cell death) by itself cause(s) cardiac failure," and "new insights on the role of myocyte death and renewal in cardiovascular physiology."
"This study provides further evidence of the broad applicability of ARIAD's cell-signaling regulation technology to create previously unattainable animal models of human disease - in this case, congestive heart failure," said Harvey J. Berger, M.D., chairman and chief executive officer of ARIAD. "Having highly predictive in vivo models to test the safety and efficacy of potential new therapies is essential for the drug discovery process, especially where long-term clinical trials are required. The new animal model developed by Dr. Kitsis and his colleague's compliments prior development of animal models for other degenerative diseases, such as hepatitis, using our patented cell-signaling technology."
Dr. Berger added, "Earlier this year, we signed the first R&D license for our ARGENT technology with GPC Biotech. We are offering licenses to other pharmaceutical and biotechnology companies to facilitate their drug discovery efforts, such as the development of new drugs to treat heart failure and hepatitis."
The paper by Wencker, et al., "A mechanistic role for cardiac myocyte apoptosis in heart failure," appears in the May 15, 2003 issue of the Journal of Clinical Investigation and can be accessed at the journal's website (http://www.jci.org/current.shtml).
The accompanying commentary by Nadal-Ginard, et al., "A matter of life and death: cardiac myocyte apoptosis and regeneration," also appears in the same issue of the Journal... |
