Cause of Human Heart Failure Discovered Using ARIAD's Cell-Signaling Technology.

Business Editors/Health/Medical Writers

BIOWIRE2K

CAMBRIDGE, Mass.--(BUSINESS WIRE)--May 16, 2003

Creation of Novel Model of Heart Failure Published

in the Journal of Clinical Investigation 

ARIAD Pharmaceuticals, Inc. (Nasdaq: ARIA) 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.

ARIAD is engaged in the discovery and development of breakthrough medicines that regulate cell signaling with small molecules. The Company is developing a comprehensive approach to the treatment of cancer and is primarily focused on a series of product candidates for targeted oncology indications. ARIAD also has an exclusive license to pioneering technology and patents related to the discovery, development and use of drugs that regulate NF-(kappa)B cell-signaling activity, which has been implicated in many major diseases.

Additional information about ARIAD can be found on the web at http://www.ariad.com.

Some of the matters discussed herein are "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. Such statements are identified by the use of words such as "anticipate," "estimate," "expect," "project," "intend," "plan," "believe," and other words and terms of similar meaning in connection with any discussion of future operating or financial performance. Such statements are based on management's current expectations and are subject to certain factors, risks and uncertainties that may cause actual results, outcome of events, timing and performance to differ materially from those expressed or implied by such forward-looking statements. These risks include, but are not limited to, risks and uncertainties regarding the Company's ability to conduct preclinical and clinical studies of its product candidates and the results of such studies, regulatory oversight, intellectual property claims, the timing, scope, cost and outcome of legal proceedings, future capital needs, key employees, dependence on the Company's collaborators and manufacturers, markets, economic conditions, products, services, prices, reimbursement rates, competition and other risks detailed in the Company's public filings with the Securities and Exchange Commission, including ARIAD's Annual Report on Form 10-K for the fiscal year ended December 31, 2002. The information contained in this document is believed to be current as of the date of original issue. The Company does not intend to update any of the forward-looking statements after the date of this document to conform these statements to actual results or to changes in the Company's expectations, except as required by law.