ARIAD Small-Molecule Drug Turns On and Controls Naturally Occuring Genes That Stimulate Growth of New Blood Vessels.

Business/Technology Editors & Health/Medical Writers

CAMBRIDGE, Mass.--(BW HealthWire)--Dec. 10, 2001

ARIAD Pharmaceuticals, Inc. (Nasdaq: ARIA) today announced, for the first time, that an ARIAD small-molecule drug robustly activates and precisely controls naturally occurring, endogenous genes that stimulate growth of new blood vessels. This drug controls a gene-specific regulatory protein introduced into target cells. Vascular endothelial growth factor (VEGF), the angiogenic gene activated in this study, has been shown to restore blood flow and is being studied as a potential new treatment for coronary artery disease and peripheral vascular disease, leading causes of death in the United States and Europe.

The results being reported at the American Society of Hematology annual meeting illustrate several medically important benefits of ARIAD's cell-signaling regulation technologies: the ability to simultaneously turn on multiple, natural forms of a gene that otherwise are inactive in target tissues, achieve high levels, control protein production in a dose-dependent manner, and terminate therapy by withdrawal of the drug. When applied to angiogenic genes, these features may provide a new approach to therapeutic intervention in cardiovascular diseases.

"The research reported today represents a major advance in the therapeutic application of our cell-signaling regulation technologies," said Harvey J. Berger, M.D., chairman and chief executive officer of ARIAD. "Our scientists have achieved what we believe will be required in clinical situations - small-molecule control and robust activation of naturally occurring genes."

The abstract of the presentation by Pollock et al (3108), "Regulation of the endogenous VEGF gene by small-molecule dimerizers," is available online at the ASH meeting website (www.abstracts-on-line.com/abstracts/hem/).

ARIAD is engaged in the discovery and development of breakthrough medicines that regulate cell signaling with small molecules. The Company's lead product candidates - treatments for bone metastases and bone pain, osteoporosis, cancer, anemia and graft-vs-host disease following T cell immunotherapy - all were developed through the integration of genomics, proteomics and structure-based drug design. ARIAD's RegTech cell-signaling regulation technologies are being used by almost 500 academic investigators providing a robust source of potential new technologies, drug targets and product candidates that the Company may develop. ARIAD also has an exclusive license to pioneering technology related to the discovery and development of drugs that modulate the cellular protein, NF-(kappa)B, and its associated pathways, which regulate the transcription of key genes involved in many major diseases. Additional information about ARIAD can be found on the web at www.ariad.com.

Some of the matters discussed herein are forward-looking statements. 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, events and performance to differ materially from those referred to or implied in such statements. These risks include, but are not limited to, risks and uncertainties regarding the Company's preclinical studies, the Company's ability to conduct clinical trials of its product candidates and the results of such trials, as well as risks and uncertainties relating to economic conditions, markets, products, competition, intellectual property, services and prices, key employees, future capital needs, dependence on the Company's collaborators and other factors. These risks are identified in ARIAD's Annual Report on Form 10-K for the fiscal year ended December 31, 2000, filed with the Securities and Exchange Commission. 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.