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Rigel’s Janus Kinase 3 (JAK3) Inhibitors Show Benefit in Organ Transplant Model and Potential Use in Immunosuppression

--Data to be Presented at 2006 World Transplant Congress--

SOUTH SAN FRANCISCO, Calif. - July 19, 2006

Rigel Pharmaceuticals, Inc. (Nasdaq: RIGL) announced today that it will present data from preclinical studies of multiple potent and selective inhibitors of Janus Kinase 3 (JAK3) at the 2006 World Transplant Congress taking place July 22-27th at the Hynes Convention Center in Boston, Massachusetts.

The Rigel JAK3 inhibitor compounds were found to significantly extend allograft survival in animal heart transplant models. These compounds effectively inhibit JAK3-dependent lymphocyte proliferation and are highly selective in an array of off-target assays. The compounds were discovered and characterized by Rigel and the heart transplant models were conducted by researchers at Stanford as part of a collaboration with Rigel.

“These promising preclinical results suggest that these drug candidates may provide a new, additional method of immunosuppression, and may result in a safer and more desirable protocol for preventing transplant rejection and treating other T cell-mediated diseases,” said Donald G. Payan, M.D., executive vice president and chief scientific officer of Rigel. “We will file an IND with one of the JAK3 inhibitors and plan to pursue JAK3 inhibition in a variety of autoimmune diseases, in addition to transplant rejection therapy.”

Organ recipients receive life-long treatment with immunosuppressive drugs in order to prevent organ rejection. With the currently available pharmaceuticals, fewer than 50% have a functioning replacement organ after 10 years. Current anti-rejection therapy suppresses the immune system with a cocktail of drugs including cyclosporin and steroids, the long-term use of which has been shown to cause kidney damage, hypertension, atherosclerosis, and diabetes.

The presentation details are as follows:

Abstract 2550: Prevention of Acute Rejection with a Novel Janus Kinase 3 (JAK3) Inhibitor in a Rodent Heterotopic Cardiac Allograft Model.
Date/time: Wednesday, July 26, 2006 at 12:30 p.m. EDT
Poster Session: Experimental Immunosuppression I

About JAK3
JAK3 is a cytoplasmic tyrosine kinase with expression limited to T cells, B cells, natural killer (NK) cells, mast cells, and macrophages. JAK3 acts in the signal transduction cascade of numerous growth factors critical for lymphocyte (white blood cell) activation, and plays an important role in lymphocyte differentiation and proliferation. Based on its limited tissue distribution and the evidence for its role in immune cell function, JAK3 may represent an optimal drug target for immunosuppression. Inhibitors of JAK3 could play a role in the treatment of autoimmune diseases and the prevention of transplant rejection.

About Rigel (www.rigel.com)
Rigel is a clinical-stage drug development company that discovers and develops novel, small-molecule drugs for the treatment of inflammatory diseases, cancer and viral diseases. Our goal is to file one new investigative new drug (IND) application in a significant indication each year. We have achieved this goal since 2002. Our pioneering research focuses on intracellular signaling pathways and related targets that are critical to disease mechanisms. Rigel’s productivity has resulted in strategic collaborations with large pharmaceutical partners to develop and market our product candidates. We have product development programs in inflammatory/autoimmune diseases such as rheumatoid arthritis, thrombocytopenia, and asthma and allergy, as well as in cancer.

This press release contains "forward-looking" statements, including statements related to Rigel's plans to pursue clinical development of product candidates and the timing thereof, and the potential efficacy of product candidates. Any statements contained in this press release that are not statements of historical fact may be deemed to be forward-looking statements. Words such as "plans," "intends," “promising,” "expects," “anticipates” and similar expressions are intended to identify these forward-looking statements. There are a number of important factors that could cause Rigel's results to differ materially from those indicated by these forward-looking statements, including risks associated with the timing and success of clinical trials and the commercialization of product candidates, as well as other risks detailed from time to time in Rigel's SEC reports, including its Form 10-Q for the quarter ended March 31, 2006. Rigel does not undertake any obligation to update forward-looking statements.

Contact: Raul Rodriguez
Phone: 650.624.1302
Email: invrel@rigel.com

Media Contact: Carolyn Bumgardner Wang, WeissComm Partners, Inc.
Phone: 415.946.1065
Email: carolyn@weisscommpartners.com