Eleven Rigel Pharmaceuticals, Inc. Product Candidate Presentations at 2009 American Society of Hematology Meeting

SOUTH SAN FRANCISCO, Calif., Dec. 1 /PRNewswire-FirstCall/ -- Rigel Pharmaceuticals, Inc. today announced that eleven presentations on preclinical studies of the company’s product candidates will be given at the upcoming American Society of Hematology (ASH) Meeting and Exposition in New Orleans, Louisiana from December 5-8, 2009. Rigel’s R788, an oral Syk kinase inhibitor, will be discussed in two oral presentations by collaborators about its activity in distinct B-cell lymphoma models. In addition, Rigel’s partner, Merck Serono, will discuss R763/AS703569, an Aurora kinase inhibitor discovered by Rigel, in two presentations.

Oral Presentations

Rational Combinations Including a Novel Syk Inhibitor, Fostamatinib Disodium (FosD) in Diffuse Large B Cell Lymphoma

December 7, 2009: 7:00 AM

Oral Session: Lymphoma

The Syk Inhibitor R788 (FosD) Inhibits Tumor Growth in the TCL1 Transgenic Mouse Model of CLL by Blocking Antigen-Dependent BCR Signaling

Tuesday, December 8, 2009: 8:30 AM

Oral Session: CLL - Therapy, excluding Transplantation

Transcriptional Repression of DAPK1 Characterizes a Resistant Phenotype of AML Enforced by Flt3 Signaling and Exclusive Nuclear Abundance of Non-Canonical NFkB2/p52: Synergistic Activity for Flt3 Inhibition along with HDAC Inhibition, or by NFkB Inhibition, for Potentiating ER Stress Apoptosis

December 6, 2009, 6:00-8:00 PM

Poster Session: Disordered Gene Expression in Hematologic Malignancy, # II-364

Antitumor Activity of Small-Molecule SYK Inhibitor R788 and Fludarabinin Mono- and Combined Therapy in a Human B-CLL Xenograft Model

December 6, 2009, 6:00-8:00 PM

Poster Session: CLL - Therapy, # II-355

Role of Spleen Tyrosine Kinase Signaling in Early B Cell Acute Lymphoblastic Leukemia

December 7, 2009, 6:00-8:00 PM

Poster Session: Acute Lymphoblastic Leukemia - Therapy, # III-29

Activity of Serono-AS703569, a Dual Inhibitor of Bcr-Abl and Aurora Kinases in Bcr-Abl Transformed Cells, is Dependent on Aurora B Inhibition, and Is Not affected by the Presence of the Highly Imatinib Resistant Bcr-Abl Mutation T3151

December 7, 2009, 6:00-8:00 PM

Poster Session: Chronic Myeloid Leukemia - Biology and Pathophysiology, # III-184

CONTACT: CONTACT: Raul Rodriguez of Rigel Pharmaceuticals, Inc.,
+1-650-624-1302, invrel@rigel.com; or Susan C. Rogers, Alchemy Consulting,
Inc., +1-650-430-3777, susan@alchemyemail.com, for Rigel Pharmaceuticals,
Inc.

Web site: http://www.rigel.com/

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