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Clinical Data Reported on Vidaza in Hematologic Malignancies and,Advanced Solid Tumors

Abstract #7083; June 2, 2007; 8:00am-12:00pm; McCormick Place Convention Center, S Hall A2

An oral dosage formulation of azacitidine: A pilot pharmacokinetic study - R. Ward, Pharmion; Abstract #7084; June 2, 2007; 8:00am-12:00pm; McCormick Place Convention Center, S Hall A2

Response to azacitidine in patients with myelodysplastic syndrome with marrow fibrosis - R. Juvvadi, Western Penn, Pennsylvania; Abstract #7089; June 2, 2007; 8:00am-12:00pm; McCormick Place Convention Center, S Hall A2

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Contact details

Breanna Burkart or Anna Sussman

Directors, Investor Relations and Corporate Communications

Pharmion Corporation

Tel: +1 720 564 9144 or +1 720 564 9143

Tara May

On-site media contact

Tel: +1 303 646 7832

About Vidaza

On May 19, 2004, Vidaza became the first drug approved by the FDA for the treatment of patients with Myelodysplastic Syndromes (MDS). The FDA approved Vidaza, the first in a new class of drugs called demethylation agents, for treatment of all five MDS subtypes, which include both low-risk and high-risk patients. These subtypes include: refractory anemia (RA) or refractory anemia with ringed sideroblasts (RARS) if accompanied by neutropenia or thrombocytopenia or requiring transfusions; refractory anemia with excess blasts (RAEB), refractory anemia with excess blasts in transformation (RAEB-T), and chronic myelomonocytic leukemia (CMMoL).

Vidaza is believed to exert its antineoplastic effects by causing hypomethylation of DNA and direct cytotoxicity on abnormal hematopoietic cells in the bone marrow. The concentration of azacitidine required for maximum inhibition of DNA methylation in vitro does not cause major suppression of DNA synthesis. Hypomethylation may restore normal function to genes that are critical for differentiation and proliferation. The cytotoxic effects of azacitidine cause the death of rapidly dividing cells, including can
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