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

Section of Myelodysplastic Syndromes, Department of Leukemia, M.D. Anderson Cancer Center. "The potential for a chronic oral demethylating agent will not only apply to MDS but to many other tumor types as well. This is a very important step forward for epigenetic therapies."

Data Presented Saturday, June 2

Phase I/II study of a novel oral isotype-selective histone deacetylase (HDAC) inhibitor MGCD0103 in combination with azacitidine in patients (pts) with high-risk Myelodysplastic Syndrome (MDS) or Acute Myelogenous Leukemia (AML) - G. Garcia-Manero, MD, MD Anderson Cancer Center; Abstract #7062; June 2, 2007; 8:00-12:00 pm; McCormick Convention Center, S Hall A2

The combination of 5-azacytidine and valproic acid is safe and active in advanced solid tumors - A.O. Soriano, MD Anderson Cancer Center; Abstract #3547; June 2, 2007; 2:00-6:00pm; McCormick Place Convention Center, S102a

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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

Vidaza was the first drug approved for the treatment of all five subtypes of myelodysplastic syndromes (MDS), including refractory anemia (RA), 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 m
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