Pharmion and MethylGene Start Phase 2 Combination Clinical Trial With MGCD0103 and Vidaza(R) in Patients With Relapsed or Refractory Hodgkin Lymphoma or Non-Hodgki...(ndDrug Administration (FDA) and has been...),Health

About Vidaza

In May 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. 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 Vidaza 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 Vidaza cause the death of rapidly dividing cells, including cancer cells that are no longer responsive to normal growth control mechanisms. Non- proliferating cells are relatively insensitive to Vidaza. Vidaza was approved for IV administration in January 2007.

About Epigenetic Therapy

DNA methylation and histone deacetylation are the two most studied epigenetic regulators of gene expression. Vidaza reverses the effects of DNA hypermethylation with subsequent tumor suppressor gene re-expression. MGCD0103 exerts its epigenetic effects by acting as an oral isotype-selective HDAC inhibitor. Together, the two act synergistically to induce suppressor gene re-expression and favorably influence the clinical course of cancer. Pharmion strongly believes that by
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