AVN944 inhibits IMPDH and induces apoptosis-related biomarkers in patients with hematologic cancers

Germantown, Md., December 11, 2006 -- Avalon Pharmaceuticals, Inc. (NASDAQ and NYSE Arca: AVRX), presented a poster detailing the effect of AVN944 on a comprehensive set of genetic and biochemical biomarkers at the American Society of Hematology 48th Annual Meeting. AVN944 demonstrated a statistically meaningful impact on IMPDH and other proteins that are critical to activities in cancer cells, including nucleotide biosynthesis, energy and metabolism, DNA replication, apoptosis and cell cycle control. The data were collected in an ongoing Phase I open-label, repeat dose-escalation study designed to evaluate the safety and tolerability of AVN944 in patients with advanced hematologic malignancies and to determine the optimal dose for Phase II efficacy trials. Further data from an interim analysis of the trial is expected to be available shortly.

"IMPDH is highly upregulated in most hematological cancers and in many solid tumors," said Beverly S. Mitchell, M.D., Deputy Director of the Stanford Comprehensive Cancer Center and George E. Becker Professor of Medicine at Stanford University. "IMPDH plays an essential role in cancer cell synthesis of DNA and RNA, and the inhibition of IMPDH represents a new and potentially important approach to the treatment of cancer."

Analysis of the selected markers in patient samples from the Phase I trial showed a correlation of changes in the expression of these genes to dose level and duration of exposure. Importantly, several of these markers have been shown to reflect a durable, sustained stress response indicative of cancer cell death, particularly in cancer cells from AML patients. Specifically, it was found that the gene HspA1A, a marker of stress response found to correlate with depleted GTP pools in cancer cell lines, is induced within hours upon the first treatment of the drug in patients, even at the trial's lowest doses. Following continued dosing of AVN944, this marker of disease cell stress was ele

Contact: Wendy Lau
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