Gemin X Presents Positive Preclinical Data of GX15-070 in Infant,ALL at AACR Meeting ( MONTREAL & MALVERN Pa.--(BUSINESS ...)

Gemin X Presents Positive Preclinical Data of GX15-070 in Infant,ALL at AACR Meeting

MONTREAL & MALVERN, Pa.--(BUSINESS WIRE)--Apr 18, 2007 - Gemin X today announced the presentation of positive preclinical data from a study of its lead compound, GX15-070 (obatoclax), in infant acute lymphoblastic leukemia (ALL). The study was discussed in an oral presentation at the Annual Meeting of the American Association for Cancer Research (AACR). According to the study, GX15-070 demonstrated potent single agent activity against ALL blast cells, and also enhanced chemosensitivity and was synergistic with cytotoxic drugs. GX15-070 is a small molecule specifically designed to inhibit all relevant members of the Bcl-2 protein family, a validated cancer target, restoring the natural cell death process of apoptosis.

In this study, researchers obtained leukemia blast cells from five infants and one child with primary ALL. The blasts were exposed to GX15-070 as a single agent in vitro for three days. In all six cases, GX15-070 exhibited potent single agent activity and IC(50) values were within clinically achievable concentrations. High BCL-2 expression and low expression of particular BH3-only BCL-2 family mRNAs in this disease correlate with GX15-070 sensitivity in vitro.

"GX15-070 is an appropriate candidate for ALL treatment because the imbalanced expression of Bcl-2 family proteins in this cancer leads to impaired apoptosis," said Gordon Shore, Ph.D., Chief Scientific Officer of Gemin X. "Additionally, this study further upholds what we already have observed about our lead candidate's utility as a single agent and in combination with other therapies."

These data were presented by Dr. Alena Zhang from Dr. Carolyn Felix's laboratory at Children's Hospital of Philadelphia on April 17 at 3:40 PM in an abstract titled, "BCL-2:BH3-only pro-apoptotic gene expression ratios correlate with in vitro sensitivity of primary MLL(+) infant acute lymphoblastic leukemia to small molecule pan-BCL-2 family
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