Data from Preclinical Studies of Gemin X's GX15-070 Presented in Five Posters at American Society of Hematology Annual Meeting.

MONTREAL -- Gemin X Biotechnologies, Inc. announced today the results of several preclinical studies of GX15-070, a small molecule specifically designed to inhibit all relevant members of the Bcl-2 protein family, a validated cancer target, thus restoring the natural cell death process of apoptosis. The data indicated that GX15-070 induced apoptosis in several types of hematological cancer cell lines, both as a single agent and in combination with other cancer drugs such as rituximab, proteasome inhibitors, other Bcl-2 inhibitors, and chemotherapy agents such as CDDP and doxorubicin. The data were presented as five separate posters at the American Society of Hematology (ASH) 48th Annual Meeting and Exposition, December 9-12, 2006 in Orlando, FL.

"These preclinical studies demonstrate the breadth of GX15-070 in a variety of blood cancers as a potent single agent as well as in combination with both targeted and traditional cancer drugs," said Dan Giampuzzi, President and CEO of Gemin X. "We are already conducting two single agent Phase 2 trials with GX15-070 and plan to initiate clinical trials in combination with other cancer drugs early next year."

The GX15-070 preclinical posters include:

* Abstract 2502: A preclinical study evaluating the effects of GX15-070 on rituximab activity, in which in vitro exposure of rituximab-sensitive cell lines (RSCL) Raji and RL to GX15-070 resulted in a dose-dependent decrease in DNA synthesis and increase in apoptosis. Additionally, GX15-070 enhanced rituximab activity and induced apoptosis in various non-Hodgkin's lymphoma (NHL) cell lines. ("Targeting BH3-Domain Anti-Apoptotic Proteins with GX15-070 Significantly Increases Rituximab-Mediated Antibody Dependent Cellular Cytotoxicity (ADCC) and Complement Mediated Cytotoxicity (CMC) Against B-Cell Lymphomas" [Hernandez-Ilizaliturri, et al.])

* Abstract 2523: A preclinical study in which GX15-070 demonstrated activity against both rituximab-sensitive cell lines (RSCL) and rituximab-resistant cell lines (RRCL). Additionally, GX15-070 induced synergistic cytotoxic and antiproliferative effects when combined with the chemotherapy agents CDDP and doxorubicin, suggesting that GX15-070 may positively impact the resistance issues common with both chemotherapy and rituximab in B-cell non-Hodgkin's lymphoma (NHL). ("Targeting BH3-Domain Anti-Apoptotic Proteins with GX15-070 Decreases DNA Synthesis, Induces Cell Death and Sensitizes Rituximab-Sensitive and Resistant Non-Hodgkin's Lymphoma Cell Lines to the Anti-Tumor Activity of Chemotherapy Agents" [Hernandez-Ilizaliturri, et al.])

* Abstract 2532: A preclinical study evaluating the activity of GX15-070 in three mantle cell lymphoma (MCL) lines (Jeko-1, Mino, and SP53). GX15-070 induced apoptosis in all three MCL cell lines and also enhanced the effectiveness of the proteasome inhibitors, bortezomib and NPI-0052, both of which have induced antiproliferative activity in MCL as single agents. Additionally, GX15-070 showed an additive effect with doxorubicin, a chemotherapy agent. ("Inhibition of the Pan-Bcl-2 Family by the Small Molecule GX15-070 Induces Apoptosis in Mantle Cell Lymphoma (MCL) Cells and Enhances the Activity of Two Proteasome Inhibitors (NPI-0052 and Bortezomib), and Doxorubicin Chemotherapy" [Yazbeck, et al.])

* Abstract 2584: A preclinical study assessing the activity of GX15-070 in acute myeloid leukemia (AML) cell lines and primary AML samples. GX15-070 induced cytochrome c release from isolated mitochondria of leukemic cells and synergized with AraC and ABT-737 to induce apoptosis in OCI-AML3 cells, a highly chemoresistant cell line. GX15-070 potently inhibited the clonogenic ability of AML blasts at sub-micromolar doses and, in 6/7 primary AML samples, induced apoptosis in CD34+ progenitor cells. ("Inhibition of Bcl-2 Signaling by Small Molecule BH3 Inhibitor GX15-070 as a Novel Therapeutic Strategy in AML" [Watt, et al.])

* Abstract 3476: A preclinical study evaluating apoptosis induced by GX15-070 in a panel of human multiple myeloma (MM) cell lines (HMCL). HMCL demonstrated sensitivity to GX15-070 at different levels which were not correlated with IL-6 dependence: 2 were very sensitive (> 60% of death cells), 3 were intermediately sensitive (> 30% < 60%) and 4 were resistant (< 30%). Additionally, GX15-070 demonstrated additive or synergistic effects when combined with melphalan, bortezomib and mapatumumab, an antibody directed against TRAIL-R1. ("The Pan-Bcl-2 Inhibitor GX15-070 Induces Apoptosis in Human Myeloma Cells by Noxa Induction and Strongly Enhances Melphalan, Bortezomib or TRAIL-R1 Antibody Apoptotic Effect" [Gomez-Bougie, et al.])

About GX15-070

GX15-070 is designed to restore apoptosis, the natural process of cell death that is often inhibited in cancer cells. Over-expression of the Bcl-2 protein family inhibits apoptosis and has been observed in a wide range of cancers, including those of the lymph, breast, lung, prostate and colon. GX15-070 is specifically designed to inhibit all of the anti-apoptotic members of the Bcl-2 protein family, thus inducing apoptosis in cancer cells without damaging normal cells, and is the first such small molecule, pan-inhibitor of Bcl-2 proteins tested in clinical trials.

Gemin X Biotechnologies Inc. specializes in the discovery and development of novel small-molecule cancer therapeutics based on the regulation of apoptosis, the body's natural ability to destroy injured or damaged cells. Gemin X's lead product, GX15-070, is a small molecule, pan-inhibitor of Bcl-2 proteins in Phase 2 clinical trials. Gemin X is also developing a small molecule that induces apoptosis in p53-defective cancers, which is slated for an IND filing at the end of the year. Gemin X is privately held and is located in Montreal, Quebec and Malvern, Pennsylvania. For additional information please visit Gemin X at www.geminx.com.