Results from Preclinical Studies of Gemin X's GX15-070 Presented in Four 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 first-in-class targeted cancer treatment designed to induce apoptosis (natural cell death) by inhibiting the Bcl-2 family of proteins, one of the most validated and well-studied cancer drug targets. The data indicated that GX15-070 induced apoptosis in several types of blood cancers, both as a single agent and in combination with other cancer drugs such as proteasome inhibitors and various chemotherapy agents. The data were presented as four separate posters at the American Society of Hematology's 47th Annual Meeting and Exposition, December 10-13, 2005 in Atlanta, GA.

"These preclinical studies demonstrate the potential breadth of use of GX15-070, both in the treatment of several types of cancer and in combination with various existing cancer treatments," said Dan Giampuzzi, President and CEO of Gemin X. "A number of other collaborations with academic and research institutes to study GX15-070 in different settings are ongoing and will inform the future development strategy for this compound."

Gemin X also presented results from a Phase 1/2 clinical trial of GX15-070 in patients with chronic lymphocytic leukemia (CLL) during the conference. The data, which indicated that GX15-070 was generally well-tolerated, was biologically active and generated clinical improvements, are fully summarized in a separate press release dated December 12, 2005.

The first preclinical study evaluated GX15-070 in the treatment of mantle cell lymphoma (MCL), both as a monotherapy and in combination with the bortezomib (Velcade(R)) proteasome inhibitor. Treatment with GX15-070 alone induced apoptosis in MCL cell lines and primary cells in vitro. Additionally, since overexpression of Bcl-2 has been associated with resistance to proteasome inhibitors, the researchers evaluated the combination of bortezomib with GX15-070, a pan-Bcl-2 inhibitor. The combination resulted in a synergistic effect, allowing a 5-20X reduction in the dose of bortezomib required to kill cancer cells. These data were summarized in a poster (Abstract 1490) entitled "The Small Molecule Pan-Bcl-2 Inhibitor GX15-070 Induces Apoptosis In Vitro in Mantle Cell Lymphoma (MCL) Cells and Exhibits a Synergistic Effect in Combination with the Proteasome Inhibitor Bortezomib" (Patricia Perez-Galan, et al).

A second preclinical study assessed GX15-070 in human myeloma cell lines and primary cells. The compound was found to induce apoptosis in all 12 cell lines tested and in the first and only primary myeloma sample tested thus far. Additionally, no cytotoxicity to normal human blood lymphocytes, stroma or bone marrow cells was observed at dose levels required to kill cancer cells. The data were presented in a poster (Abstract 1572) entitled "Studies of the Bcl Inhibitor GX15-070 in Multiple Myeloma Demonstrate Substantial Pre-clinical Activity" (A. Keith Stewart, et al).

A third preclinical study indicated that GX15-070 induced apoptosis in acute myeloid leukemia (AML) cell lines and primary samples in vitro. Treatment with GX15-070 induced apoptosis in approximately 64% of AML cells within 72 hours and in 85% of primary AML samples within 24 hours. Overexpression of Bcl-2 or Bcl-XL, which is frequently observed in several types of cancer, did not cause the cancer cells to become resistant to GX15-070. The data were presented in a poster (Abstract 3372) entitled "Inhibition of Bcl-2 Signaling by Small Molecule BH3 Inhibitor GX15-070 as a Novel Therapeutic Strategy in AML" (Rooha Contractor, et al).

The fourth preclinical study demonstrated that GX15-070 induces apoptosis in samples from leukemia patients carrying the t(4;11) mutation, which often causes resistance to standard chemotherapy. Additionally, the combination of GX15-070 with several chemotherapeutic agents suggested the ability to achieve cytotoxicity with lower doses of the chemotherapeutics. These data were summarized in a poster (Abstract 3368) entitled "Pan-BCL-2 Family Small Molecule Inhibitor GX15-070 (Gemin X, Inc.) Exhibits Single Agent Cytotoxicity, is Synergistic with Select Anti-Leukemia Cytotoxic Agents, and Induces Apoptosis in Cell Lines with t(4;11)(q21;q23) Translocations" (Jessicca M Rege, Ph.D., 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 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. Gemin X is also developing small molecules that induce apoptosis in p53-defective cancers. 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