Geron Announces Presentation of New Data Supporting the Utility of Its Small Molecule Telomerase Activator Drugs for HIV/AIDS Therapy
Friday February 3, 7:30 am ET
MENLO PARK, Calif.--(BUSINESS WIRE)--Feb. 3, 2006--Geron Corporation (Nasdaq:GERN - News) announced today the presentation of studies showing that its small molecule telomerase activators, TAT0001 and TAT0002, enhance the functional activity of immune cells from HIV/AIDS donors. The research, presented at the Gordon Research Conference "The Biology of Aging" in Ventura, California, demonstrated that the telomerase activators not only increased the proliferative capacity of cytotoxic (CD8+) T-cells and their ability to produce a virus-fighting molecule, gamma Interferon (IFN(gamma)), but also improved the ability of CD8+ cells from HIV-positive donors to inhibit virus production in infected CD4+ T-cells.
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The new data, presented by Rita Effros, Ph.D., professor of pathology and laboratory medicine at the David Geffen School of Medicine at UCLA, was the product of a joint research effort between Geron scientists, Dr. Effros and colleagues at UCLA. The ongoing research in Dr. Effros' laboratory is supported by TA Therapeutics, a joint venture between Geron Corporation and the Biotechnology Research Corporation, a company established by the Hong Kong University of Science and Technology.
During the progression of HIV disease, certain immune cells called CD8+ cytotoxic T-cells undergo accelerated replicative senescence (cellular aging), and lose their ability to proliferate and kill HIV-infected CD4+ T-cells. Previous work by Dr. Effros and colleagues demonstrated that introducing the telomerase gene into CD8+ cells from HIV/AIDS donors increased their proliferative capacity, their ability to produce IFN(gamma), and their ability to inhibit viral replication and kill HIV-infected T-cells. Dr. Effros demonstrated that the small molecule telomerase activators TAT0001 (GRN951) and TAT0002 (GRN665) improved the proliferative response of T-cells and increased IFN(gamma) production. The new data presented at the Gordon Conference showed that HIV-specific CD8+ cells pre-treated with either TAT0001 or TAT0002 had enhanced ability to inhibit viral replication when co-cultured with HIV-infected CD4+ cells.
"The new work conducted by Dr. Effros confirms and extends her earlier studies with TAT0001 and TAT0002, showing that our drug candidates enhance multiple functions of the cytotoxic T-cells that keep HIV in check," stated Calvin B. Harley, Ph.D., Geron's chief scientific officer. "These data, our ongoing safety studies and other product development activities are leading us to a novel pharmacologic approach for the treatment of HIV/AIDS."
Geron is a biopharmaceutical company developing and commercializing three groups of products: i) therapeutic products for oncology that target telomerase; ii) pharmaceuticals that activate telomerase in tissues impacted by senescence, injury or degenerative disease; and iii) cell-based therapies derived from its human embryonic stem cell platform for applications in multiple chronic diseases.
This news release may contain forward-looking statements made pursuant to the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995. Investors are cautioned that such forward-looking statements in this press release regarding future applications of Geron Corporation's technology and compounds constitute forward-looking statements involving risks and uncertainties, including, without limitation, risks inherent in the development and commercialization of potential products, need for additional capital, reliance on collaborators, need for regulatory approvals or clearances, and maintenance of our intellectual property rights. Actual results may differ materially from the results anticipated in these forward-looking statements. Additional information on potential factors that could affect our results and other risks and uncertainties are detailed from time to time in Geron's periodic reports, including the quarterly report on Form 10-Q for the quarter ended September 30, 2005. |
