Thursday, July 07, 2005

Anderson Cancer Researchers Publish Manuscript on Callisto 's Atiprimod

Anderson Cancer Researchers Publish Manuscript on Callisto Pharmaceuticals’ Atiprimod in British Cancer Journal of Cancer

NEW YORK, NY – Callisto Pharmaceuticals, Inc. (AMEX: KAL), a biopharmaceutical company primarily focused on the development of drugs to treat cancer, announced the publication of a paper entitled “Atiprimod Blocks STAT3 Phosphorylation and Induces Apoptosis in Multiple Myeloma Cells,”. It appeared in the British Journal of Cancer, Volume 92, Number 13, pp.1-11 (2005.), and was authored by a team of scientists and clinicians from the University of Texas M.D. Anderson Cancer Center, highly-regarded experts in multiple myeloma, blood cancers and bioimmunotherapy. The publication provides further evidence that Atiprimod has anti-neoplastic effects on human myeloma cells in culture, and further elucidated the biological mechanisms by which Atiprimod exerts these anti-neoplastic effects.

“The team of scientists and clinicians who participated in this study has an impressive record of advancements in the basic science of blood cancers, as well as a proven record of success in the clinic.” said Dr. Gary S. Jacob, Chief Executive Officer of Callisto Pharmaceuticals. “Atiprimod is currently being evaluated at M.D. Anderson in a Phase I/IIa clinical trial in patients with relapsed multiple myeloma, as well as in a single agent trial in advanced cancer patients.”

In the present work, Atiprimod’s effects on proliferation of myeloma cells, and on the key signaling pathways in myeloma cells were evaluated. Atiprimod was shown to inhibit proliferation in a time- and dose-dependent manner, and to arrest myeloma cell growth, preventing cell cycle progression. Furthermore, Atiprimod inhibited STAT 3 activation, blocking the signaling pathway of interleukin-6, which contributes to myeloma cell proliferation and survival. Incubation of myeloma cells with Atiprimod induced apoptosis (cell death) through the activation of caspase 3, leading to deactivation of the DNA repair enzyme PARP.

In separate experiments, Atiprimod suppressed myeloma colony-forming cell proliferation of fresh marrow cells from five patients with newly diagnosed MM in a dose-dependent fashion.

Atiprimod is currently being evaluated in a Phase I clinical trial in relapsed or refractory multiple myeloma patients at four clinical sites in the United States – the Dana-Farber Cancer Institute (Boston, MA), the M.D. Anderson Cancer Center (Houston, TX), the St. Vincent’s Comprehensive Cancer Center (New York, NY) and the Roswell Park Cancer Institute (Buffalo, NY). On May 4, 2005 Callisto announced that three patient cohorts had completed dosing at 30, 60 and 90 mg, respectively, and a fourth dosing cohort was underway at 120 mg. No dose limiting toxicities had been observed, and a fifth dose cohort at 180 mg was anticipated to begin in the following 6-8 weeks.

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