of PD166326, the mutated enzyme activity was rapidly inhibited, and the white blood count significantly decreased. Two-thirds of the PD166326-treated mice also had complete recovery from splenomegaly, an abnormal enlargement of the spleen, compared to none treated with Gleevec, Dr. Ilaria said.
In long-term use, PD166326 showed better anti-leukemia activity than Gleevec, and it also prolonged the survival of mice with the CML-like leukemia resistant to Gleevec treatment.
While PD166326 is not yet available for clinical trials, investigators at Memorial Sloan-Kettering Cancer Center in New York, who synthesized the drug, are working with a major pharmaceutical company that owns the patent for this class of drugs on its clinical development, Dr. Ilaria said. Its relatively long half-life in mice indicates once-daily dosing might be possible in humans.
PD166326 is in a different class of anti-leukemia drugs currently being investigated by other researchers for their effectiveness in Gleevec-resistant patients. Dr. Ilaria's lab is continuing research in Gleevec resistance and looking at combining this new compound with other drugs.
"CML patients may soon have multiple choices with Gleevec and any one or all of the additional classes of drugs in development," Dr. Ilaria said. "These compounds also may work on other solid tumors, so it will be very interesting to see how it all pans out."
Nicholas C. Wolff, research associate in the Nancy B. and Jake L. Hamon Center for Therapeutic Oncology Research, is first author of the Blood study.
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Contact: Scott Maier
UT Southwestern Medical Center
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