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Novel drugs help solve Gleevec resistance

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BMS-354825 has a dual mechanism of action, which gives it a 100-fold greater potency to inhibit BCR-ABL, based on preclinical tests that compared it to Gleevec, Talpaz says. Such experiments also have shown that it can treat 14 of 15 mutations that arise in Gleevec-resistant tumors, he says. Giles adds that this appears to be similar to the activity profile of AMN107.

Like AMN107, BMS-354825 binds to the active form of Bcr-Abl. It is less specific than AMN107, however, and therefore has a broader spectrum of action because it inhibits a family of tyrosine kinases known as Src, Talpaz says.

"This is an engineered drug so we know exactly how it works, but we cannot say at this point whether there are clinically meaningful differences between BMS-354825 and AMN107," he says. "Many more studies are needed to see how these drugs will perform."

The bottom line, says Giles, is that "rational drug design is a reality and effective targeted therapies will rapidly increase in number, which means that options for patients are expanding," he says. "Prognosis of diseases that were, until very recently, rapidly fatal is getting better at an unprecedented rate. Science works."


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Contact: Nancy Jensen
nwjensen@mdanderson.org
713-794-1584
University of Texas M. D. Anderson Cancer Center
5-Dec-2004


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