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Ganetespib showed activity in KRAS-mutant NSCLC

Issue: February 10, 2012

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A novel Hsp90 inhibitor, ganetespib, showed activity in slowing KRAS-mutant non–small cell lung cancer tumor cell growth, according to data presented at the AACR-IASLC Joint Conference on Molecular Origins of Lung Cancer: Biology, Therapy and Personalized Medicine meeting in San Diego.

“We saw great activity with, for example, docetaxel and ganetespib,” David A. Proia, PhD, a scientist at Synta Pharmaceuticals Corp., said in a press release. “What we are doing now is conducting a large phase 2b/phase 3 trial with docetaxel and ganetespib in NSCLC patients. Activity in the KRAS-mutant subpopulation is a coprimary endpoint in this trial.”

Proia and colleagues from Synta Pharmaceuticals conducted preclinical studies of ganetespib in KRAS-mutant NSCLC cell lines. They found that the agent displayed anticancer activity in 15 different cell lines in vitro.

When combined with antimitotics with ganetespib, there was a 44% increase in cell death compared with monotherapy. When combining alkylating agents with ganetespib, there was a 61% increase in cell death compared with monotherapy. When combining topoisomerase inhibitors with ganetespib, there was a 26% increase in cell death compared with monotherapy.

The researchers also tested ganetespib combined with a MEK inhibitor and a PI3K/mTOR inhibitor, as these two agents target two pathways known to be involved in NSCLC. Both combinations were more active in slowing tumor growth compared with ganetespib alone.

“Not only was ganetespib activity enhanced in combination with traditional chemotherapies, which may be understood in terms of the ability of the Hsp90 inhibition to block certain resistance or repair mechanisms, but activity was also enhanced in combination with a number of targeted therapies for which recent work has shown very interesting complementary inhibition of signaling pathways,” Proia said in the press release.

For more information:

• Proia D. #B1. Presented at: AACR-IASLC Joint Conference on Molecular Origins of Lung Cancer: Biology, Therapy and Personalized Medicine; Jan. 8-11, 2012; San Diego.

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