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Agios research demonstrates the effects of mutant IDH1 and IDH2 inhibitors in primary tumor models
Date:4/4/2013

Cambridge, Mass. April 4, 2013 Agios Pharmaceuticals, Inc., the leading biopharmaceutical company focused on discovering and developing novel drugs in the fields of cancer metabolism and rare metabolic genetic diseases, announced today the publication of two articles in the journal Science by Agios scientists and their collaborators demonstrating the effects of the company's small molecule isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) mutant specific inhibitors in primary human tumor models. These data add to a growing body of scientific research demonstrating the significant promise of targeting mutant IDH1 and IDH2 enzymes as novel approaches to treating cancer.

"These papers represent the first publications to show the effects of inhibiting mutant IDH1 and IDH2 enzymes in patient-derived tumor samples, extending Agios' record of scientific leadership in cancer metabolism," said David Schenkein, M.D., chief executive officer at Agios. "While IDH mutations are genetically validated cancer targets, these findings provide further preclinical support that these mutations are driving disease, and appropriately targeted therapeutics can reverse the effects. Our IDH programs continue to produce promising results, and we are excited to advance toward clinical studies that will bring a potentially transformative treatment option to patients."

Tumors carrying IDH mutations are known to produce high levels of 2-HG, as shown originally by Agios scientists in Nature in 2009. In the first Science article, titled "Targeted inhibition of mutant IDH2 in leukemia cells induces cellular differentiation," Agios scientists show that cancer-associated IDH mutations may cause a block in cellular differentiation to promote tumorigenesis. To elucidate the relationship between mutant enzyme activity, 2-HG levels and oncogenic state, Agios developed a mutant-selective IDH2 inhibitor. Primary samples of acute myeloid leukemia (AML) cells were deriv
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Contact: Dan Budwick
dan@purecommunicationsinc.com
973-271-6085
Pure Communications Inc.
Source:Eurekalert

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