On November 16, 2015 Calithera Biosciences, Inc. (Nasdaq:CALA), a clinical stage biotechnology company focused on the development of novel cancer therapeutics, reported that it will announce new preclinical data today for its lead therapeutic candidate, CB-839, at the 2015 Global Technology Community (GTC) Novel Cancer Therapeutics Summit in San Francisco, California (Press release, Calithera Biosciences, NOV 16, 2015, View Source;p=RssLanding&cat=news&id=2112877 [SID:1234508306]). CB-839 is a potent, selective, orally bioavailable glutaminase inhibitor currently in phase I clinical trials. The first preclinical studies combining CB-839 with an immune checkpoint inhibitor were presented demonstrating that CB-839 significantly increases the rate of tumor regressions in syngeneic mice when CB-839 is added to anti-PD-L1.
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"The new data presented at the GTC meeting provide us with the rationale to continue developing CB-839 in combination with multiple classes of therapeutics, and to expand our development program to include immunotherapy agents," said Susan Molineaux, PhD, President and Chief Executive Officer of Calithera. "We continue to leverage our expertise in tumor and cellular metabolism to enhance our understanding of metabolic checkpoints in cancer."
Preclinical data will be presented in an oral presentation titled, "Identification of Biomarkers and Combination Agents for the Glutaminase Inhibitor CB-839 for the Treatment of Cancer," by Francesco Parlati, PhD, Senior Director of Biology at Calithera Biosciences. Included in the presentation are the results of studies investigating the preclinical anti-tumor activity of CB-839 in combination with an anti-PD-L1 antibody. The combination of CB-839 and anti-PD-L1 increased the number of tumor regressions seen with anti-PD-L1 treatment in the CT-26 syngeneic colon carcinoma model. Synergistic effects with CB-839 and anti-PD-L1 were also observed in a B16 melanoma model. PD-L1 ligation of PD-1 on the surface of T cells blocks metabolism of glucose and glutamine, depriving T cells of nutrients necessary for activation and differentiation. The mechanism of action of anti-PD-L1 combined with CB-839, two agents that effect metabolism in the tumor microenvironment, is being explored in further studies.