Corvus Pharmaceuticals announces presentation of CPI-444, CPI-006 data

Corvus Pharmaceuticals announced the presentation of updated biomarker and clinical results from its two lead programs that target the adenosine pathway, CPI-444, an adenosine A2A receptor antagonist, and CPI-006, an anti-CD73 antibody. The data were presented at the Immuno-Oncology 360 degrees Conference. The presentation reviewed gene expression data of an adenosine gene signature recently announced by Corvus, in patients with renal cell carcinoma, or RCC, who are participating in Corvus’ ongoing Phase 1/1b study of CPI-444, a selective and potent inhibitor of the adenosine A2A receptor. In particular, the data from the study showed a relationship of this novel biomarker to angiogenesis gene expression data. Such findings indicate that expression of AdenoSig was inversely related to the angiogenesis signature, which has been well studied by others and correlates with response to vascular endothelial growth factor receptor, or VEGFR, inhibitors such as Sutent and other tyrosine kinase inhibitors. Low expression of angiogenesis genes predicts a lack of response to VEGFR inhibition. These data suggest that patients with a high AdenoSig are potentially more likely to respond to treatment with CPI-444 and less likely to respond to VEGFR inhibitors. The company also presented updated clinical results from the ongoing Phase 1/1b dose-escalation study of CPI-006 in patients with a variety of advanced cancers, including non-small cell lung cancer, or NSCLC, RCC and other cancers who have failed standard therapies. The first arm of the study is evaluating CPI-006 as a monotherapy, a second arm is evaluating CPI-006 in combination with CPI-444, and a third arm is planned to evaluate CPI-006 in combination with pembrolizumab, an anti-PD-1 antibody. CPI-006 given as a monotherapy activated B cells and led to a redistribution of these cells along with changes in other immune cells. These data are consistent with immune stimulation induced by CPI-006. CPI-006 reacted with an epitope on CD73 that led to blockade of adenosine production and expression of lymphocyte activation antigens that are independent of adenosine.
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