We are developing small-molecule kinase inhibitors that target cancer-associated alterations in FGFR2 and FGFR3 genes, which (together with BRAF mutations) are among the most commonly identified oncogenic drivers detected in solid tumor cancers. Our FGFR candidates aim to address the initial alteration and clinically observed and predicted mutations in FGFR2 fusion gene-positive intrahepatic cholangiocarcinoma (ICC) and FGFR3-altered urothelial carcinoma (UC) that drive resistance to current FGFR2- and FGFR3-targeted therapies. In preclinical studies we have observed potency across a broad range of clinically relevant mutations that drive acquired resistance. We believe that by addressing these mutations and broadly covering FGFR isoforms, we may be able to meaningfully increase the duration-of-response (DoR).