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Kura Oncology Reports Preclinical Results Showing Antitumor Activity of Tipifarnib in Combination with PI3Kα Inhibitor in Head and Neck Squamous Cell Carcinoma
– Preclinical data support potential to expand therapeutic utility of tipifarnib to HRAS/PI3K dependent tumors representing up to 50% of HNSCC – – Company
About this update from Kura Oncology, Inc.
[{"type":"text","content":"– Preclinical data support potential to expand therapeutic utility of tipifarnib to HRAS/PI3K dependent tumors representing up to 50% of HNSCC –\n – Company plans to conduct a Phase 1/2 proof-of-concept study of tipifarnib in combination with a PI3Kα inhibitor in relapsed/refractory HNSCC – SAN DIEGO, Oct. 26, 2020 (GLOBE NEWSWIRE) -- Kura Oncology, Inc. (Nasdaq: KURA), a clinical-stage biopharmaceutical company focused on the development of precision medicines for the treatment of cancer, reported new preclinical data demonstrating the Company’s late-stage drug candidate, tipifarnib, shows compelling activity when combined with a PI3Kα inhibitor in models of HRAS/PI3K-dysregulated head and neck squamous cell carcinoma (HNSCC), including tumors with PIK3CA mutations or amplifications as well as HRAS overexpression. These preclinical data were presented at the 32nd EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics on Saturday. A copy of the poster is available on Kura's website at www.kuraoncology.com/pipeline/publications. “In addition to conducting our ongoing registration-directed trial of tipifarnib in recurrent or metastatic HRAS mutant HNSCC (AIM-HN), we are also pioneering new approaches to expand the use of tipifarnib into larger patient populations,” said Troy Wilson, Ph.D., J.D., President and Chief Executive Officer of Kura Oncology. “The compelling preclinical data underscore the potential to combine tipifarnib with a PI3Kα inhibitor to treat HNSCC patients and support our rationale to prioritize a Phase 1/2 study of tipifarnib in combination with a PI3Kα inhibitor in advanced or unresectable relapsed/refractory HNSCC harboring PIK3CA mutations or amplifications and/or HRAS overexpression.” HRAS, both in the mutant and overexpressed form, acts as a key node at the center of HNSCC tumor biology, while PIK3CA represents the most commonly dysregulated oncogene in HNSCC tumors. As concluded in the presentation, Kura’s preclinical data support the observation that the HRAS and PI3K pathways are complementary in HNSCC, each providing compensatory mechanisms of resistance to single agent inhibition of the other. Specifically, additive or synergistic activity was observed with administration of the combination of tipifarnib and a PI3Kα inhibitor in a panel of 16 patient-derived xenograft models representat...