Date: 2014-09-29
Type of information: Presentation of results at a congress
phase: 2
Announcement: presentation of results at the 2014 Congress of the European Society for Medical Oncology (ESMO)
Company: Aveo Oncology (USA - MA)
Product: tivozanib (N-{2-Chloro-4-[(6,7-dimethoxy-4-quinolyl)oxy]phenyl}-N´-(5-methyl-3-isoxazolyl) urea hydrochloride monohydrate)
Action
mechanism: kinase inhibitor/tyrosine kinase inhibitor. Tivozanib is an oral, potent, selective inhibitor of vascular endothelial growth factor tyrosine kinase inhibitor (VEGF TKI) with a long half-life and activity against all three VEGF receptors.
Disease: renal cell carcinoma
Therapeutic area: Cancer - Oncology
Country:
Trial details:
Latest
news: * On September 29, 2014, Aveo Oncology announced poster presentations for two Phase 2 clinical studies of tivozanib, one in metastatic colorectal cancer (mCRC) and one in renal cell carcinoma (RCC), at the 2014 Congress of the European Society for Medical Oncology (ESMO), taking place September 25–30 in Madrid, Spain. Tivozanib is an oral, potent, selective inhibitor of vascular endothelial growth factor tyrosine kinase inhibitor (VEGF TKI) with a long half-life and activity against all three VEGF receptors. Title: Phase 2 clinical evaluation of preclinically defined biomarkers for vascular endothelial growth factor (VEGF) tyrosine kinase inhibitor (TKI) tivozanib in renal cell carcinoma (RCC): Despite significant effort, identifying predictive biomarkers for VEGF-targeted therapies remains challenging. Using population-based tumor models, Aveo Oncology identified a population of infiltrating myeloid cells associated with resistance to tivozanib. In this Phase 2, single arm trial (BATON-RCC) of tivozanib monotherapy in nephrectomized, targeted therapy-naïve RCC (n=105; 90 clear cell histology), certain myeloid cell biomarkers (immunohistochemistry [IHC] and ribonucleic acid [RNA]) were evaluated. The study results demonstrated that low myeloid signature score was associated with significantly longer PFS compared to high myeloid signature based on a median cutoff (14.7 months vs. 8.3 months; hazard ratio [HR] 0.49, p=0.035; 95% CI 0.25-0.96), and as a continuous variable (p=0.03; n=63). The IHC score exhibited a similar trend but was not significant. These results suggest a low myeloid signature score in RCC patients may predict a positive clinical response when treated with tivozanib, including significantly increased PFS.
