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Soluble in DMSO. Cobimetinib demonstrated a sustained tumor pharmacodynamic response due to longer residence times in tumor tissue than in plasma in mice. Following single doses, cobimetinib inhibited pERK in tumors with IC50 values of 780 nM in WM-266-4 and 520 nM in A375 xenograft mice. Following multiple doses, cobimetinib inhibited pERK in tumors with an increased IC50 value of 3.9 µM in WM-266-4 xenograft mice. Wong H., et al. 'Bridging the gap between preclinical and clinical studies using pharmacokinetic-pharmacodynamic modeling: an analysis of GDC-0973, a MEK inhibitor.' Clin. Cancer Res. 18: 3090-3099 (2012). 18?F-FDG-PET imaging reflected cobimetinib and vemurafenib action across a wide range of metastatic melanomas.. Baudy A.R., et al. 'FDG-PET is a good biomarker of both early response and acquired resistance in BRAF V600 mutant melanomas treated with vemurafenib and the MEK inhibitor GDC-0973.' EJNMMI Res. 2: 22 (2012). The combination treatment of cobimetinib with vemurafenib resulted in a significant improvement in progression-free survival among patients with BRAF V600-mutated metastatic melanoma. Larkin J. et al. 'Combined vemurafenib and cobimetinib in BRAF-mutated melanoma.' N. Engl. J. Med. 371: 1867-1876 (2014).
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