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2 chical randomisation algorithm to daily oral pictilisib (340 mg in part 1 and 260 mg in part 2) or pl
4 atients were analysed according to presence (pictilisib 6.5 months [95% CI 3.7-9.8] vs placebo 5.1 mo
5 median progression-free survival between the pictilisib (6.6 months [95% CI 3.9-9.8]) and placebo (5.
8 mutations were not predictive of response to pictilisib, but there was significant interaction betwee
9 athways by the small-molecule PI3K inhibitor pictilisib (GDC-0941) and the MEK inhibitor cobimetinib
10 y assessed whether adding the PI3K inhibitor pictilisib (GDC-0941) can increase the antitumor effects
11 s occurred in 54 (61%) of 89 patients in the pictilisib group and 22 (28%) of 79 in the placebo group
12 s occurred in 15 (36%) of 42 patients in the pictilisib group and seven (37%) of 19 patients in the p
16 bitors with greater selectivity than that of pictilisib might be needed to improve tolerability and p
17 orally bioavailable class I PI3K inhibitors, pictilisib or buparlisib, display elevated CMA activity,
18 of selective responses to the PI3K inhibitor pictilisib, the fatty acid synthase inhibitor GSK2194069
20 of this study is to establish if addition of pictilisib to fulvestrant can improve progression-free s
24 improve progression-free survival, dosing of pictilisib was limited by toxicity, potentially limiting