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1 rved for the structurally related 4 (BKM120, buparlisib).
3 y assigned (1:1) to receive second-line oral buparlisib (100 mg once daily) or placebo, plus intraven
4 chnology (block size of six) to receive oral buparlisib (100 mg per day) or matching placebo starting
5 e of 6) on day 15 of cycle 1 to receive oral buparlisib (100 mg/day) or matching placebo, starting on
8 nuous or intermittent (five on/two off days) buparlisib administration on an every-4-week schedule.
13 lable class I PI3K inhibitors, pictilisib or buparlisib, display elevated CMA activity, and decreased
14 for re-operation after progression received buparlisib for 7 to 13 days before surgery to evaluate b
15 s occurred in 15 (20%) of 76 patients in the buparlisib group and 17 (22%) of 78 patients in the plac
16 vival was 4.6 months (95% CI 3.5-5.3) in the buparlisib group and 3.5 months (2.2-3.7) in the placebo
17 reported for 43 (57%) of 76 patients in the buparlisib group and 37 (47%) of 78 in the placebo group
18 e reported in 62 (82%) of 76 patients in the buparlisib group and 56 (72%) of 78 patients in the plac
19 occurred in ten (3%) of 288 patients in the buparlisib group and in six (4%) of 140 in the placebo g
20 atment-related (cardiac failure [n=1] in the buparlisib group and unknown reason [n=1] in the placebo
21 reported in 134 (23%) of 573 patients in the buparlisib group compared with 90 [16%] of 570 patients
22 reported in 64 (22%) of 288 patients in the buparlisib group versus 23 (16%) of 140 in the placebo g
23 vival was 6.8 months (95% CI 4.9-7.1) in the buparlisib group versus 4.0 months (3.1-5.2) in the plac
24 vival was 6.9 months (95% CI 6.8-7.8) in the buparlisib group versus 5.0 months (4.0-5.2) in the plac
25 most common grade 3-4 adverse events in the buparlisib group versus the placebo group were increased
26 vival was 6.8 months (95% CI 5.0-7.0) in the buparlisib group vs 4.5 months (3.3-5.0) in the placebo
27 ents (occurring in >/=10% of patients in the buparlisib group vs the placebo group) were hyperglycaem
29 f this randomised phase 2 study suggest that buparlisib in combination with paclitaxel could be an ef
30 mics, and efficacy of the pan-PI3K inhibitor buparlisib in patients with recurrent glioblastoma with
33 countries were randomly assigned to receive buparlisib (n=576) or placebo plus fulvestrant (n=571).
34 PI3K pathway inhibition in tumor tissue and buparlisib pharmacokinetics in cohort 1 and 6-month prog
36 essed the efficacy of the pan-PI3K inhibitor buparlisib plus fulvestrant in patients with advanced br
39 lled and randomly assigned to receive either buparlisib plus paclitaxel (n=79) or placebo plus paclit
44 ients not eligible for re-operation received buparlisib until progression or unacceptable toxicity.
45 ree survival was significantly longer in the buparlisib versus placebo group (3.9 months [95% CI 2.8-
46 ost frequent grade 3-4 adverse events in the buparlisib versus placebo group were elevated alanine am