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1 of mature B-cell lymphoma (e.g., ibrutinib, idelalisib).
2 osphatidylinositol 3-kinase [PI3K] inhibitor idelalisib).
3 e IV MCC patient treated with PI3K inhibitor idelalisib.
4 ibitor ibrutinib and the PI3Kdelta inhibitor idelalisib.
5 s that confer the potency and selectivity of idelalisib.
6 ocked by ibrutinib and fostamatinib, but not idelalisib.
7 nositol-3'-kinase (PI3K) p110delta inhibitor idelalisib.
8 ity of inhibiting the PI3Kdelta pathway with idelalisib.
9 d basal and inducible pERK and resistance to idelalisib.
10 eptor (BCR) inhibitors such as ibrutinib and idelalisib.
11 ing autoimmune colitis in patients receiving idelalisib.
12 R-1202 in aggressive lymphoma not found with idelalisib.
13 Administration-approved p110delta inhibitor idelalisib.
14 killing by the PI3K-delta-specific inhibitor idelalisib.
15 phenotype taken on by CLL cells treated with idelalisib.
16 fficiently by sunitinib than by ibrutinib or idelalisib.
17 available small molecule PI3Kdelta inhibitor idelalisib.
19 de 10 mg on days 1-21 every 28 days and oral idelalisib 150 mg twice a day with continuous 28-day cyc
20 e 15 mg on days 1-21 in a 28 day cycle, oral idelalisib 150 mg twice a day with continuous 28-day cyc
21 ted with rituximab 375 mg/m(2) weekly x8 and idelalisib 150 mg twice daily continuously for 48 weeks.
22 eive either idelalisib plus ofatumumab (oral idelalisib 150 mg twice daily continuously plus ofatumum
23 2-6) in addition to either twice-daily oral idelalisib (150 mg) or placebo until disease progression
24 receipt of those therapies were administered idelalisib, 150 mg twice daily, until the disease progre
25 reclinical data suggested that ibrutinib and idelalisib, 2 clinically approved kinase inhibitors, inc
27 e assessed the efficacy and safety of adding idelalisib, a first-in-class targeted phosphoinositide-3
28 ased on CLL cells from patients treated with idelalisib, a phosphoinositide-3-kinase delta inhibitor
30 ho had not received previous lenalidomide or idelalisib (A051201) were started with oral lenalidomide
31 into the blood through distinct mechanisms: idelalisib actively promotes egress by upregulating S1PR
33 more, the PI3K p110delta-specific inhibitor, idelalisib, also demonstrates activity against primary l
36 tudy, we assessed the efficacy and safety of idelalisib, an oral inhibitor of the delta isoform of ph
39 hosphoinositide 3'-kinase (PI3K) inhibitors (idelalisib and duvelisib) can be prescribed for disease
41 lity of the BCR-associated kinase inhibitors idelalisib and ibrutinib, approved for treatment of CLL
42 he past year with the regulatory approval of idelalisib and ibrutinib, with other therapeutic small m
43 ts occurred in 40% of the patients receiving idelalisib and rituximab and in 35% of those receiving p
48 naling pathway inhibitors such as ibrutinib, idelalisib, and fostamatinib (respective inhibitors of B
50 2015, in six randomised trials of ibrutinib, idelalisib, and venetoclax, or at the Mayo Clinic CLL Da
55 short hairpin RNA complements the effects of idelalisib, as a single agent or in combination with car
56 ng illnesses to receive rituximab and either idelalisib (at a dose of 150 mg) or placebo twice daily.
58 se inhibitor ibrutinib or the PI3K inhibitor idelalisib block B-cell receptor induced activation of L
60 mphoma cell lines, and patients treated with idelalisib, but not ibrutinib, showed increased somatic
61 reatment with a specific PI3Kdelta inhibitor Idelalisib (CAL-101) suppresses E2F1 and c-Myc levels an
62 susceptible to PI3Kdelta inactivation using idelalisib compared with CD4(+) and CD8(+) effector T ce
63 sitivity versus CD8(+) Teff insensitivity to idelalisib could still potentially be exploited to enhan
64 approval pathway and evidence generation for idelalisib during premarketing, postmarketing, and prema
65 gs for leukaemia or lymphoma therapy such as idelalisib, duvelisib and ibrutinib block PI3Kdelta acti
68 approval of one isoform-selective inhibitor (idelalisib) for treatment of certain blood cancers and a
69 umonia, and pyrexia, were more common in the idelalisib group (140 [68%] of 207 patients) than in the
70 the placebo group and was not reached in the idelalisib group (hazard ratio for progression or death
71 al was 20.8 months (95% CI 16.6-26.4) in the idelalisib group and 11.1 months (8.9-11.1) in the place
72 o death occurred in 23 (11%) patients in the idelalisib group and 15 (7%) in the placebo group, inclu
73 including six deaths from infections in the idelalisib group and three from infections in the placeb
74 reased risk of infection was reported in the idelalisib group compared with the placebo group (grade
75 quent grade 3 or worse adverse events in the idelalisib group were neutropenia (124 [60%] of 207 pati
80 ositol 3-kinase delta (PI3K-delta) inhibitor idelalisib has been approved for treatment of chronic ly
82 e currently applied inhibitors ibrutinib and idelalisib have limited capacity however to induce cell
83 mber of single agents, such as ibrutinib and idelalisib, have demonstrated impressive efficacy with a
84 esistance, both proven and hypothesized, for idelalisib, ibrutinib, and venetoclax, describe patterns
85 randomized, double-blind, phase III study of idelalisib (IDELA) plus rituximab versus placebo plus ri
86 activation can be inhibited by ibrutinib or idelalisib.IMPORTANCE EBV establishes viral latency in B
89 e aimed to assess the efficacy and safety of idelalisib in combination with a second-generation anti-
91 ibitor ibrutinib and the PI3Kdelta inhibitor idelalisib in more than half of the cases had only a par
93 nalidomide in combination with rituximab and idelalisib in relapsed follicular and mantle cell lympho
94 verse effects in association with the use of idelalisib in the treatment of CLL, particularly as a fi
95 e and imply that ibrutinib could differ from idelalisib in their potential to induce AID in treated p
96 ated patient showed decreased sensitivity to idelalisib in vitro concomitant with enhanced MAPK signa
99 linking, whereas treatment of CLL cells with idelalisib increased S1PR1 expression and migration towa
101 ritical to B-cell development (with CAL-101 [idelalisib]), interrupts a double-negative feedback loop
110 a first-line therapy, gave indications that idelalisib may preferentially target the suppressive fun
112 in a phase 2 study consisting of 2 months of idelalisib monotherapy followed by 6 months of combinati
117 ib and tirabrutinib, and PI3Kdelta inhibitor idelalisib on malignant CLL cells but also on healthy hu
118 n this background, we examined the effect of idelalisib on the function of human Tregs ex vivo with r
119 rapy and three external-validation datasets (idelalisib or chemoimmunotherapy dataset, n=897; venetoc
120 , and all three external-validation cohorts (idelalisib or chemoimmunotherapy: CS=0.71, 0.59-0.81, lo
121 that treatment of primary mouse B cells with idelalisib or duvelisib, and to a lesser extent ibrutini
124 distinctive isoform-specificities, including idelalisib (PI3K-delta), copanlisib (PI3K-alpha/delta),
126 compared with placebo (treatment difference [idelalisib - placebo], -1.78; 95% CI, -2.53 to -1.03; P
127 one patients with allergic rhinitis received idelalisib/placebo (n = 21) or placebo/idelalisib (n = 2
128 ode, and assigned patients to receive either idelalisib plus ofatumumab (oral idelalisib 150 mg twice
130 22 treatment-related deaths occurred in the idelalisib plus ofatumumab group (the most common being
131 al was 16.3 months (95% CI 13.6-17.8) in the idelalisib plus ofatumumab group and 8.0 months (5.7-8.2
132 Serious infections were more common in the idelalisib plus ofatumumab group and included pneumonia
133 included pneumonia (23 [13%] patients in the idelalisib plus ofatumumab group vs nine [10%] in the of
134 quent grade 3 or worse adverse events in the idelalisib plus ofatumumab group were neutropenia (59 [3
136 s Treg-preferential effect could explain why idelalisib produces adverse autoimmune effects by breaki
137 tients were treated at 6 dose levels of oral idelalisib (range 50-350 mg once or twice daily) and rem
140 -CD20 monoclonal antibody), 143 treated with idelalisib-rituximab, and 100 treated with venetoclax (1
141 ce treated with the PI3Kd inhibitor (PI3Kdi) Idelalisib showed a similar transient decrease in parasi
144 nts during ibrutinib therapy, in 0.9% during idelalisib therapy, and in 7% during venetoclax therapy,
145 th grass pollen) was substantially lower for idelalisib-treated compared with placebo-treated subject
148 ymptom scores were lower during the combined idelalisib treatment periods compared with placebo (trea
159 rgistic cytotoxic activity of selinexor plus idelalisib was associated with increased regulatory effe
162 dose regimens of idelalisib were evaluated; idelalisib was taken once or twice daily continuously at
163 02, but not the approved PI3Kdelta inhibitor idelalisib, was highly synergistic with the proteasome i
166 ound GS-649443, that has superior potency to idelalisib while maintaining selectivity, reduced cGVHD
167 es were safety and tolerability of combining idelalisib with lenalidomide and rituximab in patients w