ライフサイエンスコーパス: panobinostat

1 , bortezomib, thalidomide, dexamethasone, or panobinostat).

2 were increased by the HDAC inhibitor LBH589 (panobinostat).

3 respond to the regimen immediately preceding panobinostat.

4 gent would augment the anti-CTCL activity of panobinostat.

5 in the HIV-1 DNA level during treatment with panobinostat.

6 ly 16 (all grade 1) were presumed related to panobinostat.

7 thalidomide 100 mg, dexamethasone 20 mg, and panobinostat 10, 15, or 20 mg (escalated to 20 mg accord

8 46 patients were treated with panobinostat 20 mg (the intention-to-treat population).

9 Panobinostat 20 mg in combination with bortezomib, thali

10 The MTD was established at panobinostat 20 mg plus bortezomib 1.3 mg/m(2).

11 ents were randomly assigned (1:1) to receive panobinostat (20 mg orally) or placebo, with bortezomib

12 Participants received oral panobinostat (20 mg) three times per week every other we

13 omib, to receive 21 day cycles of placebo or panobinostat (20 mg; on days 1, 3, 5, 8, 10, 12, orally)

14 Eleven of 40 patients (28%) responded to panobinostat (95% confidence interval [CI] 14.6-43.9) an

15 Panobinostat (a pan histone deacetylase inhibitor) is ap

16 Panobinostat, a histone deacetylase inhibitor, demonstra

17 evaluated the response rate and toxicity of panobinostat, a pan-HDI administered 30 mg orally 3 time

18 At the molecular level, panobinostat activated the caspase pathway, inhibited ST

19 ticancer effects of the HDACi vorinostat and panobinostat against a colon adenocarcinoma and two aggr

20 The epigenetic modifier drugs, panobinostat and azacitidine, increased CD33 expression

21 genes uniquely altered by the combination of panobinostat and decitabine were VHL, TCEB1, WT1, and DI

22 ent-derived primary tumor cells treated with panobinostat and decitabine.

23 al A/E9a deletion phenocopied the effects of panobinostat and other HDACis, indicating that destabili

24 NSCLC cells, whereas the pan-HDAC inhibitors panobinostat and SAHA significantly induced GAS5-AS1 in

25 Combination testing of panobinostat and the histone demethylase inhibitor GSK-J

26 erived histone deacetylase (HDAC) inhibitors Panobinostat and Vorinostat also enhanced AhR ligand-med

27 indings provide insights into the effects of panobinostat and vorinostat as LRAs for latent HIV-1.

28 ation PIs carfilzomib and ixazomib, the DACI panobinostat, and 2 mAbs, elotuzumab and daratumumab, ha

29 n to determine the maximum tolerated dose of panobinostat, and allocated patients to receive subcutan

30 d a decreased half-life after treatment with panobinostat, and therefore represents a newly identifie

31 ximum tolerated dose and recommended dose of panobinostat, and to estimate the proportion of patients

32 inostat-induced mTOR activation and enhanced panobinostat antiproliferative effects.

33 Vorinostat, romidepsin, belinostat, and panobinostat are Food and Drug Administration-approved f

34 and Nur77 in sensitizing human CTCL cells to panobinostat as well as suggest that cotreatment with an

35 Patients received panobinostat at 30 mg 3 times a week; 12 of 36 (33%) pat

36 o apoptosis induced by apicidin, entinostat, panobinostat, belinostat, and vorinostat.

37 Feb 29, 2012, with 387 randomly assigned to panobinostat, bortezomib, and dexamethasone and 381 to p

38 5% CI 19.6-34.3) in 73 patients who received panobinostat, bortezomib, and dexamethasone versus 19.5

39 ths (95% CI 35.0-44.8) in those who received panobinostat, bortezomib, and dexamethasone versus 35.8

40 We aimed to compare panobinostat, bortezomib, and dexamethasone with placebo

41 t of mice bearing t(8;21) AML with the HDACi panobinostat caused a robust antileukemic response that

42 ep and the pan-histone deacetylase inhibitor panobinostat caused more depletion of EZH2, induced more

43 We demonstrate that panobinostat causes a marked G(2) delay and mitotic defe

44 Our results suggest that panobinostat could be a useful addition to the treatment

45 The multi-histone deacetylase inhibitor panobinostat demonstrated therapeutic efficacy both in v

46 However, panobinostat did not reduce the number of latently infec

47 in 16 cycles of treatment at the recommended panobinostat dose in the modified intention-to-treat pop

48 Panobinostat effectively disrupts HIV latency in vivo an

49 ies (pomalidomide, carfilzomib and ixazomib, panobinostat, elotuzumab, and daratumumab).

50 ising activity in Hodgkin lymphoma including panobinostat, entinostat and mocetinostat.

51 Lapatinib and panobinostat exerted concentration-dependent antiprolife

52 was 13.14 months (95% CI 11.76-14.92) in the panobinostat group and 10.87 months (9.23-11.76) in the

53 reported in 228 (60%) of 381 patients in the panobinostat group and 157 (42%) of 377 patients in the

54 r better) was 1.51 months (1.41-1.64) in the panobinostat group and 2.00 months (1.61-2.79) in the pl

55 months (95% CI 31.34-not estimable) for the panobinostat group and 30.39 months (26.87-not estimable

56 w-up was 6.47 months (IQR 1.81-13.47) in the panobinostat group and 5.59 months (2.14-11.30) in the p

57 ponses were noted in 23 (6%) patients in the panobinostat group and in 42 (11%) in the placebo group.

58 ete response was significantly higher in the panobinostat group than in the placebo group (107 [27.6%

59 ree survival was significantly longer in the panobinostat group than in the placebo group (11.99 mont

60 included thrombocytopenia (256 [67%] in the panobinostat group vs 118 [31%] in the placebo group), l

61 Panobinostat had detrimental effects within 10 hours of

62 In this study, we demonstrate that panobinostat has potent antiproliferative activity again

63 Treatment with panobinostat improved survival of athymic nude mice impl

64 evels during treatment with the potent HDACi panobinostat in a human clinical trial involving 15 cART

65 ential of combining lapatinib with the HDACi panobinostat in colorectal cancer (CRC) cell lines with

66 PANORAMA 2 is a phase 2 trial of panobinostat in combination with bortezomib and dexameth

67 ctivity of the histone deacetylase inhibitor panobinostat in patients with relapsed/refractory Walden

68 ase II study examined safety and activity of panobinostat in this population.

69 nd determining the maximum tolerated dose of panobinostat in this regimen.

70 Panobinostat induced plasma viraemia with an odds ratio

71 family member Nor1 was necessary to inhibit panobinostat-induced apoptosis of CTCL cells.

72 These data provide mechanistic evidence of panobinostat-induced cell cycle arrest and highlight its

73 to analyse the mechanistic underpinnings of panobinostat-induced growth arrest.

74 mTOR inhibitor everolimus (RAD001) inhibited panobinostat-induced mTOR activation and enhanced panobi

75 We conclude that panobinostat induces very durable responses in some pati

76 Paradoxically, panobinostat inhibited LKB1 and AMP-activated protein ki

77 Collectively, our data demonstrate that panobinostat is a potent deacetylase inhibitor against H

78 Panobinostat is a potent deacetylase inhibitor that elic

79 Panobinostat is a potent oral pan-deacetylase inhibitor

80 We conclude that panobinostat is an active therapeutic agent in patients

81 Panobinostat is an oral pan-deacetylase inhibitor that s

82 s indicate that the combination of DZNep and panobinostat is effective and relatively selective epige

83 t that histone deacetylase inhibitor LBH589 (panobinostat) is a potent inhibitor of aromatase express

84 LBH589 (panobinostat) is an orally available HDAC inhibitor that

85 roximal promoter, which could be reversed by panobinostat (LBH-589) treatment.

86 In a preclinical study, we showed that panobinostat (LBH589) inhibits cell cycle progression of

87 The pan-deacetylase inhibitor panobinostat (LBH589) recently has been shown to have si

88 after treatment with the pan-HDAC inhibitor panobinostat (LBH589), the extracellular hsp90alpha was

89 ally, we show that sodium butyrate (NaB) and panobinostat (LBH589), two broad-spectrum HDAC inhibitor

90 lase inhibitors, for example, vorinostat and panobinostat (LBH589; Novartis Pharmaceuticals, East Han

91 Scriptaid, suberoyl anilide hydroxamic acid, panobinostat [LBH589], and belinostat [PXD101]); the ben

92 nner (belinostat < givinostat < vorinostat < panobinostat < romidepsin) via degradation of intracellu

93 nobinostat on GLUT1 expression suggests that panobinostat may modulate the results of clinical diagno

94 HL who relapsed or were refractory to ASCT, panobinostat monotherapy demonstrated antitumor activity

95 tudy and randomly assigned to receive either panobinostat (n=387) or placebo (n=381), plus bortezomib

96 re incubated with the HDAC inhibitor LBH589 (Panobinostat, Novartis, Germany); levels of proliferatio

97 y; dexamethasone on days 1, 2, 8, and 9; and panobinostat on days 1, 3, 5, 8, 10, and 12) for 16 cycl

98 Furthermore, the effect of panobinostat on GLUT1 expression suggests that panobinos

99 We found that treatment with the LRA panobinostat or a short analytical treatment interruptio

100 1 (eight 3-week cycles), patients received: panobinostat or placebo on days 1, 3, 5, 8, 10, and 12;

101 les with a 2 weeks on, 1 week off schedule), panobinostat or placebo was given three times a week, bo

102 A phase II/III clinical trial program (Panobinostat or Placebo With Bortezomib and Dexamethason

103 The administration of LRAs (panobinostat or vorinostat) to HIV-1-infected individual

104 The overall survival benefit with panobinostat over placebo with bortezomib and dexamethas

105 at all timepoints when patients were taking panobinostat (p < 0.0001).

106 Cotreatment with BA and panobinostat (pan-histone deacetylase inhibitor) or palb

107 Panobinostat (pano) is an FDA-approved histone deacetyla

108 Panobinostat plus bortezomib and dexamethasone significa

109 etermine the maximum-tolerated dose (MTD) of panobinostat plus bortezomib in patients with relapsed o

110 The MTD of panobinostat plus bortezomib was determined and demonstr

111 t with the pan-histone deacetylase inhibitor panobinostat (PS) depleted the mRNA and protein levels o

112 the pan-histone deacetylase (HDAC) inhibitor panobinostat (PS) is known to inhibit the chaperone func

113 ependent antiproliferative effects in vitro (panobinostat range 7.2-30 nmol/L; lapatinib range 7.6-25

114 Here, we demonstrate that treatment with panobinostat rapidly inhibits the in vitro and intracell

115 the effect of HDACi (belinostat, givinostat, panobinostat, romidepsin, and vorinostat) on the product

116 ability of the histone deacetylase inhibitor panobinostat to disrupt HIV-1 latency and the safety of

117 th the histone deacetylase inhibitor (HDACi) panobinostat together with Smac mimetics resulted in syn

118 Panobinostat treatment induced downregulation of EGFR, H

119 Combined lapatinib and panobinostat treatment interacted synergistically to inh

120 in cell-associated unspliced HIV RNA during panobinostat treatment was 3.5-fold (range 2.1-14.4).

121 tudy, and changes in HIV-1 DNA levels during panobinostat treatment were negatively associated with t

122 es in HIV-1 DNA levels in CD4 T cells during panobinostat treatment.

123 the promoters of these genes in response to panobinostat treatment.

124 Panobinostat triggered terminal myeloid differentiation

125 nt groups (235 [60.7%, 95% CI 55.7-65.6] for panobinostat vs 208 [54.6%, 49.4-59.7] for placebo; p=0.

126 In the dose-escalation phase (n = 47), panobinostat was administered orally thrice weekly every

127 Panobinostat was well tolerated.

128 CDK inhibitor dinaciclib and HDAC inhibitor panobinostat were the most potent inducers of apoptosis

129 n resveratrol and pan-HDACIs (vorinostat and panobinostat) were examined in human acute myelogenous l

130 Panobinostat, when combined with bortezomib and dexameth

131 induced apoptosis and sensitized HH cells to panobinostat, whereas combined knockdown of Nur77 and it

132 rovide a mechanistic rationale for combining panobinostat with mTOR inhibitors for treating Hodgkin l

133 Combining panobinostat with the mTOR inhibitor everolimus (RAD001)

134 t incorporated a 1-week treatment holiday of panobinostat, with dexamethasone added in cycle 2.