ライフサイエンスコーパス: panobinostat

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

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

3 cell-specific release of the anticancer drug panobinostat.

4 respond to the regimen immediately preceding panobinostat.

5 to the histone deacetylase (HDAC) inhibitor panobinostat.

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

7 t, likely due to increased susceptibility to panobinostat.

8 3K27ac marks, the molecular target sites for panobinostat.

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

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

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

12 46 patients were treated with panobinostat 20 mg (the intention-to-treat population).

13 Panobinostat 20 mg in combination with bortezomib, thali

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

15 The safety profile of panobinostat 20 mg three times weekly was more favourabl

16 re randomly assigned (1:1:1) to receive oral panobinostat 20 mg three times weekly, 20 mg twice weekl

17 re randomly assigned (1:1:1) to receive oral panobinostat 20 mg three times weekly, 20 mg twice weekl

18 , 248 patients were randomly assigned (82 to panobinostat 20 mg three times weekly, 83 to panobinosta

19 panobinostat 20 mg three times weekly, 83 to panobinostat 20 mg twice weekly, and 83 to 10 mg panobin

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

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

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

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

24 Panobinostat (a pan histone deacetylase inhibitor) is ap

25 delayed histone deacetylase inhibition with panobinostat, a drug used to treat hematopoietic stem ce

26 Panobinostat, a histone deacetylase inhibitor, demonstra

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

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

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

30 We identified Panobinostat, an FDA approved pan-HDAC inhibitor, could

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

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

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

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

35 Thrombocytopenia observed with vorinostat, panobinostat and romidepsin may stem from dual inhibitio

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

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

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

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

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

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

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

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

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

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

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

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

48 uman parietal epithelial cells in vitro with panobinostat attenuated stratifin expression in renal pr

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

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

51 5% CI 19.6-34.3) in 73 patients who received panobinostat, bortezomib, and dexamethasone versus 19.5

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

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

54 PT-VT-carfilzomib-lenalidomide-dexamethasone-panobinostat-bortezomib-dexamethasone had the most favor

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

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

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

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

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

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

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

62 Panobinostat effectively disrupts HIV latency in vivo an

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

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

65 Lapatinib and panobinostat exerted concentration-dependent antiprolife

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

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

68 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

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

70 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

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

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

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

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

75 Panobinostat had detrimental effects within 10 hours of

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

77 Treatment with panobinostat improved survival of athymic nude mice impl

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

79 uided FUS treatment in combination with oral panobinostat in children with relapsed DMGs.

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

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

82 y of three different dosing regimens of oral panobinostat in combination with subcutaneous bortezomib

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

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

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

86 i-inflammatory and immunosuppressive effect, panobinostat induced differentiation of an immature hype

87 Panobinostat induced plasma viraemia with an odds ratio

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

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

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

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

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

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

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

95 Panobinostat is a potent deacetylase inhibitor that elic

96 Panobinostat is a potent oral pan-deacetylase inhibitor

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

98 Panobinostat is an oral pan-deacetylase inhibitor that s

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

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

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

102 d histone deacetylase inhibitors (HDACi) and panobinostat (LBH) more specifically as the most selecti

103 Our data reveal that panobinostat (LBH-589) and romidepsin (FK-228) provide f

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

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

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

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

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

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

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

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

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

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

114 The gastrointestinal (GI) ADRs of panobinostat (n = 488, P < .05) can partly be related to

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

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

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

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

119 The effect of LBH (panobinostat) on gene expression and chromatin structure

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

121 1 (eight 3-week cycles), patients received: panobinostat or placebo on days 1, 3, 5, 8, 10, and 12;

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

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

124 retinib (VEGFR2/METi), but less sensitive to Panobinostat or Vorinostat (HDACi).

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

126 -myristate 13-acetate/ionomycin, prostratin, panobinostat, or romidepsin.

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

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

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

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

131 Panobinostat plus bortezomib and dexamethasone significa

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

133 bortezomib improves the tolerability of the panobinostat plus bortezomib plus dexamethasone regimen.

134 The MTD of panobinostat plus bortezomib was determined and demonstr

135 files of the HDACIs: vorinostat, belinostat, panobinostat, pracinostat, entinostat, romidepsin, bufex

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

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

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

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

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

141 r THZ1 and the histone deacetylase inhibitor panobinostat synergistically reduces JMJD6, E2F2, N-Myc,

142 When combined with panobinostat, Tat-LNP induces latency reversal in a sign

143 binostat 20 mg twice weekly, and 83 to 10 mg panobinostat three times weekly).

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

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

146 perone NCGC326) and proteostasis regulators (panobinostat, trans-ISRIB, and pladienolide B).

147 Panobinostat treatment induced downregulation of EGFR, H

148 Combined lapatinib and panobinostat treatment interacted synergistically to inh

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

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

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

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

153 Panobinostat triggered terminal myeloid differentiation

154 promising treatment strategies, of which the panobinostat, venetoclax and anti-CD40 triple therapy wa

155 M models, we found that FDA-approved global (panobinostat, vorinostat) and selective (romidepsin) his

156 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.

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

158 Panobinostat was well tolerated.

159 d nanoparticle (Tat-LNP) in combination with panobinostat, we show that p24+ cells from blood and lym

160 Here, FUS and panobinostat were shown to have additive therapeutic eff

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

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

163 trial that the histone deacetylase inhibitor panobinostat, when administered in combination with pegy

164 Panobinostat, when combined with bortezomib and dexameth

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

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

167 Combining panobinostat with the mTOR inhibitor everolimus (RAD001)

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