ライフサイエンスコーパス: vorinostat

1 mbination with various HDACi (MS/SNDX-275 or vorinostat).

2 cetylase (HDAC) inhibitors valproic acid and vorinostat.

3 n, entinostat, panobinostat, belinostat, and vorinostat.

4 inhibitors (HDACis) valproic acid (VPA) and vorinostat.

5 ths of maintenance therapy with single-agent vorinostat.

6 reated with the FDA-approved HDAC inhibitor, vorinostat.

7 ctivity of the histone deacetylase inhibitor vorinostat.

8 pair the DSBs despite continued culture with vorinostat.

9 nd hyponatremia also were more frequent with vorinostat.

10 DE given alone or combined with sorafenib or vorinostat.

11 erference or inhibited by the HDAC inhibitor vorinostat.

12 predicting the response of CTCL patients to vorinostat.

13 s finding a cure for beta-thalassaemia using vorinostat.

14 nalidomide, and 92 received azacitidine plus vorinostat.

15 milarly treated patients who did not receive vorinostat.

16 rall survival and safety and tolerability of vorinostat.

17 ing exposure to the latency-reversing agent, vorinostat.

18 xposure to the histone deacetylase inhibitor vorinostat.

19 AC6 with tubacin recapitulated the effect of vorinostat.

20 to evaluate the safety and activity of oral vorinostat 100 to 300 mg twice or thrice daily for 14 da

21 Vorinostat (100 mg twice daily) was started on day -10 a

22 ade 4 platelet toxicity was more common with vorinostat (18% v 3%; P < .05).

23 hypertriglyceridemia, resulting in a MTD of vorinostat 180 mg/m(2)/d 4 times per week and 13cRA 80 m

24 or, have been merged with the HDAC inhibitor vorinostat (2), leading to new molecules that are bispec

25 at analysis (n = 62), overall pCR was 27.4% (vorinostat, 25.8%; placebo, 29.0%).

26 Patients received oral vorinostat 300 mg (or matching placebo) twice daily on d

27 mg/day on days 1 to 21); or azacitidine plus vorinostat (300 mg twice daily on days 3 to 9).

28 d paclitaxel (200 mg/m(2) day 3) with either vorinostat (400 mg by mouth daily) or placebo.

29 aromatase inhibitor (AI) therapy were given vorinostat (400 mg daily) sequentially or simultaneously

30 and nab-paclitaxel (100 mg/m(2) weekly) with vorinostat (400 mg orally daily, days 1-3 of every 7-d p

31 Induction therapy was vorinostat 500 mg orally three times a day (days 1 to 3)

32 We performed a phase II study of oral vorinostat, a histone and protein deacetylase inhibitor,

33 ith either drug alone or in combination with vorinostat, a histone deacetylase inhibitor (HDACi), usi

34 PURPOSE Vorinostat, a histone deacetylase inhibitor, exerts anti

35 Vorinostat, a histone deacetylase inhibitor, represents

36 he present study, we describe the effects of vorinostat, a small-molecule inhibitor of histone deacet

37 tment of colon cancer cells with sorafenib + vorinostat activates CD95 via de novo ceramide synthesis

38 We demonstrate that vorinostat acts following viral fusion and enhances the

39 ng toxicities (DLT), and pharmacokinetics of vorinostat administered as a single agent and in combina

40 us rituximab if CD20+), alone or with 300 mg vorinostat, administered on days 1 to 5 of each cycle.

41 acetylase (HDAC) inhibitors Panobinostat and Vorinostat also enhanced AhR ligand-mediated induction a

42 Furthermore, vorinostat also interacted with a selective inhibitor of

43 ical HDACi such as the hydroxamic acid-based vorinostat (also known as SAHA and Zolinza) inhibits cla

44 as the histone deacetylase (HDAC) inhibitor vorinostat, also has been reported to trigger HIV-1 reac

45 ibitor, and suberoylanilide hydroxamic acid (vorinostat), an inhibitor of class I, II, and IV HDACs,

46 h 93% of samples treated with venetoclax and vorinostat and 73% of samples treated with venetoclax an

47 d by an increased acetylation in response to vorinostat and a reduced Ser315 phosphorylation in respo

48 the histone deacetylase inhibitors (HDACis) vorinostat and AR-42 reduced the viability of a canine m

49 th other latency-reversing agents, including vorinostat and bryostatin.

50 Combination pretreatment with vorinostat and decitabine resulted in even greater cytot

51 Weaning NOD mice received low doses of vorinostat and givinostat in their drinking water until

52 ate that the clinically well-tolerated KDACi vorinostat and givinostat revert diabetes in the nonobes

53 ant for the anticancer effects of HDACi, and vorinostat and IFN-gamma acted in concert to enhance the

54 ection and were resistant to reactivation by vorinostat and interleukin 1beta.

55 authors evaluated the effects of the HDACIs vorinostat and m-carboxycinnamic acid bis-hydroxamide on

56 r refractory lymphoma attained a response to vorinostat and niacinamide, and 57% experienced disease

57 histone deacetylase inhibitors, for example, vorinostat and panobinostat (LBH589; Novartis Pharmaceut

58 r the robust anticancer effects of the HDACi vorinostat and panobinostat against a colon adenocarcino

59 ractions between resveratrol and pan-HDACIs (vorinostat and panobinostat) were examined in human acut

60 Specifically, vorinostat and romidepsin have been approved by the US F

61 ts following the FDA approval of two HDACis, vorinostat and romidepsin.

62 hat ROS plays an important role in action of vorinostat and that combination with a redox-modulating

63 In vivo results demonstrate that combining vorinostat and the IKK inhibitor Bay 117085 significantl

64 imes unlike the hydroxamate-containing HDACi vorinostat and trichostatin-A.

65 molar inhibition of HDAC4 and HDAC5, whereas vorinostat and TSA inhibit HDAC4 and HDAC5 in the higher

66 acetylase (HDAC) inhibitors, including SAHA (vorinostat) and LBH589, which are currently being tested

67 ound that FDA-approved global (panobinostat, vorinostat) and selective (romidepsin) histone deacetyla

68 one deacetylase inhibitors (e.g. romidepsin, vorinostat, and balinostat), purine analogs and agents t

69 After a 24-h culture of cells with vorinostat, and reculture without the HDACi, gammaH2AX w

70 T cells, were implicated as effectors of the vorinostat antitumor immune response.

71 depsin) and suberoylanilide hydroxamic acid (vorinostat) are histone deacetylase inhibitors (HDACi) a

72 HDAC inhibitors, particularly vorinostat, are currently being investigated clinically

73 ne deacetylase (HDAC) inhibitors, especially vorinostat, are currently under investigation as potenti

74 l (13.0 months v 9.7 months; P = .17) in the vorinostat arm.

75 Chemosensitivity testing identified vorinostat as a potential therapeutic agent.

76 by Makki and Haqqi that proposes the use of vorinostat as a therapeutic agent for the management of

77 nsights into the effects of panobinostat and vorinostat as LRAs for latent HIV-1.

78 The finding that vorinostat augments the effectiveness of doxorubicin pro

79 ry of suberoylanilide hydroxamic acid (SAHA, vorinostat) began over three decades ago with our studie

80 Low doses of sorafenib and vorinostat, but not the individual drugs, rapidly increa

81 Therapeutic effects of pan-HDAC (Vorinostat), class-selective (VPA) and isoform-selective

82 The effect of vorinostat co-treatment on the development of resistance

83 trials of the histone deacetylase inhibitor vorinostat combined with either the vascular endothelial

84 we further demonstrated that decitabine and vorinostat cooperate to suppress colon carcinoma metasta

85 ed that epigenetic inhibitors decitabine and vorinostat cooperate to upregulate Fas expression in met

86 The median number of vorinostat cycles received was nine.

87 B-IVA MF/SS were treated with 400 mg of oral vorinostat daily until disease progression or intolerabl

88 pregulates BNIP3 and Bik expression, whereas vorinostat decreased Bcl-x(L) expression.

89 ely to benefit from combination therapy, but vorinostat did not change ER expression at the level of

90 EPOCH-vorinostat did not eliminate HIV reservoirs, resulted in

91 Wide interpatient variability was noted in vorinostat disposition, with area under the concentratio

92 The histone deacetylase (HDAC) inhibitor vorinostat disrupts EBV/HHV-8 latency, enhances chemothe

93 Vorinostat does not enhance viral fusion with cells but

94 The daily vorinostat dose was escalated within each hepatic dysfun

95 The recommended vorinostat doses in mild, moderate, and severe hepatic d

96 Finally, subeffective vorinostat doses markedly increased CFZ-mediated tumor g

97 One week later, daily vorinostat dosing was begun and continued until toxicity

98 Vorinostat downregulated baseline NF-kappaB activity and

99 Coadministration of vorinostat dramatically increased MK-0457 lethality in K

100 However, CFZ/vorinostat dramatically induced resistant cell apoptosis

101 n, implicating HIF-2alpha as a biomarker for Vorinostat efficacy in STS.

102 Vorinostat (either 100 mg or 200 mg, twice a day) was in

103 BET inhibitor (+)-JQ1 and the HDAC inhibitor vorinostat, either alone or and in combination, highligh

104 one deacetylase (HDAC) inhibitors, including vorinostat, enhanced GD2 expression in neuroblastoma cel

105 CONCLUSION Vorinostat enhances the efficacy of carboplatin and pacl

106 ), erlotinib, lapatinib, and combinations of vorinostat/erlotinib and vorinostat/lapatinib.

107 ed the safety and efficacy of pazopanib plus vorinostat, everolimus, lapatinib or trastuzumab, and ME

108 We further show that vorinostat exhibits these synergistic beneficial effects

109 ase CD95 plasma membrane levels; sorafenib + vorinostat exposure killed HCT116 cells via an intrinsic

110 uptake did not systematically increase with vorinostat exposure, indicating no change in regional ER

111 Vorinostat for GVHD prevention is an effective strategy

112 ll patients received a single 400-mg dose of vorinostat for pharmacokinetic studies.

113 e studies are needed to assess the effect of vorinostat for prevention of GVHD in broader settings of

114 d by the US Food and Drug Administration for vorinostat for treatment of cutaneous T-cell lymphoma.

115 ed this phase 3 trial to investigate whether vorinostat given as a second-line or third-line therapy

116 In this randomised trial, vorinostat given as a second-line or third-line therapy

117 fatigue or malaise (51 [16%] patients in the vorinostat group vs 25 [8%] in the placebo group]) and d

118 against highly aggressive HIV-NHLs, whereas vorinostat had no benefit; patients with Myc-driven DLBC

119 In clinical trials, vorinostat has activity against hematologic and solid ca

120 ly, the histone deacetylase (HDAC) inhibitor vorinostat has been demonstrated to induce HIV transcrip

121 Vorinostat has demonstrated significant anticancer activ

122 Further evaluation of vorinostat in AML/MDS is warranted.

123 ngs can explain, in part, the selectivity of vorinostat in causing cancer cell death at concentration

124 Additional testing of vorinostat in combination regimens is warranted.

125 o-controlled study evaluated the efficacy of vorinostat in combination with carboplatin and paclitaxe

126 uture clinical studies looking at the use of vorinostat in combination with conventional chemotherapy

127 Administration of vorinostat in combination with standard GVHD prophylaxis

128 The IL-8/CXCL8 expression induced by vorinostat in EOC cells is dependent on IkappaB kinase (

129 , significantly enhanced the cytotoxicity of vorinostat in leukemia cell lines and primary leukemia c

130 ion analysis performed in a phase 1 trial of vorinostat in leukemia indicated that overexpression of

131 TAT3, and STAT5 correlate with resistance to vorinostat in lymphoma cell lines.

132 ximum-tolerated dose and pharmacokinetics of vorinostat in patients with hepatic dysfunction.

133 uding depsipeptide and MGCD0103, differ from vorinostat in structure and isoenzyme specificity, and h

134 s and RNA expression profiling indicate that vorinostat in this dose and schedule affects target path

135 doxorubicin and the pan-HDAC inhibitor SAHA (vorinostat) in transformed cells (LNCaP, MCF-7), an effe

136 that the histone deacetylase inhibitor drug, vorinostat, in addition to its beneficial effects for pa

137 We aimed to study the safety and activity of vorinostat, in combination with standard immunoprophylax

138 s observed with the combination of 13cRA and vorinostat included thrombocytopenia, neutropenia, anore

139 In SW480 cells, sorafenib + vorinostat increased CD95 plasma membrane levels and pro

140 Vorinostat increased p53 expression and activated caspas

141 the small molecule HDAC inhibitors, ISOX and vorinostat, increased MBNL1 expression in DM1 patient-de

142 We demonstrate here that vorinostat increases the susceptibility of uninfected CD

143 HDACIs, such as vorinostat, induce caspase-dependent apoptosis in Rb cel

144 his study, we report that the HDAC inhibitor vorinostat induced p21 expression and decreased Bcl-xL l

145 CFZ/vorinostat induced pronounced lethality in 3 primary DLB

146 Vorinostat induced reactive oxygen species (ROS) through

147 Vorinostat induced the accumulation of acetylated histon

148 and -3, whereas caspase inhibition abrogated vorinostat-induced apoptosis.

149 Suppression or neutralization of vorinostat-induced IL-8/CXCL8 potentiates the vorinostat

150 Previously, we found that vorinostat induces DNA breaks in normal and transformed

151 Thus, the HDACi, vorinostat, induces DNA damage which normal but not canc

152 Furthermore, vorinostat inhibited STAT6 phosphorylation and decreased

153 orinostat-induced IL-8/CXCL8 potentiates the vorinostat inhibitory effect on cell viability and proli

154 Vorinostat inhibits STS tumour growth, an effect amelior

155 The targeted therapeutics sorafenib and vorinostat interact in a synergistic fashion to kill car

156 Vorinostat is a histone deacetylase inhibitor that chang

157 Vorinostat is a histone deacetylase inhibitor that induc

158 duction of cytosolic Ca(2+) by sorafenib and vorinostat is a primary event that elevates dihydroceram

159 Oral vorinostat is a promising agent in FL and MZL, with an a

160 Vorinostat is an inhibitor of histone deacetylases and w

161 Vorinostat is the first US Food and Drug Administration-

162 In children with recurrent solid tumors, vorinostat is well-tolerated at 230 mg/m(2)/d, with a mo

163 e oral histone deacetylase (HDAC) inhibitor (vorinostat) is safe and results in low incidence of acut

164 clinical trials, and one drug of this class, vorinostat, is US Food and Drug Administration approved

165 and combinations of vorinostat/erlotinib and vorinostat/lapatinib.

166 L-60/LR) cells that are resistant to LAQ824, vorinostat, LBH589, and sodium butyrate.

167 Thus, the HDACi vorinostat leads to both transcriptional and posttranscr

168 rbonyl)-aminomethyl]-benzamide (MS-275), and vorinostat led to differential increases in H3K4 methyla

169 ells, knockdown of CD95 enhanced sorafenib + vorinostat lethality, which correlated with less drug-in

170 JNK inhibition significantly diminished CFZ/vorinostat lethality.

171 -dependent manner (belinostat < givinostat < vorinostat < panobinostat < romidepsin) via degradation

172 ore DNA content, whereas coadministration of vorinostat markedly enhanced aurora kinase inhibition by

173 Finally, vorinostat markedly induced Bim expression, while blocka

174 We found that vorinostat markedly inhibited proliferation and induced

175 Pharmacokinetic analysis showed lower vorinostat maximum concentration and area under the curv

176 Our results suggest that vorinostat may have therapeutic potential for the treatm

177 ion with HIV, raising clinical concerns that vorinostat may reseed the viral reservoirs it is meant t

178 including the histone deacetylase inhibitor vorinostat, may sensitize tumors to chemotherapy and enh

179 is via cathepsin D accumulation and enhances vorinostat-mediated cell death in breast cancer models.

180 g a critical role for FasL in decitabine and vorinostat-mediated tumor suppression in vivo.

181 8(+) T cells are FasL(+), and decitabine and vorinostat-mediated tumor-suppression efficacy was signi

182 sion profiling and qRT-PCR demonstrated that vorinostat modulated the mRNA levels of genes important

183 CONCLUSION:Vorinostat monotherapy is well tolerated in patients wit

184 ), those who were treated with pazopanib and vorinostat (n = 11) had a significantly higher rate of c

185 id tumors who were treated with ixazomib and vorinostat (n = 59), those who were treated with pazopan

186 lled and randomly assigned to receive either vorinostat (n=329) or placebo (n=332) and included in th

187 trate that the histone deacetylase inhibitor vorinostat not only reprograms the aberrant gene express

188 cally approved histone deacetylase inhibitor vorinostat not only restored spatial memory, but also ex

189 enzamide) showed similar effects compared to vorinostat on inhibition of cellular HDACs in a pan-HDAC

190 t, givinostat, panobinostat, romidepsin, and vorinostat) on the productive infection of macrophages.

191 that suberoylanilide hydroxamic acid (SAHA; vorinostat), one of the histone deacetylase inhibitors d

192 Exposure to the pan-HDACIs vorinostat or LBH-589 induced phosphorylation of IKKalph

193 oparticle albumin-bound paclitaxel (CP) with vorinostat or placebo in women with stage II/III, human

194 Preoperative CP with vorinostat or placebo is associated with similar pCR rat

195 Vorinostat or placebo was given on days 1 through 14 of

196 block size of four to either treatment with vorinostat or placebo.

197 with a histone deacetylase (HDAC) inhibitor, vorinostat or romidepsin.

198 ally achievable concentrations of the HDACIs vorinostat or sodium valproate.

199 selectivity profile of 19i in comparison to vorinostat or trichostatin A (TSA).

200 Vorinostat or trichostatin A decreased MYC mRNA and prot

201 ithdrawn mice incubated with the HDACi SAHA (vorinostat) or trichostatin A (TSA) for 2 h, the hyposen

202 v azacitidine), and 27% for azacitidine plus vorinostat ( P = .16 v azacitidine).

203 CR rates were 74% vs 68% for EPOCH vs EPOCH-vorinostat (P = .72).

204 in PBMC was observed after administration of vorinostat, particularly at higher doses.

205 There were no significant differences in vorinostat pharmacokinetic parameters among the normal o

206 quire appropriate dose reduction even though vorinostat pharmacokinetics are unaltered.

207 obtained from CTCL patients enrolled in the vorinostat phase IIb trial showed that nuclear accumulat

208 Vorinostat plasma concentrations were quantitated by a v

209 lanilidehydroxamic acid (SAHA, also known as vorinostat) potently reactivates KSHV lytic replication

210 n of the class I and II HDAC inhibitor SAHA (vorinostat) preserved the antipsychotic profile of LY379

211 dine-based combinations with lenalidomide or vorinostat produce superior overall response rates (ORRs

212 rafenib and vorinostat together (sorafenib + vorinostat) promoted colocalization of CD95 with caspase

213 ity toward androgens and the anticancer drug vorinostat (R > 0.9, P < .001).

214 Addition of vorinostat reactivated proapoptotic genes and enhanced l

215 cell function, all the LRAs except the HDACi Vorinostat reduced, but did not abolish, one or more mea

216 Notably, the MK-0457/vorinostat regimen was highly active against primary CD3

217 No excess vorinostat-related toxicity was observed.

218 eregulation of STAT activity plays a role in vorinostat resistance in CTCL, and strategies that block

219 ses sensitivity to HDACIs and also overcomes vorinostat resistance.

220 Antioxidant gene expression may confer vorinostat resistance.

221 udy was to identify biomarkers predictive of vorinostat response in CTCL using preclinical model syst

222 rategies that block this pathway may improve vorinostat response.

223 h the histone deacetylase inhibitor (HDAC-I) vorinostat restored physiological levels of histone H3 a

224 a) and broad-spectrum HDAC inhibitors (e.g., Vorinostat, Romidepsin).

225 Vorinostat, romidepsin, belinostat, and panobinostat are

226 cells increases their sensitivity to HDACi (vorinostat, romidepsin, or entinostat) induced cell deat

227 limited response to the broad-spectrum HDACi Vorinostat (SAHA) in A549 cells, we find that combinatio

228 iferative activity with greater potency than vorinostat (SAHA), erlotinib, lapatinib, and combination

229 stone deacetylase (HDAC) inhibitors, such as vorinostat (SAHA), have shown promise as therapeutic age

230 suppression by histone deacetylase inhibitor vorinostat (SAHA).

231 acid, which is found in the anticancer drug vorinostat (SAHA).

232 latency disrupting compounds such as JQ1 or vorinostat/SAHA, the CARM1 inhibitor achieved synergisti

233 ga-position of the polyethylene chain of the vorinostat scaffold, allowed the selection of a new clas

234 bitor suberoylanilide hydroxamic acid (SAHA; vorinostat) show increases in unspliced cellular HIV-1 R

235 n in apoptosis sensitization, decitabine and vorinostat significantly increased the efficacy of CTL a

236 Here, we demonstrate that vorinostat significantly increases the susceptibility of

237 In addition, vorinostat significantly inhibited JAK2V617F-expressing

238 marginally lethal concentrations of HDACIs (vorinostat, SNDX-275, or SBHA) synergistically increased

239 The clinically approved HDAC inhibitor Vorinostat specifically increases HIF-2alpha, but not HI

240 show that sublethal doses of doxorubicin and vorinostat still increased cellular ceramide, which was

241 Together, these findings indicate that vorinostat strikingly increases MK-0457 activity against

242 se cells were treated with trichostatin A or vorinostat (suberoylanilide hydroxamic acid [SAHA]) to e

243 ent histone deacetylase inhibitors (HDACIs): vorinostat (suberoylanilide hydroxamic acid) and valproi

244 safety of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid) in persiste

245 Hydroxamic acid-based HDACIs such as vorinostat (suberoylanilide hydroxamic acid) induce the

246 Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a

247 safety of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid, SAHA) were

248 ive HDAC inhibitors trichostatin A (TSA) and vorinostat (suberoylanilide hydroxamic acid, SAHA), alth

249 Here, we show that the HDACi, vorinostat (Suberoylanilide hydroxamic acid, SAHA), indu

250 samples showed changes in genes regulated by vorinostat, such as upregulation of E-cadherin (P = .02)

251 Further, we found that vorinostat suppressed DNA DSB repair proteins, e.g., RAD

252 nd to characterize the pharmacokinetics of a vorinostat suspension in children.

253 Sorafenib and vorinostat synergized (sorafenib + vorinostat) to kill H

254 34 patients received vorinostat, tamoxifen and pembrolizumab with no excessiv

255 ecursor of the histone deacetylase inhibitor vorinostat that was efficiently uncaged by heterogeneous

256 r ART plus the histone deacetylase inhibitor vorinostat (the kick) and replication-deficient viral ve

257 The administration of LRAs (panobinostat or vorinostat) to HIV-1-infected individuals on antiretrovi

258 fenib and vorinostat synergized (sorafenib + vorinostat) to kill HCT116 and SW480 cells.

259 bitor pacritnib with the pan-HDAC inhibitor, vorinostat, to create bispecific single molecules with b

260 agged proteins, treatment with sorafenib and vorinostat together (sorafenib + vorinostat) promoted co

261 patient-matched to SW480 cells, sorafenib + vorinostat toxicity was significantly lower, which corre

262 e resultant doxorubicin-resistant (DoxR) and vorinostat-treated doxorubicin resistant (DoxR-v) cells

263 = .041; ST2, P = .002) at day 30 post-HCT in vorinostat-treated subjects compared with similarly trea

264 on of JAK2, Stat5, Stat3, Akt, and Erk1/2 in vorinostat-treated, JAK2V617F-expressing human erythrole

265 Sorafenib + vorinostat treatment activated the c-Jun NH(2)-terminal

266 ore potent against established lymphoma than vorinostat treatment alone.

267 Vorinostat treatment also decreased the mutant allele bu

268 and ART intensification are warranted during vorinostat treatment and indicate that HDAC inhibitors t

269 In HCT116 cells, sorafenib + vorinostat treatment caused DISC formation without reduc

270 Vorinostat treatment increased the frequency of function

271 More importantly, we observed that vorinostat treatment normalized the peripheral blood cou

272 Sorafenib and vorinostat treatment radiosensitized liver and pancreati

273 alysis performed in paired baseline and post-vorinostat treatment samples in a separate surgical subg

274 Further, sorafenib and vorinostat treatment suppressed the growth of pancreatic

275 ssion of SOCS1 and SOCS3 was up-regulated by vorinostat treatment.

276 drug application has been approved for SAHA (vorinostat) treatment of cutaneous T-cell lymphoma.

277 The confirmed response rate was 34% with vorinostat versus 12.5% with placebo (P = .02).

278 mbined impact of the latency reversing agent vorinostat (VOR) and AGS-004, an autologous dendritic ce

279 The histone deacetylase (HDAC) inhibitor vorinostat (VOR) can increase HIV RNA expression in vivo

280 the HDACi suberoylanilide hydroxamic acid or vorinostat (VOR) resulted in increases in HIV gag RNA an

281 le dose of the histone deacetylase inhibitor vorinostat (VOR) up-regulates HIV RNA expression within

282 The HDACi suberoylanilide hydroxamic acid (vorinostat [VOR]) has been employed in several clinical

283 beroylanilide hydroxamic acid (also known as vorinostat, VOR) can disrupt HIV-1 latency in vitro, the

284 Median overall survival for vorinostat was 30.7 weeks (95% CI 26.7-36.1) versus 27.1

285 Vorinostat was administered at a dose of 200 mg orally t

286 Oral vorinostat was administered at a dose of 200 mg twice da

287 Vorinostat was administered orally daily starting at 180

288 Oral vorinostat was effective in treatment refractory MF/SS w

289 The effect of vorinostat was recapitulated using the cytoplasmic histo

290 Vorinostat was safe and tolerable.

291 l mesothelioma treated in a phase 1 study of vorinostat, we designed this phase 3 trial to investigat

292 K-0457 and the histone deacetylase inhibitor vorinostat were examined in Bcr/Abl(+) leukemia cells, i

293 rse adverse events for patients treated with vorinostat were fatigue or malaise (51 [16%] patients in

294 levels increased with continued culture with vorinostat, whereas in normal cells, this marker decreas

295 While vorinostat will be given in the context of antiretrovira

296 dose reduction being required when combining vorinostat with 13cRA.

297 combining the histone deacetylase inhibitor vorinostat with a PI3K inhibitor led to enhanced FOXO-de

298 Furthermore, we show that a combination of vorinostat with alpha-galactosylceramide (alpha-GalCer),

299 The combination of vorinostat with idarubicin and cytarabine is safe and ac

300 cover suberoylanilide hydroxamic acid (SAHA; vorinostat (Zolinza)), which is a histone deacetylase in