ライフサイエンスコーパス: HDAC inhibitor

1 etylation, demonstrating that acetate was an HDAC inhibitor.

2 preclinical validation of a novel selective HDAC inhibitor.

3 entrations of JNJ-26481585, a broad-spectrum HDAC inhibitor.

4 e beneficial effect of the class I-selective HDAC inhibitor.

5 tment with CI-994, a brain-permeable class I HDAC inhibitor.

6 reviously cytotoxic properties attributed to HDAC inhibitors.

7 65P, conferred increased cell sensitivity to HDAC inhibitors.

8 influences the antiproliferative effects of HDAC inhibitors.

9 vide implications for the therapeutic use of HDAC inhibitors.

10 lly attenuated with either AR antagonists or HDAC inhibitors.

11 r monitoring the pharmacodynamic activity of HDAC inhibitors.

12 TAT3/IL-17 pathway as an important target of HDAC inhibitors.

13 ot require catalytic activity using specific HDAC inhibitors.

14 tivity and increased sensitivity to selected HDAC inhibitors.

15 3 proteins are decreased upon treatment with HDAC inhibitors.

16 artially rescued cellular sensitivity to the HDAC inhibitors.

17 econsideration of the mechanism of action of HDAC inhibitors.

18 rrogate indicator of cellular sensitivity to HDAC inhibitors.

19 r mechanism of action and therapeutic use of HDAC inhibitors.

20 from LNs and suggest caution with the use of HDAC inhibitors.

21 that may affect the therapeutic efficacy of HDAC inhibitors.

22 w molecules that are bispecific targeted JAK/HDAC inhibitors.

23 chain fatty acid (SCFA) histone deacetylase (HDAC) inhibitor.

24 d-acting drugs known as histone deacetylase (HDAC) inhibitors.

25 kinetics for a panel of histone deacetylase (HDAC) inhibitors.

26 on for design of potent histone deacetylase (HDAC) inhibitors.

27 odifying drugs, such as histone deacetylase (HDAC) inhibitors.

28 ir potent activities as histone deacetylase (HDAC) inhibitors.

29 A methyltransferase and histone deacetylase (HDAC) inhibitors.

30 ensitizes DIPG cells to histone deacetylase (HDAC) inhibitors.

31 he first small molecule histone deacetylase (HDAC) inhibitor (3, BRD73954) capable of potently and se

32 ation, and unlike many natural product based HDAC inhibitors, 4a was found to be nontoxic under in vi

33 o monitor cellular responses to the DNMT and HDAC inhibitors 5-Aza-2'-deoxycytidine and suberoylanili

34 t-term treatment of preleukemic mice with an HDAC inhibitor accelerated leukemogenesis.

35 HDAC inhibitor activity was detected by Western blotting

36 three oxazolinyl inhibitors evaluated; those HDAC inhibitors also lowered cyclin E expression in U937

37 Several other HDAC inhibitors also mimicked NaBu.

38 In mouse models, HDAC inhibitors also suppress oxidative stress, CCF, inf

39 The study reveals that a class I HDAC inhibitor alters the formation of auditory memory b

40 n levels increased upon treatment with a pan-HDAC inhibitor, an HDAC6-specific inhibitor, or depletio

41 ink between the global acetylation caused by HDAC inhibitor and gene promoter recruitment of CDK8 was

42 synergistic antitumor combination of PDI and HDAC inhibitors and demonstrates a mechanistic and tumor

43 tudies that go beyond the traditional use of HDAC inhibitors and have begun to dissect the roles of i

44 of IFN-lambda, revealing the combination of HDAC inhibitors and IFN-lambda to be a potential antitum

45 In an miR-22-dependent manner, HDAC inhibitors and RA reduced HDAC1, HDAC4, and sirtuin

46 Thus, HDAC inhibitors and RA-induced miR-22 resulted in simult

47 ve the way for the development of allosteric HDAC inhibitors and regulators to improve the therapy fo

48 cation, we tested known histone deacetylase (HDAC) inhibitors and a focused library of structurally s

49 Histone deacetylase (HDAC) inhibitors and DNA-damaging agents were identified

50 agents (LRAs), such as histone deacetylase (HDAC) inhibitors and protein kinase C (PKC) modulators,

51 ampal sphingosine-1-phosphate, an endogenous HDAC inhibitor, and reduced histone acetylation, and dis

52 ver, many of these classical agents are "pan-HDAC" inhibitors, and their use makes it difficult to de

53 cells were treated with histone-deacetylase (HDAC) inhibitors, and expression of Fam65b and interacti

54 a potent zinc-dependent histone deacetylase (HDAC) inhibitor appeared.

55 he first time, the present studies show that HDAC inhibitors are clearly beneficial for hypothyroidis

56 roles in fundamental cellular processes, and HDAC inhibitors are emerging as promising cancer therape

57 Histone deacetylase (HDAC) inhibitors are an important new class of therapeut

58 ltransferase (DNMT) and histone deacetylase (HDAC) inhibitors are currently in use and under developm

59 Histone deacetylase (HDAC) inhibitors are effective in killing pancreatic can

60 IFICANCE STATEMENT Some histone deacetylase (HDAC) inhibitors are known to have neuroprotective and c

61 In addition, histone deacetylase complex (HDAC) inhibitors are known to reverse BRM silencing, but

62 Broad-spectrum histone deacetylase (HDAC) inhibitors are useful in the treatment of allergic

63 ene expression, such as histone deacetylase (HDAC) inhibitors, are among the new agents being used in

64 igenetic drugs, such as histone deacetylase (HDAC) inhibitors, are finding their way into clinical pr

65 guiding the development of isoform specific HDAC inhibitors as effective therapeutics.

66 ation in irinotecan resistance and establish HDAC inhibitors as potential therapeutic means to overco

67 munoprecipitation, small interfering RNA and HDAC inhibitor assays.

68 ity of malignancies of hematologic origin to HDAC inhibitor-based therapy.

69 Histone deacetylase (HDAC) inhibitors blocked GRP78 release by inducing its a

70 t trichostatin A, a pan-histone deacetylase (HDAC) inhibitor, blocked all high glucose-induced effect

71 ux and carbon-tracing analyses revealed that HDAC inhibitors blunted glycolysis in a c-Myc-dependent

72 results demonstrate that glucocorticoids and HDAC inhibitors, both of which are currently in clinical

73 t with three additional histone deacetylase (HDAC) inhibitors, but not other antipsychotics, chemical

74 of the DNMT inhibitor 5-azacytidine and the HDAC inhibitor butyrate markedly reduced CSC abundance a

75 designed and synthesized as novel dual PI3K/HDAC inhibitors by incorporating an HDAC pharmacophore i

76 These findings indicate that HDAC inhibitors can elicit transgenerational effects, vi

77 However, it is not yet known whether HDAC inhibitors can modulate age-related epigenetic chan

78 ncreasing evidence that histone deacetylase (HDAC) inhibitors can (re)sensitize cancer cells for chem

79 arental, CRC cells with histone deacetylase (HDAC) inhibitors can effectively overcome resistance.

80 shown that nonselective histone deacetylase (HDAC) inhibitors can protect the retina from ischemic in

81 a strong rationale for using the proteasome/HDAC inhibitor combination therapy in PEL.

82 Additionally, some reported HDAC inhibitors contain hydroxamate moiety that chelates

83 of MYD88 exhibited increased sensitivity to HDAC inhibitors; conversely, low expression coincided wi

84 treatment of patients with class I-specific HDAC inhibitors could induce latent viruses without incr

85 identified Panobinostat, an FDA approved pan-HDAC inhibitor, could elevate and restore SOX7 expressio

86 ity, highly competitive with the most potent HDAC inhibitors, currently under clinical trials.

87 re-induction of HLA class-I by interferons, HDAC inhibitors did not interfere with the expression of

88 ACs, thus contributing to the selectivity of HDAC inhibitors discovered in this study.

89 ort that treatment with histone deacetylase (HDAC) inhibitors downregulates renal CLDN14 mRNA and dra

90 n (e.g., Dacogen, Vidaza) and broad-spectrum HDAC inhibitors (e.g., Vorinostat, Romidepsin).

91 or entinostat (a clinically relevant class-I HDAC inhibitor) efficiently promoted apoptosis in colore

92 Importantly, HDAC inhibitors elevate receptor expression and restore

93 selective (romidepsin) histone deacetylase (HDAC) inhibitors elicited metabolic reprogramming in con

94 ndings reveal that sialic acid analogues and HDAC inhibitors enhance GD2 expression and could potenti

95 with a class I- but not a class II-selective HDAC inhibitor enhanced oxidative metabolism in skeletal

96 Both HDAC4 knockdown and HDAC inhibitor enhanced radiation-induced cell death and

97 HC toxin, another HDAC inhibitor, enhances beta-cell function in primary m

98 id (VPA) and enhanced by the narrow-spectrum HDAC inhibitor entinostat.

99 small-molecule Class 1 histone deacetylase (HDAC) inhibitor Entinostat (MS-275) enhances GLP-1R agon

100 While pharmacological doses of HDAC inhibitors exert positive effects on Bdnf gene tran

101 d HDAC-targeting drugs are nonselective, pan-HDAC inhibitors, exhibiting adverse side effects at ther

102 r treatment, as shown by the approval of two HDAC inhibitors for the treatment of cutaneous T-cell ly

103 Off-label use of VPA and other HDAC inhibitors for the treatment of RP should be limite

104 However, MC1568 (class II HDAC inhibitor) had no discernible effect.

105 ently, the development and implementation of HDAC inhibitors has proven to be therapeutically benefic

106 HDAC inhibitors have been reported to produce antidepres

107 Since then, five HDAC inhibitors have received regulatory approval for ca

108 However, while studies of VOR or other HDAC inhibitors have reported reversal of latency, none

109 Because current pan-HDAC inhibitors have shown disappointing results in clin

110 Histone deacetylase (HDAC) inhibitors have been associated primarily with an

111 Small molecule histone deacetylase (HDAC) inhibitors have been shown to suppress cardiac hyp

112 Histone deacetylase (HDAC) inhibitors have been used to promote neuronal surv

113 Histone deacetylase (HDAC) inhibitors have proven useful therapeutic agents f

114 Neither a VDR agonist (VDA) nor an HDAC inhibitor (HDACI) nor a demethylating agent (DAC) i

115 ed autophagosomes in rod inner segments with HDAC inhibitor (HDACi) treatment, potentially linking th

116 Mice were treated with class I and IIb HDAC inhibitor (HDACi) via drinking water for 2 and 4 we

117 therefore support the further assessment of HDAC inhibitors (HDACi's) in FRDA and diseases caused by

118 HDAC inhibitors (HDACi) are widely used in the clinic to

119 ublications have demonstrated that selective HDAC inhibitors (HDACi) can influence tumor immunogenici

120 HDAC inhibitors (HDACi) employing different zinc chelati

121 this report, we demonstrate the efficacy of HDAC inhibitors (HDACi) in vivo We show that daily admin

122 HDAC inhibitors (HDACi) increase transcription of some g

123 NAD(+), and the influence of small molecule HDAC inhibitors (HDACi) on cancer cell resistance to gen

124 CD48 messenger RNA, and that treatment with HDAC inhibitors (HDACi) restores the expression of CD48.

125 HDAC inhibitors (HDACi) suppress inflammatory activation

126 e also demonstrate that clinically available HDAC inhibitors (HDACi) targeting HDAC1 and HDAC7 can be

127 GABA sensitivity of pDAergic VTA neurons by HDAC inhibitors (HDACi), and also measured the levels of

128 nhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic

129 further the depth of the SAR of 3HPT-derived HDAC inhibitors (HDACi), we have extended the SAR studie

130 mesangial cells treated with class-specific HDAC inhibitors (HDACi).

131 Histone deacetylase (HDAC) inhibitors (HDACi) are clinically approved antican

132 evidence has shown that histone deacetylase (HDAC) inhibitors (HDACi) can have significant benefit in

133 HDAC inhibitors (HDACIs) are currently being explored as

134 echanisms underlying AUD and the efficacy of HDAC inhibitors (HDACIs) in different animal models of A

135 cal assessment indicated that treatment with HDAC inhibitors (HDACis) may be effective in t(8;21) AML

136 We examine HDAC inhibitors (HDACis) targeting class I, II, and IV H

137 TSC2(+/-) mice that is also normalized with HDAC inhibitors (HDACis).

138 Histone deacetylase (HDAC) inhibitors (HDACis) have been widely tested in cli

139 Histone deacetylase (HDAC) inhibitors (HDACis) have demonstrated activity in

140 et al demonstrate that histone deacetylase (HDAC) inhibitors (HDACis) in glucose-6-phosphate dehydro

141 Histone deacetylase (HDAC) inhibitors (HDACis) reactivate latent KSHV and dra

142 duced histone acetylation and sensitivity to HDAC inhibitors (HDIs) (Figure 4A-B).

143 Histone deacetylase (HDAC) inhibitors (HDIs) are promising anticancer therapi

144 Compound 4j, the most potent HDAC inhibitor in the cellular HDAC assay, revealed rema

145 69 genome was not induced in the presence of HDAC inhibitors in either KG-1 or Kasumi-3 cells.

146 reasing numbers of clinical trials involving HDAC inhibitors in human cancers, our observations stron

147 evidence for an anti-inflammatory potency of HDAC inhibitors in models of experimental colitis.

148 sts there may be a therapeutic potential for HDAC inhibitors in this disease.

149 We examined the role of histone deacetylase (HDAC) inhibitors in regulating sGCalpha1 and -beta1 expr

150 KSHV was reactivated by all SCFAs that are HDAC inhibitors, including phenylbutyrate.

151 retinoic acid (RA) and histone deacetylase (HDAC) inhibitors, including short-chain fatty acids and

152 c combined with various histone deacetylase (HDAC) inhibitors, including vorinostat, enhanced GD2 exp

153 ed as corepressors of YY1, and, accordingly, HDAC inhibitors increased EAAT2 promoter activity and re

154 The class I HDAC inhibitors increased the expression of sGCbeta1 mor

155 transcription factor involved in regulating HDAC inhibitor-induced AQP3 expression.

156 reased transcriptional activity, as shown by HDAC inhibitor-induced chromatin relaxation and observed

157 Surprisingly, hypoxia preferentially blocks HDAC inhibitor-induced differentiation of the BRCA1-reco

158 the use of a loop diuretic in mice abrogated HDAC inhibitor-induced hypocalciuria.

159 e more sensitive to the histone deacetylase (HDAC) inhibitor-induced loss of stemness than the BRCA1-

160 Valproic acid (VPA), another SCFA and an HDAC inhibitor, induces the lytic cycle of KSHV but bloc

161 ry of isozyme-selective histone deacetylase (HDAC) inhibitors is critical for understanding the biolo

162 ontinued improvement of histone deacetylase (HDAC) inhibitors is finding alternative motifs equipoten

163 nt of isoform-selective histone deacetylase (HDAC) inhibitors is important in elucidating the functio

164 a unique and unexplored histone deacetylase (HDAC) inhibitor, is reported.

165 of two hits revealed that the small molecule HDAC inhibitors, ISOX and vorinostat, increased MBNL1 ex

166 des have provided potent and class-selective HDAC inhibitors, it will be challenging to distinguish b

167 he goal of developing a second generation of HDAC inhibitors lacking this hydroxamate, we designed a

168 e highly potent class I histone deacetylase (HDAC) inhibitor largazole cooperated to induce E-cadheri

169 synthesis of a focused histone deacetylase (HDAC) inhibitor library with peptoid-based cap groups an

170 cific memory promoting properties of class I HDAC inhibitors may depend on isoform selectivity and th

171 l cell transdifferentiation, suggesting that HDAC inhibitors may enhance repair by promoting acquisit

172 r results suggest that hydroxamic acid-based HDAC inhibitors may mediate neuroprotection via HDAC-ind

173 These results suggest that class I HDAC inhibitors may provide a pharmacologic approach to

174 Histone deacetylase (HDAC) inhibitors may have therapeutic utility in multipl

175 the class IIa selective histone deacetylase (HDAC) inhibitor MC1568 are described.

176 However, use of more specific HDAC inhibitors might limit the toxicities caused by HDA

177 ells, Trichostatin A, a histone deacetylase (HDAC) inhibitor, mimics juvenile hormone (JH) in inducin

178 phenotypic changes seen with broad spectrum HDAC inhibitors, most notably a block in the differentia

179 (RX) (24 h), the neuroprotection of Class I HDAC inhibitor MS-275 was counteracted, whereas in neuro

180 le of ATRA with a 2-aminoanilide tail of the HDAC inhibitor MS-275, yielding MC2392.

181 rate group of rats, the histone deacetylase (HDAC) inhibitor, MS275, was delivered to the renal medul

182 investigating combination therapy including HDAC inhibitors, no HDAC drug or combination therapy wit

183 By acting as HDAC inhibitors, not as energy substrates or through GPR

184 previously unknown cytoplasmic mechanism of HDAC inhibitors on HIV replication that is distinct from

185 his study explores the regulatory potency of HDAC inhibitors on T cell polarization as a mechanistic

186 , a selective class IIa histone deacetylase (HDAC) inhibitor, on the development and progression of r

187 nd an ectopic xenograft were pretreated with HDAC inhibitor or short hairpin RNA to knock down expres

188 Majors rarely forage, but injection of a HDAC inhibitor or small interfering RNAs against the HDA

189 ifically, we showed that HDAC1 inhibition by HDAC inhibitors or by siRNA shortened the half-life of T

190 Treatment of HCC cells with HDAC inhibitors or knockdown of HDAC1 and/or HDAC2 resto

191 dies showed that either histone deacetylase (HDAC) inhibitors or tumor necrosis factor-related apopto

192 195 or TMP269, which are selective class IIa HDAC inhibitors, or shRNA-mediated knockdown of HDAC5 bu

193 d the selection of a new class of potent pan-HDAC inhibitors (pan-HDACis).

194 found that the CDK inhibitor dinaciclib and HDAC inhibitor panobinostat were the most potent inducer

195 ate GAS5-AS1 in NSCLC cells, whereas the pan-HDAC inhibitors panobinostat and SAHA significantly indu

196 ases sensitivity to the histone deacetylase (HDAC) inhibitor panobinostat.

197 ydroxyamic acid-derived histone deacetylase (HDAC) inhibitors Panobinostat and Vorinostat also enhanc

198 DAC4 silencing and the administration of the HDAC inhibitor parthenolide during obstructive cholestas

199 HDAC inhibitors, particularly vorinostat, are currently

200 The precise molecular mechanisms whereby HDAC inhibitors prevent neuronal death are currently the

201 All of the HDAC inhibitors prevented degradation of BNC, in which T

202 usion criteria included previous exposure to HDAC inhibitors; previous allogeneic stem-cell transplan

203 gain by elimination of histone deacetylase (HDAC) inhibitor-producing microbes, which are anti-infla

204 l a previously unknown cytoplasmic effect of HDAC inhibitors promoting productive infection of CD4(+)

205 A novel class IIa-selective HDAC inhibitor reduced recombinant human HDAC7 enzyme ac

206 -induced plasticity, and previous studies of HDAC inhibitors report conflicting effects on cocaine-el

207 As memory enhancement by HDAC inhibitors requires CREB-CBP interaction and Nr4a g

208 R-9 and miR-374 genes, and treatment with an HDAC inhibitor rescued the phenotypes of cell and animal

209 Systemic administration of an HDAC inhibitor rescues the detrimental effects of ELS wh

210 Importantly, we show that low-dose HDAC inhibitors restore expression of most nuclear-encod

211 In line with these results, HDAC inhibitors restore in part C/EBPalpha target gene e

212 ent with 109, a class I histone deacetylase (HDAC) inhibitor, resulted in increased level of FXN tran

213 Treatment with HDAC inhibitor results in an increase in TAF9 acetylatio

214 We used a class I HDAC inhibitor, RGFP966 (C21H19FN4O), to test the role o

215 s of Xyzidepsin, a depsipeptidic analogue of HDAC inhibitor Romidepsin (FK228), using a solid-phase s

216 tralized effects of the histone deacetylase (HDAC) inhibitor romidepsin.

217 tly, co-administration of the class I and II HDAC inhibitor SAHA (vorinostat) preserved the antipsych

218 Importantly, we show that treatment with the HDAC inhibitor SAHA restores sensitivity to prednisolone

219 treating cells with the histone deacetylase (HDAC) inhibitor SAHA led to detectable clusters of DNA-P

220 The histone deacetylase (HDAC) inhibitor SAHA synergizes with JQ1 to augment cell

221 folds to mimic the niche for 5-days with the HDAC inhibitor Scriptaid and cytokines.

222 Many of the new HDAC inhibitors showed higher solubilities and lower bin

223 HDAC4 knockdown with or without an HDAC inhibitor significantly delayed tumor growth in a r

224 itor, and mocetinostat (MGCD0103), a class I HDAC inhibitor, significantly enhanced Npr1 promoter act

225 Strikingly, coadministration of the HDAC inhibitor sodium butyrate with PNFlx prevented the

226 Treatment with histone deacetylase (HDAC) inhibitor sodium butyrate (NaBu) induced PKCdelta

227 etinoic acid (ATRA) and histone deacetylase (HDAC) inhibitor, sodium butyrate (NaBu) to examine the e

228 Furthermore, treatment of mice with HDAC inhibitors stimulated the transcription of renal mi

229 rent study, we sought to study the effect of HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) on

230 ease in BDNF mRNA induced by the class I/IIb HDAC inhibitor suberoylanilide hydroxamic acid (SAHA).

231 The broad-spectrum HDAC inhibitor suberoylanilide hydroxamic acid induced A

232 is study, we found that histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) i

233 Histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA),

234 ID/DeltaID) mice with a histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxyamic acid (SAHA)

235 ination of Btz with the histone deacetylase (HDAC) inhibitor suberoylanilidehydroxamic acid (SAHA, al

236 Despite the abundant presence of HDAC inhibitors such as butyrate in the intestine, we fo

237 uggests a combination approach where class I HDAC inhibitors such as valproic acid or MS-275 (entinos

238 However, several fatty acid HDAC inhibitors, such as isobutyrate and phenylbutyrate,

239 the antidepressant-like properties of other HDAC inhibitors, such as SAHA and MS-275, in the tail su

240 Histone deacetylase (HDAC) inhibitors, such as vorinostat (SAHA), have shown

241 Here we found that histone deacetylase (HDAC) inhibitors suppress both wild-type and mutant p53

242 nosis of HCC and restored FBP1 expression by HDAC inhibitors suppresses HCC growth.

243 HDAC inhibitors synergize with BPTF knockdown against HG

244 Significantly, these isoform-targeted HDAC inhibitors synergize with PKC modulators, namely br

245 Hdac3 is a key target for Hdac inhibitors that are efficacious in cutaneous T cell

246 Selective HDAC inhibitors that bind to the 14 A cavity have also b

247 ogical brain states may be more receptive to HDAC inhibitors that improve network function by enhanci

248 uring vorinostat treatment and indicate that HDAC inhibitors that selectively target nuclear class I

249 syntheses of a class of cyclic tetrapeptide HDAC inhibitors, the azumamides, by a concise route in w

250 HDAC inhibition, and DIPG cells resistant to HDAC inhibitor therapy retain sensitivity to CDK7 blocka

251 try aimed at identifying a new generation of HDAC inhibitors, through the introduction of a thiol zin

252 gical inhibition of HDAC9 with the class IIa HDAC inhibitor TMP195 attenuates lesion formation by red

253 ass selective class IIa histone deacetylase (HDAC) inhibitor, TMP195, influenced human monocyte respo

254 Cs in HIV latency, and recent efforts to use HDAC inhibitors to reactivate latent HIV in vitro and in

255 lation about the use of histone deacetylase (HDAC) inhibitors to treat skin diseases led us to invest

256 tubule perfusion techniques, we showed that HDAC inhibitors transiently increase the paracellular ca

257 Furthermore, HDAC inhibitor treatment increased mRNA expression of th

258 ged to the genes most strongly responding to HDAC inhibitor treatment of neuroblastoma cells in a gen

259 Mechanistically, HDAC inhibitor treatment suppressed HDAC6 activity and l

260 P53 gene and that MYC recruitment drops upon HDAC inhibitor treatment.

261 ous betaOHB and class I histone deacetylase (HDAC) inhibitor treatment.

262 Notably, the HDAC inhibitor trichostatin A had no effect on MeCP2-med

263 cardiac sarcomeres and that a class I and II HDAC inhibitor, trichostatin A, enhances contractile act

264 ells, consistent with effects elicited by an HDAC inhibitor, trichostatin A.

265 nd panobinostat (LBH589), two broad-spectrum HDAC inhibitors up-regulate hsa-miR-31 (miR-31).

266 ned a series of potent and selective class I HDAC inhibitors using a hydrazide motif.

267 ensitive to many ASD risk factors, including HDAC inhibitor valproic acid and a variety of endocrine

268 lls is inhibited by the histone deacetylase (HDAC) inhibitor valproic acid (VPA) and enhanced by the

269 hibitor hydralazine and histone deacetylase (HDAC) inhibitor valproic acid (VPA) will reverse this in

270 and in combination with histone deacetylase (HDAC) inhibitors valproic acid and vorinostat.

271 nized with the class III histone deactylase (HDAC) inhibitor vitamin B3 (nicotinamide) which activate

272 JAK1/2 inhibitor, have been merged with the HDAC inhibitor vorinostat (2), leading to new molecules

273 The clinically approved HDAC inhibitor Vorinostat specifically increases HIF-2al

274 tency than the BET inhibitor (+)-JQ1 and the HDAC inhibitor vorinostat, either alone or and in combin

275 eted by RNA interference or inhibited by the HDAC inhibitor vorinostat.

276 The histone deacetylase (HDAC) inhibitor vorinostat (VOR) can increase HIV RNA ex

277 The histone deacetylase (HDAC) inhibitor vorinostat disrupts EBV/HHV-8 latency, e

278 Recently, the histone deacetylase (HDAC) inhibitor vorinostat has been demonstrated to indu

279 The oral histone deacetylase (HDAC) inhibitor (vorinostat) is safe and results in low

280 e JAK2/FLT3 inhibitor pacritnib with the pan-HDAC inhibitor, vorinostat, to create bispecific single

281 d in combination with a histone deacetylase (HDAC) inhibitor, vorinostat or romidepsin.

282 pression patterns to elucidate the effect of HDAC inhibitors VPA and entinostat (MS-275) on behaviora

283 in cells treated with a histone deacetylase (HDAC) inhibitor was accompanied by increased histone ace

284 m-selective (CAY10398, Romidepsin, PCI34051) HDAC inhibitors were evaluated ex vivo (IPAH-PAAF, IPAH-

285 azoline-1-oxyl-3-oxide or trichostatin A (an HDAC inhibitor) were quantified, thereby identifying gen

286 inhibitors may increase the effectiveness of HDAC inhibitors when treating ovarian cancer and other s

287 IPAH-PAAFs was augmented by HDAC8 siRNA and HDAC inhibitors, which also attenuated IPAH-associated h

288 se 3 (Hdac3) is a target of the FDA approved HDAC inhibitors, which are used for the treatment of lym

289 dies indicated that 12 functions as a potent HDAC inhibitor with an IC50 value of 0.1 muM.

290 the first HDAC6 degrader by tethering a pan-HDAC inhibitor with cereblon (CRBN) E3 ubiquitin ligase

291 e synthesis of a series of class I-selective HDAC inhibitors with 2-aminoanilides as zinc-binding gro

292 l evaluation of new potent hydroxamate-based HDAC inhibitors with a novel alkoxyamide connecting unit

293 Use of HDAC inhibitors with different specificities limited our

294 -hydroxypyrrolidine cap for the synthesis of HDAC inhibitors with good potency.

295 A goal shared by many is to develop HDAC inhibitors with increased isoform selectivity in or

296 wever, the underling mechanisms of combining HDAC inhibitors with TRAIL in the treatment of breast ca

297 While known HDAC inhibitors with varied inhibitory profiles proved t

298 terrogated the biological effects of class I HDAC inhibitors with varying selectivity and assessed a

299 , hydroxamic-containing histone deacetylase (HDAC) inhibitor with broad anti-inflammatory properties,

300 inhibitors with VPA or histone deacetylase (HDAC) inhibitors with lithium synergistically increased