ライフサイエンスコーパス: hydroxamic acid

1 nducers tunicamycin or SAHA (suberoylanilide hydroxamic acid).

2 stone deacetylase inhibitor, suberoylanilide hydroxamic acid.

3 inhibitors trichostatin A or suberoylanilide hydroxamic acid.

4 ipotent to the classic and ubiquitously used hydroxamic acid.

5 f the naturally occurring iron(III) chelator hydroxamic acid.

6 e that is more active than the corresponding hydroxamic acid.

7 tone deacetylase inhibitor, suberolylanilide hydroxamic acid.

8 antibacterial LpxC inhibitors represented by hydroxamic acid.

9 and can be applied to aliphatic and aromatic hydroxamic acids.

10 identified as the main metabolic enzymes for hydroxamic acids.

11 y inhibited by 1:1 complexes of vanadate and hydroxamic acids.

12 of their transformation to the corresponding hydroxamic acids.

13 he synthesis of 2-substituted N-alkylmalonyl hydroxamic acids.

14 her esters of heterocyclic hydroxylamines or hydroxamic acids.

15 centrations of 1:1 complexes of vanadate and hydroxamic acids.

16 also proceeds with N-hydroxysulfonamides and hydroxamic acids.

17 or effective intermolecular alkenylations of hydroxamic acids.

18 proceeds in metal complexes of deprotonated hydroxamic acids.

19 sulting in variable NDA yields (13-51%) from hydroxamic acids 1-10 with cyclohexa-1,3-diene and 2,3-d

20 to afford predominantly monocyclic anti-1,2-hydroxamic acids 12.

21 itors (11c,c') relative to the corresponding hydroxamic acids (16a,a').

22 The hydroxamic acid (2) and amino (6) analogues did not inhi

23 to afford predominantly monocyclic anti-1,4-hydroxamic acids 3.

24 eocontrolled synthesis of substituted cyclic hydroxamic acids (3-amino-1-hydroxy-3,4-dihydroquinolino

25 and does so without the intermediacy of the hydroxamic acid, 3, and with 18O exchange from the solve

26 ucleophiles to give functionalized protected hydroxamic acids, 3, in good to excellent yields.

27 tivity of the ring opening to afford syn-1,4-hydroxamic acids 4.

28 We found that mycophenolic hydroxamic acid (9, MAHA) inhibits both IMPDH (Ki=30 nM)

29 te that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of histone deacetyla

30 ith the exception of the recently discovered hydroxamic acids, all bioisosteric attempts to replace t

31 by using trichostatin A and suberoylanilide hydroxamic acid alone or in combination with the tyrosin

32 acetylase inhibitors such as suberoylanilide hydroxamic acid (also known as vorinostat, VOR) can disr

33 le to or better than that of suberoylanilide hydroxamic acid, an inhibitor of histone deacetylase cur

34 t studies show that LBH589, a novel cinnamic hydroxamic acid analog histone deacetylase inhibitor, in

35 Hydroxamic acid analog pan-histone deacetylase (HDAC) in

36 (Novartis Pharmaceutical, Inc.), a cinnamyl hydroxamic acid analogue inhibitor of histone deacetylas

37 DA cycloadducts were not obtained from other hydroxamic acid analogues [RCONHOH (R = PhCH2 4; Ph(CH2)

38 preliminary iron(III) binding study of these hydroxamic acid analogues is presented, demonstrating bi

39 hibitors: amide analogues of trichostatin A, hydroxamic acid analogues of trapoxin, and scriptaid and

40 ivity relationship (SAR) studies on cinnamic hydroxamic acid and benzo[b]thiophen-2-hydroxamic acid g

41 of four heterocyclic/spacer moieties, and a hydroxamic acid and evaluated the LpxC inhibition of the

42 with the pan-HDAC inhibitor, suberoylanilide hydroxamic acid and HDAC3 siRNA resulted in increased mi

43 acetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824.

44 coupling them with Zn(2+)-chelating motifs (hydroxamic acid and o-phenylenediamine) through aromatic

45 mplications for the study of suberoylanilide hydroxamic acid and other HDAC inhibitors in the prevent

46 With the exception of suberoyl anilide hydroxamic acid and PXD101, all of the other HDAC inhibi

47 tone deacetylase inhibitors, suberoylanilide hydroxamic acid and trichostatin A, fit into the catalyt

48 tic modifiers 5-azacytidine and suberoyl bis-hydroxamic acid and under conditions where individual ge

49 f the enzyme complex with 4-nitrobenzo[(13)C]hydroxamic acid and vanadate yields a coordination-induc

50 erent zinc chelating functionalities such as hydroxamic acids and benzamides have shown promising res

51 distinct clusters of dissimilar activity for hydroxamic acids and orthoamino anilides.

52 ve broad implications for future research on hydroxamic acids and polyhalogenated quinoid carcinogens

53 o assess and control the plasma stability of hydroxamic acids and realize their full potential as in

54 bitors (HDACIs): vorinostat (suberoylanilide hydroxamic acid) and valproic acid (VPA).

55 as bortezomib, depsipeptide, suberoylanilide hydroxamic acid, and a host of other compounds, though a

56 AC activity, trichostatin A, suberoylanilide hydroxamic acid, and apicidin, induced acetylation of H3

57 e chemical HDACis PCI-24781, suberoylanilide hydroxamic acid, and MS-275 on a panel of human NF1-asso

58 inhibitors (trichostatin A, suberoylanilide hydroxamic acid, and sodium butyrate) prevent induction

59 by butyrate, trichostatin A, suberoylanilide hydroxamic acid, and STAT1 small interfering RNA.

60 inhibitors (trichostatin A, suberoylanilide hydroxamic acid, and tributyrin).

61 o primary, secondary, tertiary, and aromatic hydroxamic acids, and the acidity of the protons adjacen

62 Hydroxamic acids are an important class of chelators of

63 Hydroxamic acids are outstanding zinc chelating groups t

64 demonstrate that meta substituents of phenyl hydroxamic acids are readily accommodated upon binding t

65 Although hydroxamic acids are utilized universally in the develop

66 1' using an anti-succinate-based macrocyclic hydroxamic acid as a template led to the identification

67 The design involves: incorporation of hydroxamic acid as the bidentate chelating agent for cat

68 Small molecules bearing hydroxamic acid as the zinc binding group (ZBG) have bee

69 of azaindole carboxylic acids and azaindole hydroxamic acids as potent inhibitors of the HIV-1 IN en

70 ement is demonstrated with other hydrophobic hydroxamic acids, as well as with additional thioether s

71 f this enzyme are oxazolines incorporating a hydroxamic acid at the 4-position, which is believed to

72 ter hydrolysis to generate the corresponding hydroxamic acids at pH <2, while the more reactive 2c an

73 Release is blocked by either the hydroxamic acid based inhibitor, KD-IX-73-4 or by 1,10-p

74 Hydroxamic acid based small molecules have proven to be

75 Here, we report hydroxamic acid-based and benzoic acid-based inhibitors

76 We also demonstrated that synthetic hydroxamic acid-based compounds efficiently inhibited th

77 Our results suggest that hydroxamic acid-based HDAC inhibitors may mediate neurop

78 ic acid (SAHA), the prototype of a series of hydroxamic acid-based HDAC inhibitors, in cell lines and

79 Hydroxamic acid-based HDACIs such as vorinostat (suberoy

80 Hydroxamic acid-based histone deacetylase inhibitors lim

81 The results suggest that hydroxamic acid-based hybrid polar compounds inhibit pro

82 d to the synthesis of a unique cyclopentenyl hydroxamic acid-based inhibitor of 5-lipoxygenase.

83 gn, synthesis, and evaluation of a series of hydroxamic acid-based inhibitors and demonstrate the com

84 acterization, and biological activity of new hydroxamic acid-based inhibitors with nanomolar affinity

85 sAPPalpha release was blocked by the hydroxamic acid-based metalloprotease inhibitor Ro31-979

86 Because hydroxamic acid-based metalloprotease inhibitors prevent

87 Here, we show that a hydroxamic acid-based small-molecule N-hydroxy-4-(2-[(2-

88 Classical HDACi such as the hydroxamic acid-based vorinostat (also known as SAHA and

89 Weak acids, such as hydroxamic acids, bind in their neutral form and then tr

90 le, thiazolidine-2,4-dione, methyldinitrile, hydroxamic acid, boronic acid, 2-oxoaldehyde, and ethyl

91 finity of the HDAC inhibitor suberoylanilide hydroxamic acid by 5-fold.

92 he initiation pathway involves activation of hydroxamic acid by nitriles and subsequent Lossen rearra

93 on conditions and readily revert back to the hydroxamic acid by treatment with Nafion-H in 2-propanol

94 Hydroxamic acids can be incorporated into dye molecules

95 Cyclic hydroxamic acids can undergo a thermal ring contraction

96 ge of metal binding groups (MBGs), including hydroxamic acid, carboxylate, hydroxypyridinonate, thiol

97 s was efficiently promoted by a tungsten/bis(hydroxamic acid) catalytic system, furnishing various an

98 on mechanism for the Lossen rearrangement of hydroxamic acids catalyzed by basic salts is presented.

99 histone deacetylase inhibitors derived from hydroxamic acid, caused a dramatic decrease (90%) in pro

100 ition of LpxC by a novel N-aroyl-l-threonine hydroxamic acid (CHIR-090) from a recent patent applicat

101 These results indicate that the hydroxamic acid class of HDAC inhibitors activates SMN2

102 to establish whether the potent and specific hydroxamic acid class of histone deacetylase (HDAC) inhi

103 The N-heterocyclic carbene and hydroxamic acid cocatalyzed kinetic resolution of cyclic

104 the low formation constants of the vanadate-hydroxamic acid complex.

105 complexed with a sulfonamide derivative of a hydroxamic acid compound (WAY-151693) has been determine

106 dative amidation has been used to synthesize hydroxamic acid-containing bicyclic beta-lactam cores.

107 A number of non-hydroxamic acid-containing compounds that showed a high

108 ndicate that the protective effects of these hydroxamic acid-containing small molecules are likely un

109 ally restrained HDAC inhibitors based on the hydroxamic acid dacinostat (LAQ824, 7).

110 LBH589 is a novel hydroxamic acid derivative that at low nanomolar concent

111 Here we show that NVP-LAQ824, a novel hydroxamic acid derivative, induces apoptosis at physiol

112 u generation of nitrosocarbonyl species from hydroxamic acid derivatives.

113 nhibitors (trichostatin A or suberoylanilide hydroxamic acid), despite induction of global histone ac

114 of pyridine N-oxide substrates in O-pivaloyl hydroxamic acid-directed Rh(III)-catalyzed (4+2) annulat

115 Some hydroxamic acids display a high plasma clearance resulti

116 comparison, the hydroxamate suberoylanilide hydroxamic acid does not discriminate between these enzy

117 ionalized through diazonium chemistry with a hydroxamic acid end group that both renders the SWCNTs w

118 lase inhibitors butyrate and suberoylanilide hydroxamic acid, followed by culture in MEK/ERK and GSK3

119 and a focused library of structurally simple hydroxamic acids for inhibition of a HCV subgenomic repl

120 Required hydroxamic acids for the Lossen rearrangements were synt

121 Both aryl and alkyl hydroxamic acids form inhibitory ternary complexes with

122 l ligands, which incorporate sulfonamide and hydroxamic acid fragments.

123 tructure-activity studies indicated that the hydroxamic acid functional group was essential to this i

124 The metal-coordinating, N-substituted hydroxamic acid functional groups exist in solution as a

125 pon coordination of a ditopic linker bearing hydroxamic acid functional groups.

126 namic hydroxamic acid and benzo[b]thiophen-2-hydroxamic acid gave rise to compounds 22 and 53, which

127 Indeed, treatment with suberoylanilide hydroxamic acid greatly reduced the expression of the in

128 guanadinium group of Arg38, and between the hydroxamic acid group and the indole nitrogen of Trp41.

129 e, thiophosphoglycolohydroxamate, contains a hydroxamic acid group linked to a thiophosphate moiety.

130 smidomycin with a reverse orientation of the hydroxamic acid group were synthesized and evaluated for

131 Exochelin MN has two hydroxamic acid groups and an unusual threo-beta-hydroxy

132 o modulate the metal chelating properties of hydroxamic acid groups by bioorthogonal chemistry using

133 The hydroxamic acid (HAA) analogue pan-histone deacetylase (

134 istone deacetylase inhibitor suberoylanilide hydroxamic acid has strikingly distinct targets compared

135 h achiral N-heterocyclic carbenes and chiral hydroxamic acids has emerged as a promising method to ob

136 rovide guidance for the design of novel, non-hydroxamic acid HDAC inhibitors.

137 Importantly, use of a selective linkerless hydroxamic acid HDAC8 inhibitor increases Hsp20 acetylat

138 on of miRNA levels in response to the potent hydroxamic acid HDACi LAQ824 in the breast cancer cell l

139 h is coordinated to the zinc ion through the hydroxamic acid hydroxyl and carbonyl oxygen atoms.

140 istone deacetylase inhibitor suberoylanilide hydroxamic acid in induction of the hypermethylated gene

141 e expression and response to suberoylanilide hydroxamic acid in levels of antiapoptotic and proapopto

142 The protonation state of hydroxamic acids in the active site and the origin of th

143 for dehydrative alkyne annulation by NH-free hydroxamic acids in water.

144 tylase inhibitor vorinostat (suberoylanilide hydroxamic acid) in persistent, progressive, or recurren

145 hibitors, valproic acid, and suberoylanilide hydroxamic acid, in models of pulmonary arterial hyperte

146 micromolar concentrations of suberoylanilide hydroxamic acid induce the expression of 15-lipoxygenase

147 d HDACIs such as vorinostat (suberoylanilide hydroxamic acid) induce the differentiation and apoptosi

148 road-spectrum HDAC inhibitor suberoylanilide hydroxamic acid induced AQP3 mRNA and protein expression

149 -1 significantly reduced the suberoylanilide hydroxamic acid-induced effects.

150 poxygenase-1 correlates with suberoylanilide hydroxamic acid-induced increase in 13-S-hydroxyoctadeca

151 Both valproic acid and suberoylanilide hydroxamic acid inhibited the imprinted highly prolifera

152 Because suberoylanilide hydroxamic acid is already approved to treat cutaneous T

153 Because of its low toxicity, suberoylanilide hydroxamic acid is currently in clinical trials for the

154 A versatile new method for O-arylation of hydroxamic acids is also reported herein, as well as a m

155 One such agent, suberoylanilide hydroxamic acid, is a potent inhibitor of HDACs that cau

156 CHIR-090, a novel N-aroyl-l-threonine hydroxamic acid, is a potent, slow, tight-binding inhibi

157 Combining b-AP15 with suberoylanilide hydroxamic acid, lenalidomide, or dexamethasone induces

158 ynthesis, and biological evaluation of novel hydroxamic acid LpxC inhibitors, exemplified by 1, where

159 ms by which HDAC inhibitors (suberoylanilide hydroxamic acid, m-carboxycinnamic acid bis-hydroxamide,

160 cell lines could be similarly inhibited by a hydroxamic acid, metalloprotease inhibitor compound.

161 indings were observed in mice treated with a hydroxamic acid MMP inhibitor from 3 hr to 3 d after inj

162 The pK(a) values for the two hydroxamic acid moieties, the histidine imidazole ring a

163 about the pharmacokinetic liabilities of the hydroxamic acid moiety have stimulated research efforts

164 The hydroxamic acid moiety of the inhibitor binds to the zin

165 The hydroxamic acid moiety was introduced via the reaction o

166 bstituted cyclopentenes while regenerating a hydroxamic acid moiety, thus enhancing the chemical vers

167 mpounds, BRD9715 and BRD8461, which lack the hydroxamic acid motif and showed that they stably penetr

168 chelators containing alpha,beta-unsaturated hydroxamic acid motifs appended to a citric acid platfor

169 inhibitors (trichostatin A, suberoylanilide hydroxamic acid, MS-275, and OSU-HDAC42) led to increase

170 Four HDAI (depsipeptide, suberoylanilide hydroxamic acid, MS-275, and trichostatin A) were studie

171 ine derivatives, including N-hydroxy amides (hydroxamic acids), N-hydroxy sulfonamides, and N-hydroxy

172 nt classes of key starting materials such as hydroxamic acids, N-hydroxy carbamates, N-hydroxyureas,

173 cetylase inhibitors, such as suberoylanilide hydroxamic acid, not only inhibit deacetylase activity b

174 ation of Akt/p300 pathway by suberoylanilide hydroxamic acid occurs at the chromatin level, resulting

175 Hydroxamic acids of structure RCON(OH)CH(2)CH(CH(2)C(6)H

176 and sodium butyrate (NaB) or suberoylanilide hydroxamic acid on the day of, the day before, or the da

177 minal carboxylate of DmTR was converted to a hydroxamic acid or a thiocarboxylate.

178 HDAC inhibition using suberoylanilide hydroxamic acid or MS-275 significantly increased MCSFR

179 equent exposure to the HDACi suberoylanilide hydroxamic acid or vorinostat (VOR) resulted in increase

180 g treatment with bortezomib, suberoylanilide hydroxamic acid, or the combination, showing tumor selec

181 y acids (sodium butyrate and valproic acid); hydroxamic acids (oxamflatin, Scriptaid, suberoyl anilid

182 2 is suitably placed to hydrogen bond to the hydroxamic acid oxygen atom.

183 ids (oxamflatin, Scriptaid, suberoyl anilide hydroxamic acid, panobinostat [LBH589], and belinostat [

184 etylase (HDAC) inhibitors such as the phenyl hydroxamic acid PCI-24781 have emerged recently as a cla

185 In acid dissociation these residues yield hydroxamic acid pK(a) values that vary from 7.6 to 10.3.

186 s via a novel concerted pathway in which the hydroxamic acid plays a key role in directing proton tra

187 In our study, the statin hydroxamic acids prepared by a fused strategy are most p

188 Para-substituted phenyl-hydroxamic acids presented a more potent inhibition of H

189 utyrate, trichostatin A, and suberoylanilide hydroxamic acid, prevented IFNgamma-induced JAK1 activat

190 The use of the chiral hydroxamic acid, (R)-1-hydroxy-3-(1-phenylethylurea) 3 (

191 O-Methyl hydroxamic acids, readily available from carboxylic acid

192 istone deacetylase inhibitor suberoylanilide hydroxamic acid, restored miR-200a expression and reduce

193 nhibitors, valproic acid and suberoylanilide hydroxamic acid, restored the expression of RELN and DAB

194 lly approved HDAC inhibitor (suberoylanilide hydroxamic acid) reverses the dysregulation of the major

195 cals derived from the common class of cyclic hydroxamic acid root exudates directly affect the chroma

196 n A (CyA) with the pan-HDACi suberoylanilide hydroxamic acid (SAHA) and a novel HDAC6-specific inhibi

197 ting agents are derived from suberoylanilide hydroxamic acid (SAHA) and anthracycline daunorubicin, p

198 action of 2 HDAC inhibitors, suberoylanilide hydroxamic acid (SAHA) and ITF 2357, on mouse DC respons

199 tudy we found that the HDACi suberoylanilide hydroxamic acid (SAHA) and MS-275, a benzamide, cause an

200 tivity to the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) and PARP inhibitor olaparib, and

201 two HDAC inhibitors, namely suberoylanilide hydroxamic acid (SAHA) and romidepsin, have been recentl

202 cetylase (HDAC) inhibitors suberanoylanilide hydroxamic acid (SAHA) and sodium butyrate (SB) and the

203 cetylase inhibitors (HDACIs) suberoylanilide hydroxamic acid (SAHA) and sodium butyrate (SB) and the

204 C3T3 cells were treated with suberoylanilide hydroxamic acid (SAHA) and subjected to microarray gene

205 finity of the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) and the Michaelis constant, with

206 se (HDAC) inhibitors such as suberoylanilide hydroxamic acid (SAHA) are known to induce apoptosis of

207 deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) corrected the VLCFA derangement b

208 nib mesylate and 2.0 micro M suberoylanilide hydroxamic acid (SAHA) for 24 h, exposures that were min

209 Suberoylanilide hydroxamic acid (SAHA) has been approved as a drug to tr

210 s) sodium butyrate (NaB) and suberoylanilide hydroxamic acid (SAHA) have been examined in human leuke

211 deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) increased AQP5 expression and Sp1

212 Suberoylanilide hydroxamic acid (SAHA) is a histone deacetylase inhibito

213 Suberoylanilide hydroxamic acid (SAHA) is a potent inhibitor of histone

214 Suberoylanilide hydroxamic acid (SAHA) is an HDAC inhibitor which is in

215 deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) is being evaluated for imatinib-r

216 Suberoylanilide hydroxamic acid (SAHA) is currently in clinical trials a

217 istone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) is currently in clinical trials.

218 nonical broad-spectrum HDACi suberoylanilide hydroxamic acid (SAHA) is described.

219 The HDACi suberoylanilide hydroxamic acid (SAHA) is in phase I/II clinical trials

220 Suberoylanilide hydroxamic acid (SAHA) is the first HDAC inhibitor to be

221 Suberoylanilide hydroxamic acid (SAHA) is the prototype of a family of h

222 deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) led to a dramatic induction of RI

223 istone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) only after DNMT-1 dissociation fr

224 tions of bortezomib + either suberoylanilide hydroxamic acid (SAHA) or sodium butyrate (SB) resulted

225 as trichostatin A (TSA) and suberonylanilide hydroxamic acid (SAHA) permits the study of the role of

226 sses of HDAC inhibitors, and suberoylanilide hydroxamic acid (SAHA) reactivated EBV in HH514-16 cells

227 s study, we demonstrate that suberoylanilide hydroxamic acid (SAHA) reactivates HIV from latency in c

228 hat inhibition of STAT6 with suberoylanilide hydroxamic acid (SAHA) restores protease expression and

229 e (NaB), valproate (VPA) and suberoylanilide hydroxamic acid (SAHA) were tested for their ability to

230 xy-N(1)-phenyloctanediamide (suberoylanilide hydroxamic acid (SAHA)), providing the product in 79.8%

231 ary screening, we identified suberoylanilide hydroxamic acid (SAHA), a Food and Drug Administration-a

232 e tested the hypothesis that suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor

233 amplified when combined with suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor.

234 study, we determined whether suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor:

235 , it is also noteworthy that suberoylanilide hydroxamic acid (SAHA), a polar compound that was initia

236 Suberoylanilide hydroxamic acid (SAHA), a potent differentiation agent a

237 deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA), acting in part through HDAC7 sil

238 Suberoylanilide hydroxamic acid (SAHA), an orally administered inhibitor

239 thylene bisacetamide (HMBA), suberoylanilide hydroxamic acid (SAHA), and other histone deacetylase in

240 ing of trichostatin A (TSA), suberoylanilide hydroxamic acid (SAHA), and two other SAHA derivatives t

241 f the general HDAC inhibitor suberoylanilide hydroxamic acid (SAHA), as well as benzophenone and alky

242 onstrate that prostratin and suberoylanilide hydroxamic acid (SAHA), but not hexamethylene bisacetami

243 bitor, OSU-HDAC42, vis-a-vis suberoylanilide hydroxamic acid (SAHA), in in vitro and in vivo models o

244 DAC inhibitors, butyrate and suberoylanilide hydroxamic acid (SAHA), induced caspase-3 activation and

245 One of the HDAC inhibitors, suberoylanilide hydroxamic acid (SAHA), is currently being used for trea

246 stration of sodium butyrate, suberoylanilide hydroxamic acid (SAHA), or trichostatin with perifosine

247 hat HDAC inhibitors, such as suberoylanilide hydroxamic acid (SAHA), potently induce apoptosis of hum

248 eacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA), restored Ogg1 expression in cell

249 of HDAC inhibitors, such as suberoylanilide hydroxamic acid (SAHA), that were initially identified b

250 characterized the effect of suberoylanilide hydroxamic acid (SAHA), the prototype of a series of hyd

251 caffolds of enzalutamide and suberoylanilide hydroxamic acid (SAHA), with weakened intrinsic pan-HDAC

252 drugs-namely, prostratin and suberoylanilide hydroxamic acid (SAHA)-overcomes the limitations of sing

253 tin (TSA, 1), MS-275 (2) and suberoylanilide hydroxamic acid (SAHA, 3) arrest growth in transformed c

254 The path to the discovery of suberoylanilide hydroxamic acid (SAHA, vorinostat) began over three deca

255 tidine [5azaD]), followed by suberoylanilide hydroxamic acid (SAHA; 5azaD/SAHA), or trichostatin A (5

256 path that led us to discover suberoylanilide hydroxamic acid (SAHA; vorinostat (Zolinza)), which is a

257 istone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA; vorinostat) show increases in uns

258 We showed that suberoylanilide hydroxamic acid (SAHA; vorinostat), one of the histone d

259 richostatin A or vorinostat (suberoylanilide hydroxamic acid [SAHA]) to evaluate the activation of p2

260 Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deacetylase inhibito

261 tylase inhibitor vorinostat (suberoylanilide hydroxamic acid, SAHA) were evaluated in patients with r

262 atin A (TSA) and vorinostat (suberoylanilide hydroxamic acid, SAHA), although largazole upregulated e

263 that the HDACi, vorinostat (Suberoylanilide hydroxamic acid, SAHA), induces DNA double-strand breaks

264 e deactetylase (HDAC) inhibitor suberoyl bis-hydroxamic acid (SBHA) was employed to determine whether

265 xpected to be competitive with aggrecan, the hydroxamic acid, SC81956, demonstrated noncompetitive in

266 l-amidine and HDAC inhibitor suberoylanilide hydroxamic acid show additive effects in inducing p21, G

267 Several 4-fluorobenzyl substituted azaindole hydroxamic acids showed potent antiviral activities in c

268 istone deacetylase inhibitor suberoylanilide hydroxamic acid significantly decreased colitis activity

269 utant proteins, we find that suberoylanilide hydroxamic acid stimulates Akt activity, which is requir

270 ere we provide evidence that suberoylanilide hydroxamic acid stimulates NF-kappaB transcription throu

271 tors valproic acid (VPA) and suberoylanilide hydroxamic acid than SW620 or HT-29 cells (both expressi

272 A new strategy for the preparation of hydroxamic acids that uses readily available N-benzyloxy

273 eacetylase inhibitor, NVP-LAQ824, a cinnamic hydroxamic acid, that inhibited in vitro enzymatic activ

274 adenine ring joined to a metal-coordinating hydroxamic acid through flexible acyclic linkers.

275 The direct conversion of a hydroxamic acid to an amine has been accomplished in a s

276 a manganese(III)-mediated alpha-oxidation of hydroxamic acids to aminals.

277 We designed a 57-member library of hydroxamic acids to explore the structure-plasma stabili

278 deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid) to animals reared in a standard cage mi

279 gulated by valproic acid and suberoylanilide hydroxamic acid treatment.

280 Trichostatin A and suberoylanilide hydroxamic acid, two broad spectrum HDAC inhibitors, blo

281 Trichostatin A and suberoylanilide hydroxamic acid, two structurally related inhibitors of

282 tease activity of ADAM19 is sensitive to the hydroxamic acid-type metalloprotease inhibitor BB94 (bat

283 e ring system joined to a metal-coordinating hydroxamic acid via various linkers.

284 stone deacetylase inhibitor, suberoylanilide hydroxamic acid (vorinostat), a new anticancer drug.

285 class I HDAC inhibitor, and suberoylanilide hydroxamic acid (vorinostat), an inhibitor of class I, I

286 ing a promoiety, sensitive to thiols, to the hydroxamic acid warhead (termed SAHA-TAP).

287 hibitors (HDACIs) MS-275 and suberoylanilide hydroxamic acid was associated with hyperacetylation and

288 xposure to valproic acid and suberoylanilide hydroxamic acid was associated with increased levels of

289 structure, linked by an aliphatic chain to a hydroxamic acid, was designed and synthesized.

290 Enolization of O-methyl hydroxamic acids (Weinreb amides) in tetrahydrofuran sol

291 Hydroxamic acids were designed, synthesized, and evaluat

292 Some of the synthesized hydroxamic acids were found to be potent MMP inhibitors

293 hods developed with N-(benzoyloxy)amines and hydroxamic acids were used in the synthesis of N-(hydrox

294 ing phospho-Akt, followed by suberoylanilide hydroxamic acid, whereas MS-275 shows only a marginal ef

295 Oxazolines incorporating a hydroxamic acid, which is believed to coordinate to the

296 When cells were treated with suberoylanilide hydroxamic acid, which releases P-TEFb from the 7SK smal

297 cally stable anchors, such as silatranes and hydroxamic acids, which are oxidation resistant and stab

298 st currently studied HDAC inhibitors contain hydroxamic acids, which are potentially problematic in t

299 istone deacetylase inhibitor suberoylanilide hydroxamic acid, WIF1 promoter activity increased signif

300 of nitrosocarbonyl precursors, N-substituted hydroxamic acids with pyrazolone leaving groups (NHPY),