ライフサイエンスコーパス: mesylate

1 n=269 3-day intravenous and oral casopitant mesylate).

2 ay select for resistant clones (ie, imatinib mesylate).

3 the tyrosine kinase inhibitor (TKI) imatinib mesylate.

4 drugs: paclitaxel, ixabepilone, and eribulin mesylate.

5 ogically targeted therapies such as imatinib mesylate.

6 the tyrosine kinase inhibitor (TKI) imatinib mesylate.

7 s targeted by the antifibrotic drug imatinib mesylate.

8 ion loop mutants are insensitive to imatinib mesylate.

9 ants resistant to the Kit inhibitor imatinib-mesylate.

10 ces targeting of CML progenitors by imatinib mesylate.

11 assessing the response of GISTs to imatinib mesylate.

12 hibited by the Abl kinase inhibitor imatinib mesylate.

13 tant mutants were also resistant to imatinib mesylate.

14 predicting a favorable response to imatinib mesylate.

15 s from a clinical trial of adjuvant imatinib mesylate.

16 e products of both are inhibited by imatinib mesylate.

17 (95% CI, -0.90 to 0.26 hour) for rasagiline mesylate 1 mg/d.

18 r 10 mg twice daily), placebo, or rasagiline mesylate (1 mg/d) in a 1:1:1:1:1 ratio.

19 The Bcr-Abl kinase inhibitor imatinib mesylate (1 microM) and two Jak2 kinase inhibitors stron

20 re randomly assigned 1:1 to receive eribulin mesylate (1.4 mg/m(2) intravenously on days 1 and 8) or

21 anthracycline and a taxane received eribulin mesylate (1.4 mg/m(2)) as a 2- to 5-minute intravenous (

22 itochondria-targeted antioxidant mitoquinone mesylate {[10-(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cycl

23 rent mutations were identified with imatinib mesylate, 10 with nilotinib (including only 1 novel muta

24 dria-targeted antioxidant MitoQ (mitoquinone mesylate: [10-(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cycl

25 a panel of probe molecules [dexamethasone 21-mesylate, 15-deoxy-Delta-((12,14))-prostaglandin J(2), 2

26 cebo (n=269), single oral dose of casopitant mesylate (150 mg oral, n=271), or 3-day intravenous plus

27 clic substrate, that is, cyclopropylcarbinyl mesylate (19); in contrast, 11 reacted only three times

28 Imatinib mesylate, 1a, inhibits production of beta-amyloid (Abeta

29 tudies (1 administering dabigatran etexilate mesylate, 2 administering rivaroxaban, and 3 administeri

30 tion of the silyl carbamate derived from Boc mesylate 27 to produce the key cyclic carbamate 28.

31 domly assigned (1:1) to receive deferoxamine mesylate (32 mg/kg per day) or placebo (saline) infusion

32 hesized by the cyclization of 1-thioacetyl-3-mesylate (4/38) under basic conditions.

33 and tolerability of an oral dose of imatinib mesylate 400 mg twice daily in patients with recurrent o

34 Imatinib mesylate, 400 mg orally twice daily.

35 ), or 3-day intravenous plus oral casopitant mesylate (90 mg intravenous on day 1 plus 50 mg oral on

36 g the peptide to Desferal (desferrioxamine B mesylate), a chelator in therapeutic use, increased the

37 s in turn led to the development of imatinib mesylate, a clinically successful inhibitor of the BCR-A

38 Eribulin mesylate, a novel microtubule-targeting analogue of the

39 Ts can be successfully treated with imatinib mesylate, a selective small-molecule protein kinase inhi

40 ntrast, treatment of cells with methiothepin mesylate, a serotonin antagonist, enhanced infection by

41 gum, fluids), dexamethasone, and dolasetron mesylate, a serotonin receptor antagonist.

42 Imatinib mesylate, a small-molecule inhibitor against several rec

43 eting these activated proteins with imatinib mesylate, a small-molecule kinase inhibitor, has proven

44 this tumor, and the development of imatinib mesylate, a specific inhibitor of KIT tyrosine kinase fu

45 Imatinib mesylate, a tyrosine kinase inhibitor, has revolutionize

46 ition of BCR-ABL kinase activity by imatinib mesylate abrogates such activation.

47 myeloid leukemia (CML) treated with imatinib mesylate achieve a complete cytogenetic response (CCR),

48 y 85% of GIST patients treated with imatinib mesylate achieve disease stabilization, however, often i

49 so found evidence that long-term mitoquinone mesylate administration did not reduce mitochondrial rea

50 long-term mitochondria-targeted mitoquinone mesylate administration failed to attenuate age-related

51 ncogene and a favorable response to imatinib mesylate [also known as STI571 (Gleevec)] therapy.

52 e have been published on the use of Apatinib Mesylate (AM) against EGFR-TKI resistance in lung adenoc

53 Ten (7%) participants in the deferoxamine mesylate and 11 (7%) in the placebo group died.

54 enetic response rates were 87% with imatinib mesylate and 28% with interferon-alpha (P < .001).

55 only 2.6 times faster than endo-2-norbornyl mesylate and 9.4 times faster in CF3CH2OH.

56 receptor tyrosine kinase inhibitor imatinib mesylate and a monoclonal antibody against PDGF receptor

57 o other serine protease inhibitors (camostat mesylate and aprotinin), affords protection against neut

58 The kinase inhibitors imatinib mesylate and dasatinib are the preferred treatment for P

59 he resistance to inhibitors such as imatinib mesylate and malignant progression of the disease.

60 Imatinib mesylate and new TKIs along with allogeneic stem cell tr

61 e tyrosine kinase inhibitors (TKIs) imatinib mesylate and nilotinib represents a successful applicati

62 chronic myeloid leukemia (CML) with imatinib mesylate and other second- and/or third-generation c-Abl

63 Imatinib mesylate and other tyrosine kinase inhibitors (TKIs) tha

64 Emergence of imatinib mesylate and other, second-generation tyrosine kinase in

65 In silico profiling of Imatinib mesylate and PD-173955 kinase inhibitors with protein ty

66 for TGFbeta-induced EndoMT and that imatinib mesylate and rottlerin or similar kinase inhibitor molec

67 The inhibitory effects of imatinib mesylate and rottlerin were mediated by inhibition of ph

68 Deferoxamine mesylate and starch-deferoxamine (1 mM) prevented bafilo

69 The efficacy of the inhibitors imatinib mesylate and sunitinib malate in GIST patients has been

70 es, alkynes, aldehydes, alkyl halides, alkyl mesylates and disulfides.

71 with high selectivity toward triflates over mesylates and proved to be compatible with sensitive fun

72 ntylglycolboronates with aryl and heteroaryl mesylates and sulfamates containing both electron-donati

73 ntylglycolboronates with aryl and heteroaryl mesylates and sulfamates in THF at room temperature.

74 With the exception of mesylates and sulfamates the efficiency of all other 2-n

75 ed electron-rich and electron-deficient aryl mesylates and tosylates.

76 second slope of -0.0057 +/- 0.0038 (imatinib mesylate) and -0.0019 +/- 0.0013 (nilotinib) per day rep

77 he first slope of -0.052 +/- 0.018 (imatinib mesylate) and -0.042 +/- 0.015 (nilotinib) per day repre

78 e involving an efficient cleavage of an aryl mesylate, and an efficient and practical method of intro

79 ifferential sensitivity to the drug imatinib mesylate, and differential self-renewal capacity.

80 ment with specific c-Abl inhibitor, imatinib mesylate, and knock down of c-Abl significantly decrease

81 ng reactions with the two C-O electrophiles, mesylates, and sulfamates was compared.

82 lectron-poor, and heterocyclic tosylates and mesylates, and the reaction shows wide functional group

83 enzylic or allylic chlorides, tosylates, and mesylates are possible.

84 This catalyst system enables the use of aryl mesylates as a coupling partner in C-N bond-forming reac

85 Electronically varied aryl tosylates and mesylates, as well as benzyl acetates, afford the arylat

86 tients were treated with daily oral imatinib mesylate at 220 mg/m(2) twice a day for children and 400

87 ease and NSF were treated with oral imatinib mesylate at a dosage of 400 mg/day.

88 th newly diagnosed CML treated with imatinib mesylate at our institution (2000-2004) to 650 patients

89 that pretreatment of CML cells with imatinib mesylate augments the antigrowth effects of IFNalpha.

90 Imatinib mesylate blocked activation of the Smad1 pathway in tran

91 A potent tryptase inhibitor, nafamostat mesylate, blocked DENV-induced vascular leakage in vivo.

92 B431542 and by the c-Abl inhibitor, imatinib mesylate, but not by the p38 map kinase inhibitor, SB203

93 s formed by intramolecular displacement of a mesylate by the deprotected amine.

94 achieved by nucleophilic displacement of the mesylates by the radioactive fluoride ion with 31% incor

95 rial to test whether treatment with imatinib mesylate can decrease the volume burden of clinically si

96 We have therefore examined whether imatinib mesylate can delay relapse and postpone the requirement

97 Resistance to imatinib mesylate can occur in chronic myelogenous leukemia (CML)

98 tor everolimus and PDGFRA inhibitor imatinib mesylate confirmed that this drug combination can impact

99 Imatinib mesylate could be used to treat plexiform neurofibromas

100 The mesylate derivative of the (S) enantiomer (1c) is conver

101 those of three metal chelators; deferoxamine mesylate (DFO), 1,10-phenanthroline (o-phen) and 1,2-Bis

102 the nose-to-brain transport of deferoxamine mesylate (DFO), a neuroprotector unable to cross the blo

103 n of PP-IX or the iron chelator deferoxamine mesylate (DFO), with the first committed heme precursor

104 PC12 with the iron chelator, desferrioxamine mesylate (DFO, 50 microM for 24 h), significantly decrea

105 ibrated against the marketed desferrioxamine mesylate (DFOM) siderophore and applied with experiments

106 ttacks can be treated with dihydroergotamine mesylate (DHE), an ergot derivative that is especially e

107 l), and c-Abl inhibitors, including imatinib mesylate, diminishing the fibrogenic effects of TGF-beta

108 Eribulin mesylate (E7389), a nontaxane microtubule dynamics inhib

109 Eribulin mesylate (E7389), a synthetic analogue of the marine nat

110 the Kit tyrosine kinase inhibitor, imanitib mesylate, eliminated or reduced action potentials and Ca

111 ression or Abl kinase activity with imatinib mesylate enhanced HNSCC matrix degradation and 3D collag

112 Moreover, imatinib mesylate enhanced rat cardiac allograft vasculopathy, ca

113 f the hydroxybenzocycloalkanonyl acetate and mesylate esters (7a-d, 8a-c) has provided new insight in

114 itochondria-targeted antioxidant mitoquinone mesylate fails to attenuate age-related oxidative damage

115 one for those patients able to take imatinib mesylate for 6 months.

116 Of the 23 patients who received imatinib mesylate for at least 6 months, six (26%, 95% CI 10-48)

117 d in the patient who resumed taking imatinib mesylate for longer than 2 weeks.

118 valuable functionalities like triflates and mesylates for follow-up reactions as well as the compari

119 nt the first examples of using tosylate- and mesylate-functionalized arenes as the electrophile partn

120 tions with respective release of acetone and mesylate furnished the corresponding unsaturated alcohol

121 he Smad1/CCN2 pathway is blocked by imatinib mesylate further clarifies the mechanism of the antifibr

122 Imatinib mesylate (Gleevec) is effective therapy against Philadel

123 Although the ABL kinase inhibitor imatinib mesylate (Gleevec) provides highly effective treatment f

124 the small molecule kinase inhibitor imatinib mesylate (Gleevec), complete remissions are rare and the

125 eated with the targeted therapeutic imatinib mesylate (Gleevec).

126 neutralizing antibody to PDGF or by imatinib mesylate (Gleevec).

127 T) can be successfully treated with imatinib mesylate (Gleevec); however, complete remissions are rar

128 e and the antileukemia drug STI571 [imatinib mesylate (Gleevec); Novartis], which potently and select

129 the Kit tyrosine kinase inhibitor, imatinib mesylate (Gleevec, formerly STI-571), has caught the att

130 Imatinib mesylate (Gleevec, STI571), a selective inhibitor of a r

131 n the 3-day intravenous plus oral casopitant mesylate group (p=0.0004 vs control]).

132 228 [86%] in the single-dose oral casopitant mesylate group [p<0.0001 vs control], and 214 [80%] in t

133 of 144 patients assigned to the deferoxamine mesylate group and 147 assigned to the placebo group.

134 patients in the single-dose oral casopitant mesylate group and 203 (75%) patients in the 3-day intra

135 in the 3-day intravenous and oral casopitant mesylate group compared with 194 (73%) of patients in th

136 n the 3-day intravenous plus oral casopitant mesylate group), and dehydration (n=4 [2%] in the contro

137 n the 3-day intravenous plus oral casopitant mesylate group), febrile neutropenia (n=1 [<1%] in the c

138 n the 3-day intravenous plus oral casopitant mesylate group).

139 34%) of 140 participants in the deferoxamine mesylate group, and 47 (33%) of 143 patients in the plac

140 39 (27%) of 144 patients in the deferoxamine mesylate group, and 78 serious adverse events were repor

141 n=2 [<1%] in the single-dose oral casopitant mesylate group, and n=1 [<1%] in the 3-day intravenous p

142 n=3 [1%] in the single-dose oral casopitant mesylate group, and n=11 [4%] in the 3-day intravenous p

143 n=4 [1%] in the single-dose oral casopitant mesylate group, and n=6 [2%] in the 3-day intravenous pl

144 ed with the selective Abl inhibitor imatinib mesylate had a reduced capability to migrate into breast

145 Obatoclax mesylate has biologic activity and modest single-agent a

146 achieve similar disease control as imatinib mesylate has produced in chronic myeloid leukemia.

147 dazo[1,2-a]pyridines with aryl tosylates and mesylates has been accomplished by employing palladium(I

148 Kit/Pdgfra inhibitors such as imatinib mesylate have increased progression-free survival in met

149 Inhibitors of Bcr-abl such as imatinib mesylate have replaced the cytokine IFNalpha as the prim

150 The radical cation formed by mesylate heterolysis from the 1,1-dimethyl-7,7-diphenyl-

151 is, and seminoma are insensitive to imatinib mesylate (IC50 > 5-10 micromol/L), and acquired KIT acti

152 eukemia (CML) patients treated with imatinib mesylate (IM) become drug resistant by mutations within

153 Imatinib mesylate (IM) blocks the CSF-1 receptor.

154 myeloid leukemia were treated with imatinib mesylate (IM) for 6 to 12 months to establish disease co

155 AMN107 was more potent than imatinib mesylate (IM) in inhibiting Bcr-Abl tyrosine kinase (TK)

156 Previous studies demonstrated that imatinib mesylate (IM) induces autophagy in chronic myeloid leuke

157 Imatinib mesylate (IM) is effective at inducing complete cytogene

158 Imatinib mesylate (IM) therapy for chronic myeloid leukemia (CML)

159 osedly contribute to the failure of imatinib mesylate (IM) to eradicate chronic myeloid leukemia (CML

160 ll survival and self-renewal during imatinib mesylate (IM) treatment.

161 nd nuclear import were increased by imatinib mesylate (IM), a selective ABL inhibitor, but prevented

162 cells, including those resistant to imatinib mesylate (IM), particularly those with the T315I mutatio

163 Despite excellent responses to imatinib mesylate (IM), patients are relapsing.

164 CML stem cells (CMLSCs) to the drug imatinib mesylate (IM).

165 /Abl(+) leukemia cells resistant to imatinib mesylate (IM).

166 press BcrAbl and are insensitive to imatinib mesylate (IM).

167 play a major role in resistance to imatinib mesylate (IM).

168 Imatinib mesylate (IM, Gleevec) has largely supplanted allogeneic

169 se (ABL1) kinase inhibitors such as imatinib mesylate (imatinib) are effective in managing chronic my

170 Imatinib mesylate (imatinib) is a tyrosine kinase inhibitor devel

171 Imatinib mesylate (imatinib) is highly effective in the treatment

172 Adjuvant therapy with imatinib mesylate improves recurrence-free survival rates and may

173 o evaluate the tryptase inhibitor nafamostat mesylate in a mouse model for severe DENV viremia.

174 lysis of 1-(trimethylsilylmethyl)cyclopropyl mesylate in CD(3)CO(2)D gives ring-opened products as we

175 tiapoptotic BCL-2 family inhibitor obatoclax mesylate in diagnostic leukemia cells from 54 infants wi

176 t of a randomized phase II trial of imatinib mesylate in patients with incurable GIST detailed high r

177 the safety of the iron chelator deferoxamine mesylate in patients with intracerebral haemorrhage and

178 se 2 study demonstrated efficacy of imatinib mesylate in patients with metastatic GIST harboring a KI

179 e BRAF inhibitors vemurafenib and dabrafenib mesylate in the treatment of metastatic melanoma have be

180 1- and 3-year durations of adjuvant imatinib mesylate in the treatment of patients with gastrointesti

181 the effects of KIT inhibition using imatinib mesylate in this molecular subset of disease.

182 data suggest a possible utility for imatinib mesylate in treating smallpox or MPX infections or compl

183 apamycin and the Bcr-Abl inhibitor, imatinib mesylate, in Bcr-Abl-expressing cell lines and primary C

184 ercially available siderophore, deferoxamine mesylate, in both the free ligand and Fe-bound forms.

185 randomized to 1 of 2 dose levels of imatinib mesylate, including 400 mg once daily (400 mg/d) vs 400

186 imals with the ABL kinase inhibitor imatinib mesylate induced specific modulation of blasts and proge

187 whereas IL-33 counteracts in vitro imatinib mesylate-induced growth arrest in CML CD34(+) progenitor

188 ve shown that the BCR-ABL inhibitor imatinib mesylate induces both apoptosis and autophagy, and that

189 Overall, our findings indicate that eribulin mesylate induces less neuropathy in mice than paclitaxel

190 Imatinib mesylate inhibited Pdgfr-beta activation and Acta2(-/-)

191 After imatinib mesylate initiation, metabolic response by (18)F-FDG PET

192 aseline, 1-7 d, and 4 or 8 wk after imatinib mesylate initiation.

193 ith PMR, and the biologic action of imatinib mesylate interacts with glycolysis and GLUT4 expression.

194 targeted tyrosine kinase inhibitor imatinib mesylate is a dramatically effective agent, but the dura

195 -molecule tyrosine kinase inhibitor imatinib mesylate is a potent inhibitor of wild-type (WT) KIT and

196 Obatoclax mesylate is a small molecule pan-Bcl-2 antagonist with i

197 Imatinib mesylate is a small molecule that inhibits activation of

198 Imatinib mesylate is a tyrosine kinase inhibitor that was approve

199 Resistance to imatinib mesylate is an emerging problem in the treatment of chro

200 Furthermore, we show that imatinib mesylate is effective in a mouse model of infection with

201 e BCR/ABL tyrosine kinase inhibitor imatinib mesylate is highly effective in the treatment of chronic

202 Imatinib mesylate is standard treatment for patients who have adv

203 r (GIST) and treated long-term with imatinib mesylate is unknown.

204 re of the 2'-hydroxyl group onto a secondary mesylate leaving group with clean inversion of stereoche

205 nt of mice with the c-KIT inhibitor imatinib mesylate limited effusion precipitation by mouse and hum

206 The KIT tyrosine kinase inhibitor imatinib mesylate markedly prolongs the survival of patients with

207 1.3-53.2), decreasing after 1 wk of imatinib mesylate (mean, 5.5; range, -0.5-47.7, P < 0.001, n = 44

208 3 months after CCR (29 months after imatinib mesylate; median 6 RQ-PCR assays), 23 patients (27%) had

209 The clinical applications of imatinib mesylate might thus be expanded with its use as a potent

210 gioisomer and the corresponding 2-chloroaryl mesylates (Ms) deliver the other in a selectable manner.

211 5 control, n=266 single-dose oral casopitant mesylate, n=269 3-day intravenous and oral casopitant me

212 de the antiproliferative effects of imatinib mesylate on CD34(+) progenitors in CML.

213 have investigated the influence of imatinib mesylate on CD4(+)CD25(+)FoxP3(+) regulatory T cells (Tr

214 uppressive effects of nilotinib and imatinib mesylate on leukemic progenitor colony formation, sugges

215 tor receptor (PDGFR)-beta inhibitor imatinib mesylate on tissue repair.

216 response category was similar with imatinib mesylate or interferon-alpha, suggesting that the surviv

217 mited treatment success with either imatinib mesylate or other anti-KIT D816V kinase inhibitors.

218 lly, the near universal exposure to imatinib mesylate or other kinase inhibitors before transplant co

219 f study drug (containing 0.4 mg phentolamine mesylate or placebo) was injected per cartridge of local

220 the c-Abl tyrosine kinase inhibitor imatinib mesylate or the protein kinase Cdelta (PKCdelta) inhibit

221 Enantioenriched propargyl mesylates or perfluorobenzoates react with alpha-(N-carb

222 mg of dexamethasone and 100 mg of dolasetron mesylate orally 2 h before therapy and every 12 h for an

223 vere neuropathy in mice relative to eribulin mesylate, paralleling their toxicity profiles in clinic.

224 PDGF-BB-overexpressing tumors with imatinib mesylate (PDGFR inhibitor) resulted in increased growth

225 intravenous plus oral regimen of casopitant mesylate plus dexamethasone and ondansetron significantl

226 ine-18 via displacement of the corresponding mesylate precursor with [18F]fluoride.

227 3-N-benzoyl-3',5'-di-O-benzoyl-protected 5-O-mesylate precursors in 17-35% radiochemical yield (decay

228 The corresponding mesylate precursors of 3 and 4 were radiolabeled with (1

229 In contrast, eribulin mesylate produced no significant deleterious effects on

230 Adjuvant imatinib mesylate prolongs recurrence-free survival (RFS) after r

231 rowth factor receptor with Gleevec (imatinib mesylate) reduced overall contractile ability and the el

232 eloid leukemia (CML) often manifest imatinib mesylate resistance associated with point mutations in B

233 op mutations can be associated with imatinib mesylate resistance in GIST.

234 c cells exhibiting various forms of imatinib mesylate resistance, including Bcr/Abl overexpression, L

235 iologies of disease progression and imatinib mesylate resistance, leading to the development of new t

236 this pathway in CML maintenance and imatinib mesylate resistance.

237 fenib potently induced apoptosis in imatinib mesylate-resistant cells expressing high levels of Bcr/A

238 ies, particularly in the setting of imatinib mesylate-resistant disease.

239 The mutations included 6 known imatinib mesylate-resistant mutations, including T315I, which sho

240 hick embryos to the PDGFR inhibitor imatinib mesylate resulted in spina bifida in the absence of NTDs

241 ing KIT alterations, treatment with imatinib mesylate results in significant clinical responses in a

242 ation was also detected in d(6)-DMSO for the mesylate salt, assigned to the alpha conformation, in wh

243 xhibited good oral bioavailability (F = 42%, mesylate salt, rat) and rate of prodrug conversion to AD

244 rane-impermeable iron chelator, deferoxamine mesylate salt, was able to increase MT2 levels.

245 ,4-benz oxazinyl]-(1-naphthalenyl) methanone mesylate salt] (Win55,212-2) inhibited gp120-induced IL-

246 1,4-benz oxazinyl]-(1-naphthalenyl)methanone mesylate salt] (Win55212-2) (100 nM) and 2-arachidonylgl

247 wn, and recent clinical trials with imatinib mesylate showed limited success due to normal tissue tox

248 Furthermore, imatinib mesylate significantly enhanced antitumor immune respons

249 tyrosine kinases and is blocked by imatinib mesylate (STI-571; Gleevec), an Abl family kinase inhibi

250 The efficiency of mesylates, sulfamates, esters, carbonates, carbamates, a

251 advanced GIST who were treated with imatinib mesylate survived for more than 5 years, regardless of a

252 efficacious therapeutics that, like imatinib mesylate, target the oncogenic kinase activity of BCR-AB

253 Imatinib mesylate targets mutated KIT oncoproteins in gastrointes

254 Additionally, imatinib mesylate that inhibits release of VEGF induces nuclear e

255 s recurred after discontinuation of imatinib mesylate, the duration for which treatment may be requir

256 occurred after the introduction of imatinib mesylate, the first tyrosine kinase inhibitor (TKI).

257 Within weeks of stopping imatinib mesylate, the skin changes recurred in each patient.

258 was less than 12% in favour of deferoxamine mesylate, then to move to a phase 3 efficacy trial would

259 tumor, GLUT4 levels decrease after imatinib mesylate therapy in most patients with PMR, and the biol

260 By multivariate analysis, imatinib mesylate therapy was identified as an independent favora

261 rexpression is normalized following imatinib mesylate therapy, whereas IL-33 counteracts in vitro ima

262 tromal tumor undergoing neoadjuvant imatinib mesylate therapy.

263 geted KIT/PDGFRA inhibitors such as imatinib mesylate, these treatments are rarely curative.

264 e the kinase inhibitory activity of imatinib mesylate; thus, agents that target Bcr/Abl through uniqu

265 The capacity of imatinib mesylate to reverse established pulmonary arterial hyper

266 atalyzed carbonylation of aryl tosylates and mesylates to form esters has been developed using a cata

267 development of drugs, particularly imatinib mesylate, to treat chronic myelogenous leukemia.

268 that cheaper and more stable aryl chlorides, mesylates, tosylates, and sulfamates can be used to yiel

269 Imatinib mesylate treatment decreases fibrosis and results in the

270 We found that mitoquinone mesylate treatment failed to prevent age-dependent loss

271 Imatinib mesylate treatment markedly reduces the burden of leukem

272 us leukemia (CML) and resistance to imatinib mesylate treatment remain poorly investigated.

273 ling approach that used the 10-year imatinib mesylate treatment response of patients with CML and a p

274 aining for type I procollagen after imatinib mesylate treatment, but essentially unchanged tissue gad

275 ed Smad1 signaling may benefit from imatinib mesylate treatment.

276 e MRSS, following the initiation of imatinib mesylate treatment.

277 ificantly altered in response to mitoquinone mesylate treatment.

278 erve class I MHC expression despite imatinib mesylate treatment.

279 hat accumulated in tumor foci after imatinib mesylate treatment.

280 rast, anti-7-trimethylsilyl-endo-2-norbornyl mesylate undergoes solvolysis in CD3CO2D only 2.6 times

281 A survival benefit for imatinib mesylate versus interferon-alpha therapy could not be de

282 esting that the survival benefit of imatinib mesylate (versus interferon-alpha in newly diagnosed CML

283 neurokinin-1-receptor antagonist casopitant mesylate was able to prevent acute and delayed CINV even

284 Imatinib mesylate was well tolerated but had minimal single-agent

285 early CP CML patients treated with imatinib mesylate, we performed an analysis in a large series of

286 Survival rates with imatinib mesylate were significantly better than with interferon-

287 g of aryl neopentylglycolboronates with aryl mesylates were developed.

288 Formation of a benzylic mesylate (which is not isolated), followed by treatment

289 erapy was developed, initially with imatinib mesylate, which has transformed our treatment algorithms

290 In contrast, imatinib mesylate, which inhibits KIT kinase activity but does no

291 give stereochemically defined 3-aminopropyl mesylates, which were cyclized to 1,2,3,4-tetrasubstitut

292 monitored 85 patients treated with imatinib mesylate who achieved a CCR.

293 benzoxaz in-6-yl)-(1-naphthalenyl) methanone mesylate [WIN 55,212-2 (WIN)] and (R,S)-3-(2-iodo-5-nitr

294 1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate (WIN55,212,2) depolarized MCH cells and increas

295 1,4-b enzoxazinyl]-(1-naphthalenyl)methanone mesylate (WIN55,212-2) in a concentration-dependent mann

296 urther study of the efficacy of deferoxamine mesylate with anticipation that the drug would significa

297 n-deficient aryl triflates, -tosylates, and -mesylates with alkylbis(catecholato)silicates is present

298 basis, had an objective response to imatinib mesylate, with a 20% or more decrease in tumour volume.

299 over (90%) from interferon-alpha to imatinib mesylate within a year of study entry.

300 al injection of the vasodilator phentolamine mesylate would shorten the duration of soft-tissue anest