ライフサイエンスコーパス: vemurafenib

1 he cells more resistant to targeted therapy (vemurafenib).

2 suggested disease acceleration triggered by vemurafenib.

3 but lacked sensitivity to the BRAF inhibitor vemurafenib.

4 tiation of treatment with the BRAF inhibitor vemurafenib.

5 isted even 732 days after discontinuation of vemurafenib.

6 han one-fifth of patients being treated with vemurafenib.

7 OR pathway inhibition by the B-Raf inhibitor vemurafenib.

8 al600Glu are sensitive to the BRAF inhibitor vemurafenib.

9 roquinolones ciprofloxacin and ofloxacin and vemurafenib.

10 l patients who received at least one dose of vemurafenib.

11 dacarbazine crossed over from dacarbazine to vemurafenib.

12 increased sensitivity to the BRAF inhibitor vemurafenib.

13 educed the development of resistance against Vemurafenib.

14 tance and sensitivity to the BRAF inhibitor, vemurafenib.

15 ical responses when chloroquine was added to vemurafenib.

16 e of melanoma cells chronically treated with vemurafenib.

17 entifying mutations conferring resistance to Vemurafenib.

18 Photosensitivity was more common with vemurafenib (14 patients [38.9%]) compared with dabrafen

19 of BRAF V600E downstream targets showed that vemurafenib (480 mg/d) completely abrogated extracellula

20 lation phase of our study, patients received vemurafenib 720 mg or 960 mg twice a day continuously an

21 Patients received vemurafenib 960 mg orally twice daily.

22 on of QTc; and two patients on a schedule of vemurafenib 960 mg twice a day and cobimetinib 60 mg 28/

23 re than 7 days; one patient on a schedule of vemurafenib 960 mg twice a day and cobimetinib 60 mg onc

24 One patient on a schedule of vemurafenib 960 mg twice a day and cobimetinib 80 mg onc

25 noma and a BRAF(V600) mutation received oral vemurafenib 960 mg twice a day.

26 e voice recognition system to receive either vemurafenib (960 mg orally twice daily) or dacarbazine (

27 to irinotecan and cetuximab with or without vemurafenib (960 mg PO twice daily).

28 e daily) and trametinib (2 mg once daily) or vemurafenib (960 mg twice daily) orally as first-line th

29 cycle) or placebo, in combination with oral vemurafenib (960 mg twice daily).

30 Mutant ARAF activity was inhibited by vemurafenib, a BRAF inhibitor, indicating the importance

31 cing COMET markedly increased sensitivity to vemurafenib, a common inhibitor of mutated B-raf.

32 A-Raf molecule is sensitive to inhibition by vemurafenib, a potent and selective Raf kinase inhibitor

33 a developed EMN while receiving therapy with vemurafenib, a selective BRAF inhibitor.

34 Vemurafenib, a selective inhibitor of RAF kinases, has c

35 Vemurafenib, a specific BRAF(V600E) inhibitor, has signi

36 enes whose loss is involved in resistance to vemurafenib, a therapeutic RAF inhibitor.

37 ioprine, the fluoroquinolone antibiotics and vemurafenib-a BRAF inhibitor used to treat metastatic me

38 nase (MEK) inhibitor reverses the benefit of vemurafenib-accelerated wound healing.

39 Here we show how the BRAF inhibitor vemurafenib accelerates skin wound healing by inducing t

40 rally bioavailable B-Raf inhibitors, such as vemurafenib, achieve dramatic responses initially, but t

41 ue of the JCI, Ma and colleagues report that vemurafenib activates ER stress and autophagy in BRAF(V6

42 Preliminary vemurafenib activity was observed in non-small-cell lung

43 on therapy with atezolizumab + cobimetinib + vemurafenib, after a 28-d run-in period with cobimetinib

44 ession-free survival than those treated with vemurafenib alone.

45 Vemurafenib, an oncogenic BRAF kinase inhibitor approved

46 Vemurafenib, an oral BRAF V600 inhibitor, has pronounced

47 Hypokalemia (6 cases in patients receiving vemurafenib and 2 cases in patients receiving dabrafenib

48 n the trials: 568 patients were treated with vemurafenib and 287 patients were treated with dacarbazi

49 7 patients were randomly assigned to receive vemurafenib and 338 to receive dacarbazine.

50 d cobimetinib: 66 had recently progressed on vemurafenib and 63 had never received a BRAF inhibitor.

51 follow-up was 12.5 months (IQR 7.7-16.0) on vemurafenib and 9.5 months (3.1-14.7) on dacarbazine.

52 nib-resistant melanoma with a combination of vemurafenib and an autophagy inhibitor reduced tumor loa

53 patients with colorectal cancer who received vemurafenib and cetuximab.

54 patients with colorectal cancer who received vemurafenib and cetuximab.

55 F V600 mutation-positive melanoma to receive vemurafenib and cobimetinib (combination group) or vemur

56 In cycle 1, all patients received vemurafenib and cobimetinib only; atezolizumab placebo w

57 Vemurafenib and cobimetinib was associated with a nonsig

58 ion of atezolizumab to targeted therapy with vemurafenib and cobimetinib was safe and tolerable and s

59 All patients treated with vemurafenib and cobimetinib were included in safety and

60 ere treated at ten dosing regimens combining vemurafenib and cobimetinib: 66 had recently progressed

61 The BRAF inhibitors vemurafenib and dabrafenib have shown efficacy as monoth

62 The selective BRAF inhibitors vemurafenib and dabrafenib have shown significant improv

63 neous adverse effects of the BRAF inhibitors vemurafenib and dabrafenib mesylate in the treatment of

64 low-up data after at least 50% crossover (in vemurafenib and dabrafenib phase 3 trials) weakened the

65 by selective BRAF inhibitors (BRAFis; e.g., vemurafenib and dabrafenib) has led to a sea change in t

66 n are insensitive to BRAF inhibitors such as vemurafenib and dabrafenib, and also may evade immune su

67 The development of targeted inhibitors, vemurafenib and dabrafenib, has led to improved clinical

68 The kinase inhibitors vemurafenib and dabrafenib, which target oncogenic BRAF

69 R-211 was up-regulated by the BRAF inhibitor vemurafenib and in vemurafenib-resistant melanoma cells,

70 sole BRAF inhibition with the BRAF inhibitor vemurafenib and may provide a novel targeted therapeutic

71 nd efficacy of combined BRAF inhibition with vemurafenib and MEK inhibition with cobimetinib in patie

72 vents of grade 3 or higher, as compared with vemurafenib and placebo (65% vs. 59%), and there was no

73 fenib and cobimetinib (combination group) or vemurafenib and placebo (control group).

74 re unresponsive to both generations of RAFi, vemurafenib and PLX8394, highlighting a distinct respons

75 ibitor TAK-931 sensitized resistant cells to Vemurafenib and reduced the number of cell colonies.

76 linical benefit of cobimetinib combined with vemurafenib and support the use of the combination as a

77 fit over monotherapy with the BRAF inhibitor vemurafenib and supports the combination therapy as stan

78 the Food and Drug Administration approval of vemurafenib and the development of other RAF and MEK (mi

79 ed melanoma resistance to the BRAF inhibitor vemurafenib and the MAPK/ERK kinase inhibitor cobimetini

80 luated the combination of the BRAF inhibitor vemurafenib and the MEK inhibitor cobimetinib.

81 o combined treatment with the BRAF inhibitor vemurafenib and the mitogen-activated protein kinase/ext

82 s of incomplete leukemic cell eradication by vemurafenib and to explore chemotherapy-free combination

83 signed 1:1 to 28-day cycles of atezolizumab, vemurafenib, and cobimetinib (atezolizumab group) or ate

84 atezolizumab group) or atezolizumab placebo, vemurafenib, and cobimetinib (control group).

85 effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametin

86 partial metabolic responders at 6 months of vemurafenib, and the median reduction in maximum standar

87 these, 119 patients received dabrafenib; 36, vemurafenib; and 30, CombiDT therapy.

88 /relapsed HCL patients to the BRAF inhibitor vemurafenib approached 100%, with 35% to 40% complete re

89 al signs of ocular inflammation treated with vemurafenib at the Department of Ophthalmology, Cochin-H

90 hase 2, single-group, multicenter studies of vemurafenib (at a dose of 960 mg twice daily)--one in It

91 s, ectopic CK2alpha decreased sensitivity to vemurafenib (BRAF inhibitor), dabrafenib (BRAF inhibitor

92 hint of an underlying sensitization against vemurafenib but found evidence suggesting that vemurafen

93 However, vemurafenib can be continued while the ocular symptoms a

94 Selective BRAF inhibitors such as vemurafenib cause multiple cutaneous adverse effects, in

95 Blockade of BRAF(V600E) by vemurafenib causes feedback upregulation of EGFR, whose

96 Treatment with RAF inhibitors such as vemurafenib causes the development of cutaneous squamous

97 The vemurafenib clinical trials were a multicenter series in

98 enib/trametinib, encorafenib/binimetinib, or vemurafenib/cobimetinib should be offered in BRAF-mutant

99 The orally available BRAF kinase inhibitor vemurafenib, compared with dacarbazine, shows improved r

100 nce of cutaneous toxic effects differs among vemurafenib, dabrafenib, and CombiDT therapies.

101 wed further exploration into the novel drugs vemurafenib, dabrafenib, trametinib, and ibrutinib.

102 om 26 patients to clinically available BRAF (vemurafenib; dabrafenib) or MEK (trametinib) inhibitors.

103 ith BRAF V600E-mutant melanoma, single-agent vemurafenib did not show meaningful clinical activity in

104 Combined treatment of polycations and vemurafenib diminishes the metabolic flexibility of mela

105 At the same time, vemurafenib directly activated the fibroblasts through p

106 Here, we examine how vemurafenib disposition, particularly through cytochrome

107 Patients' demographics, vemurafenib dosages, and the intervals between the onset

108 The vemurafenib dose was 960 mg twice per day in 6 patients

109 and kinetics of response were independent of vemurafenib dosing.

110 riven melanoma respond to the BRAF inhibitor vemurafenib due to subsequent deactivation of the prolif

111 eness of the three clinically approved BRAFi vemurafenib, encorafenib, and dabrafenib and the preclin

112 murafenib but found evidence suggesting that vemurafenib enhances proinflammatory responses by inhibi

113 ll lines, A375 and DM443, by serial in vitro vemurafenib exposure.

114 y stimulated Ras and MAPK upregulation after vemurafenib exposure.

115 clib, suggesting that initial treatment with vemurafenib followed by palbociclib with or without mTOR

116 fety was similar to that in prior studies of vemurafenib for melanoma.

117 evaluated tumors from patients treated with vemurafenib for the presence of human papilloma virus (H

118 anoma was initiated on twice-daily 960 mg of vemurafenib for treatment of progressive and recurrent s

119 the risk of uveitis in patients treated with vemurafenib for unresectable or metastatic cutaneous mel

120 hibited by targeted therapies (e.g. PLX-4032/vemurafenib), glucose metabolism is reduced, and cells i

121 rapy group and 65% (95% CI, 59 to 70) in the vemurafenib group (hazard ratio for death in the combina

122 bination-therapy group and 7.3 months in the vemurafenib group (hazard ratio, 0.56; 95% CI, 0.46 to 0

123 nd randomly assigned to the cobimetinib plus vemurafenib group (n=247) or placebo plus vemurafenib gr

124 us vemurafenib group (n=247) or placebo plus vemurafenib group (n=248).

125 the combination-therapy group and 51% in the vemurafenib group (P<0.001).

126 nts: 109 (93%) of 117 in the cobimetinib and vemurafenib group and 133 (94%) of 142 in the vemurafeni

127 have died: 117 (47%) in the cobimetinib and vemurafenib group and 142 (58%) in the vemurafenib group

128 in 92 patients (37%) in the cobimetinib and vemurafenib group and 69 patients (28%) in the vemurafen

129 ormal liver function tests (38 [11%]) in the vemurafenib group and neutropenia (26 [9%] of 287 patien

130 Eight (2%) patients in the vemurafenib group and seven (2%) in the dacarbazine grou

131 frequency in patients in the cobimetinib and vemurafenib group compared with the vemurafenib group we

132 all survival was significantly longer in the vemurafenib group than in the dacarbazine group (13.6 mo

133 se increase (36 [15%] in the cobimetinib and vemurafenib group vs 25 [10%] in the placebo and vemuraf

134 00K) disease, median overall survival in the vemurafenib group was 14.5 months (95% CI 11.2-not estim

135 inib and vemurafenib group compared with the vemurafenib group were gamma-glutamyl transferase increa

136 rafenib group vs 25 [10%] in the placebo and vemurafenib group), blood creatine phosphokinase increas

137 emurafenib group and 133 (94%) of 142 in the vemurafenib group.

138 murafenib group and 69 patients (28%) in the vemurafenib group.

139 b and vemurafenib group and 142 (58%) in the vemurafenib group.

140 verse events reported in the cobimetinib and vemurafenib group.

141 nation-therapy group and 18% of those in the vemurafenib group.

142 fter a 28-d run-in period with cobimetinib + vemurafenib, had substantial but manageable toxicity.

143 Vemurafenib has an objective and sustained efficacy in B

144 In recent years, the BRAF inhibitor vemurafenib has been successfully established in the the

145 veral small molecule BRAF inhibitors such as vemurafenib have been developed and demonstrate remarkab

146 end point, was improved with the addition of vemurafenib (hazard ratio, 0.50, P = .001).

147 versus 7.2 months (5.6-7.5) for placebo and vemurafenib (HR 0.58 [95% CI 0.46-0.72], p<0.0001).

148 .4 months (95% CI 15.0-19.8) for placebo and vemurafenib (HR 0.70, 95% CI 0.55-0.90; p=0.005).

149 The combination of cobimetinib with vemurafenib improves progression-free survival compared

150 Inhibition of BRAF with vemurafenib improves survival in patients with the most

151 tology-independent phase 2 "basket" study of vemurafenib in BRAF V600 mutation-positive nonmelanoma c

152 ls testing selective BRAF inhibitors such as vemurafenib in BRAF(V600E)-mutant patients.

153 mal melanocytes and act synergistically with vemurafenib in effectuating bioenergetic crisis, DNA dam

154 or, profoundly reduced circulating levels of vemurafenib in humanized mice.

155 e major enzyme involved in the metabolism of vemurafenib in in vitro assays with human liver microsom

156 wed the initial success of the RAF inhibitor vemurafenib in mutant V600 BRAF melanoma patients.

157 We aimed to establish the activity of vemurafenib in patients with BRAF(V600E)-positive papill

158 fety and activity of the oral BRAF inhibitor vemurafenib in patients with hairy-cell leukemia that ha

159 th objective responses to the BRAF inhibitor vemurafenib in patients with metastatic colorectal cance

160 xclusive with KRAS and define sensitivity to vemurafenib in PDA models.

161 sion-free survival compared with placebo and vemurafenib in previously untreated patients with BRAF(V

162 the clinical success of BRAF inhibitors like vemurafenib in treating metastatic melanoma, resistance

163 Topical treatment with vemurafenib in two wound-healing mice models accelerates

164 ted short-term efficacy of a BRAF inhibitor (vemurafenib) in three patients with multisystemic ECD.

165 he single-agent BRAF inhibitor dabrafenib or vemurafenib included Grover disease (51 patients [42.9%]

166 Inhibition of BRAF(V600E) using vemurafenib, independently of its cytostatic effects, su

167 The BRAF inhibitors dabrafenib and vemurafenib induce remarkable clinical responses in pati

168 m to protect against UVB-, chemotherapy- and vemurafenib-induced apoptosis.

169 Herein, a case of severe vemurafenib-induced granulomatous hepatitis leading to c

170 te, the molecular and cellular mechanisms of vemurafenib-induced rashes have remained largely elusive

171 requent TGFBR1 and TGFBR2 mutations in human vemurafenib-induced skin lesions and in sporadic cSCC.

172 We here demonstrate that vemurafenib inhibits the downstream signaling of the can

173 spliced, truncated BRAF(V600E) that promotes vemurafenib-insensitive MAPK pathway signaling.

174 stance to the oncogenic BRAF(E600) inhibitor vemurafenib is a major clinical challenge in the treatme

175 Vemurafenib is a potent RAF kinase inhibitor with remark

176 Vemurafenib is a revolutionary treatment for melanoma, b

177 noma cells treated with the kinase inhibitor vemurafenib is driven by downregulation of the transcrip

178 Despite its superior efficacy, the use of vemurafenib is limited by frequent inflammatory cutaneou

179 aken together, our findings demonstrate that vemurafenib is unlikely to exhibit a clinically signific

180 Retreatment with vemurafenib led to similar response patterns (n = 6).

181 athways may contribute more significantly to vemurafenib metabolism in vivo.

182 e-daily) and trametinib (2 mg once-daily) or vemurafenib monotherapy (960 mg twice-daily) orally as f

183 l in favour of the combination compared with vemurafenib monotherapy for most domains across all thre

184 Dabrafenib plus trametinib, as compared with vemurafenib monotherapy, significantly improved overall

185 ned to dabrafenib plus trametinib (n=352) or vemurafenib (n=352).

186 with metastatic melanoma who did not receive vemurafenib nor immune checkpoint-blocking antibodies.

187 Among the 568 patients treated with vemurafenib, ocular adverse effects developed in 22% (95

188 se in T-regulatory cells, as observed in the vemurafenib-only run-in period.

189 d CRAF isoforms with similar affinity, while vemurafenib or dabrafenib have little or modest CRAF act

190 iduals who had either recently progressed on vemurafenib or never received a BRAF inhibitor.

191 d the course of 21 HCL patients treated with vemurafenib outside of trials with individual dosing reg

192 In tumors with wild-type B-Raf, vemurafenib paradoxically activates downstream signaling

193 ompetitive, first-generation RAF inhibitors (vemurafenib/PLX4720, RAFi) cause paradoxical activation

194 t alternating dosing schedules of Gant61 and vemurafenib prevented the onset of BRAFi resistance, sug

195 s, a short course of the oral BRAF inhibitor vemurafenib produced an almost 100% response rate, inclu

196 noma treatment with the BRAF V600E inhibitor vemurafenib provides therapeutic benefits but the common

197 0E) mutation with kinase inhibitors, such as vemurafenib, reduces tumor burden, but these tumors freq

198 erized a novel ZNF767-BRAF fusion found in a vemurafenib-refractory respiratory tract PMM, from which

199 ate that ~50-60% of melanoma cell lines with vemurafenib resistance acquired in vitro show activation

200 uman melanoma cells was sufficient to confer vemurafenib resistance and more robust tumor growth in v

201 ate the biological role of CDC7 in promoting Vemurafenib resistance and the anticipated benefits of d

202 aive BRAF-mutant LAs and those with acquired vemurafenib resistance caused by an alternatively splice

203 nome expression analysis and discovered that vemurafenib resistance correlated with the loss of micro

204 gulation of miR-3613-3p were associated with Vemurafenib resistance in BRAF(V600E)- bearing melanoma

205 ate it as a potential new target to overcome vemurafenib resistance in BRAF-mutated and MET-addicted

206 lyethylenimines and poly(l-lysine)s, prevent vemurafenib resistance in melanoma cells through inducti

207 We developed a CRAF-mediated model of vemurafenib resistance in melanoma cells to assess the i

208 ression and dysregulation is a mechanism for vemurafenib resistance in melanoma.

209 previously responsive melanomas, we induced vemurafenib resistance in two V600E BRAF+ve melanoma cel

210 the results indicate a mechanism of acquired vemurafenib resistance in V600E BRAF+ve melanoma cells t

211 Here, we found that EGFR-induced vemurafenib resistance is ligand dependent.

212 Vemurafenib resistance is poorly understood; however, av

213 Vemurafenib resistance mediated by ACK1 inhibition can b

214 iRNA-mediated NRAS suppression both reversed vemurafenib resistance significantly in A375rVem and DM4

215 An inverse relationship between MITF, vemurafenib resistance, and EGFR was then observed in pa

216 a cell lines, with acquired in vitro-induced vemurafenib resistance, show increased levels of glioma-

217 , induced MAP kinase signaling and conferred vemurafenib resistance.

218 h pre-mRNA splicing as a mechanism to combat vemurafenib resistance.

219 a known critical factor that contributes to vemurafenib resistance.

220 s a novel, druggable target in CRAF-mediated vemurafenib resistance.

221 drug-naive lines, two of which are innately vemurafenib resistant.

222 of MITF in drug response is corroborated in vemurafenib-resistant biopsies, including MITF-high and

223 f GMPR accompanies downregulation of MITF in vemurafenib-resistant BRAF(V600E)-melanoma cells and und

224 1 isoform is related to autophagic status in vemurafenib-resistant BRAF(V600E)-mutant melanoma cells

225 We tested this hypothesis in vemurafenib-resistant brain tumors.

226 The resulting approximately 10-fold more vemurafenib-resistant cell lines, A375rVem and D443rVem,

227 Our results demonstrated that Vemurafenib-resistant cells exhibited a persistent expre

228 on of miR-204-5p and miR-211-5p occurring in vemurafenib-resistant cells was determined to impact vem

229 Treatment of vemurafenib-resistant cells with the GLI1/GLI2 inhibitor

230 own of GLI1 and GLI2 restored sensitivity to vemurafenib-resistant cells, an effect associated with b

231 production and limit in-vitro cell growth of vemurafenib-resistant cells.

232 ted by the BRAF inhibitor vemurafenib and in vemurafenib-resistant melanoma cells, with miR-211 loss

233 modulates EGFR turnover, is downregulated in vemurafenib-resistant melanoma cells.

234 In preclinical studies, treating vemurafenib-resistant melanoma with a combination of vem

235 has been recurrently identified in a set of vemurafenib-resistant melanomas, but little is known abo

236 provide an avenue to overcome recurrence of vemurafenib-resistant metastatic disease.

237 Strikingly, we found that vemurafenib-resistant tumors remain sensitive to palboci

238 revents tumour formation and slows growth of vemurafenib-resistant tumours.

239 of Hsp90 and BRAF signaling using 17-AAG and vemurafenib, respectively.

240 nib-resistant cells was determined to impact vemurafenib response.

241 ns for mechanism-based strategies to improve vemurafenib responses.Significance: Identification of mi

242 y biomarker data show that the cobimetinib + vemurafenib run-in was associated with an increase in pr

243 Vemurafenib safety in this diverse population of patient

244 3222 patients received at least one dose of vemurafenib (safety population).

245 Vemurafenib seems to be more nephrotoxic than dabrafenib

246 ne the role of CDC7 in drug resistance using Vemurafenib-sensitive and resistant melanoma cells.

247 pparent mechanisms of acquired resistance in vemurafenib-sensitive patient-derived xenograft models.

248 ent a viable therapeutic strategy to restore vemurafenib sensitivity, reducing or even inhibiting the

249 Vemurafenib showed antitumour activity in patients with

250 hibitors, the first-generation RAF inhibitor vemurafenib stimulated in vitro and in vivo growth and i

251 Finally, vemurafenib strongly induced PXR activity in vitro, but

252 e after failure of the BRAF(V600E) inhibitor vemurafenib, suggesting autophagy inhibition overcame th

253 or and side effects are observed with 480 mg vemurafenib, suggesting that dosing regimens in BRAF-dri

254 ion, imparting resistance to inhibitors like vemurafenib that bind the alphaC "out" conformation.

255 mour, and selective BRAF inhibitors, such as vemurafenib that blocks tumour cell proliferation in pat

256 therapy, which justified the continuation of vemurafenib therapy because the benefits regarding the p

257 The effect of the discontinuation of vemurafenib therapy on ocular manifestations was assesse

258 All were successfully managed while vemurafenib therapy was continued.

259 Clinical improvement occurred when vemurafenib therapy was stopped in 5 of 7 patients.

260 of acute kidney injury in patients receiving vemurafenib therapy were reported.

261 mice expressing human CYP3A4 did not process vemurafenib to a greater extent than CYP3A4-null animals

262 Our results argue that HPV cooperates with vemurafenib to promote tumorigenesis, in either the pres

263 elerated fibrosarcoma (RAF) kinase inhibitor vemurafenib to treat unresectable melanoma.

264 tested the in vitro and in vivo efficacy of vemurafenib, trametinib, BKM120 or LEE011 alone and in c

265 sults were validated in vivo in samples from vemurafenib-treated HCL patients within a phase 2 clinic

266 Furthermore, 55% of the cSCCs arising in vemurafenib-treated mice exhibited a wild-type Ras genot

267 Vemurafenib treatment elevated MAPK markers and increase

268 ation of miR-204-5p and miR-211-5p following vemurafenib treatment enables the emergence of resistanc

269 Vemurafenib treatment improved blood counts in all patie

270 Vemurafenib treatment led to the release of transforming

271 emains higher in melanoma cells resistant to vemurafenib treatment than in untreated cells.

272 Their expression was rapidly affected by vemurafenib treatment through RNA stabilization.

273 In case 2, after 5 months of vemurafenib treatment, the patient developed a granuloma

274 ever, patients rapidly develop resistance to vemurafenib treatment.

275 (CLL) in the absence of RAS mutations during vemurafenib treatment.

276 erved in a cohort of melanoma patients after vemurafenib treatment.

277 s in liver biochemistries were reported with vemurafenib use in 30% of subjects, 11% developed severe

278 f first-generation RAF inhibitors, including vemurafenib (VEM) and dabrafenib led to initial exciteme

279 % CI 20.3-not estimable) for cobimetinib and vemurafenib versus 17.4 months (95% CI 15.0-19.8) for pl

280 months (95% CI 9.5-13.4) for cobimetinib and vemurafenib versus 7.2 months (5.6-7.5) for placebo and

281 Off-label use of vemurafenib (VMF) to treat BRAF(V600E) mutation-positive

282 ERKi-resistant cells were also resistant to vemurafenib (VMF), trametinib (TMT), and combined treatm

283 ntical intravenous placebo, and blinding for vemurafenib was achieved by means of a placebo tablet.

284 Although vemurafenib was also highly phototoxic to cultured cells

285 The addition of cobimetinib to vemurafenib was associated with a significant improvemen

286 In the BRIM-3 trial, vemurafenib was associated with risk reduction versus da

287 Vemurafenib was given to eight patients with multisystem

288 A short oral course of vemurafenib was highly effective in patients with relaps

289 TP/RAS ratio in primary CLL cells exposed to vemurafenib was reduced upon SYK inhibition.

290 as well as the effect of rechallenging when vemurafenib was reintroduced.

291 The safety profile for cobimetinib and vemurafenib was tolerable and manageable, and no new saf

292 sponse to the BRAF(V600E)-targeted inhibitor vemurafenib, which decreased the cytotoxicity of the dru

293 was placed on a clinical trial that combined vemurafenib with a MEK inhibitor, cobimetinib.

294 testing a combination of the BRAF inhibitor vemurafenib with ipilimumab (anti-CTLA4), with significa

295 e generated A375 melanoma cells resistant to vemurafenib with the goal of investigating changes in mi

296 eneral symptoms and a persistent response to vemurafenib, with a median follow-up time of 10.5 months

297 f 66 patients who had recently progressed on vemurafenib, with a median progression-free survival of

298 es of these PTEN-null melanoma cell lines to vemurafenib, with enhanced cytotoxicity observed followi

299 lines were insensitive to the BRAF inhibitor vemurafenib, with IC(50) values greater than 5 muM, but

300 Vemurafenib (Zelboraf; Genentech, CA) is a highly effect