ライフサイエンスコーパス: nilotinib

1 ly to the surprisingly large accumulation of nilotinib.

2 e was inhibited by daily oral treatment with nilotinib.

3 letion of alpha4 sensitized leukemia cell to nilotinib.

4 hagy might be a major mechanism of action of nilotinib.

5 inically important tyrosine kinase inhibitor nilotinib.

6 e between ABL001 and the catalytic inhibitor nilotinib.

7 ilar persistent grade 2 nonhematologic AE on nilotinib.

8 e (CHR) at baseline (n = 52) achieved CHR on nilotinib.

9 ted with dasatinib and 45 (52%) treated with nilotinib.

10 her these cells were efficiently targeted by nilotinib.

11 ter treatment failure with both imatinib and nilotinib.

12 atients after failure with both imatinib and nilotinib.

13 or dasatinib and Y253H, E255V, and T315I for nilotinib.

14 of patients remained on imatinib, and 30% on nilotinib.

15 approach with selective, early switching to nilotinib.

16 ent or to the pharmacodynamics properties of nilotinib.

17 rate of EMR failure on imatinib, but not on nilotinib.

18 iled imatinib, should one offer dasatinib or nilotinib?

19 imatinib group, n=1 [1%, after crossover to nilotinib]).

20 6), dasatinib (0.28, 0.12-0.66, p=0.004), or nilotinib (0.42, 0.20-0.89, p=0.024) predicted for bette

21 nts (21) on imatinib 400 mg once daily as on nilotinib (11 patients each on nilotinib 300 mg twice da

22 was achieved in 3 of 6 patients treated with nilotinib, 2 of 2 with imatinib, and 0 of 3 with dasatin

23 inib 200 mg daily, dasatinib 50 mg daily, or nilotinib 200 mg twice daily) for 12 months.

24 ts were randomly assigned (1:1:1) to receive nilotinib 300 mg twice a day, nilotinib 400 mg twice a d

25 e daily as on nilotinib (11 patients each on nilotinib 300 mg twice daily and nilotinib 400 mg twice

26 ly, and 29 [10%] with imatinib; p<0.0001 for nilotinib 300 mg twice daily vs imatinib, p=0.0004 for n

27 ce daily, and 17 with imatinib; p=0.0003 for nilotinib 300 mg twice daily vs imatinib, p=0.0089 for n

28 nilotinib than with imatinib (201 [71%] with nilotinib 300 mg twice daily, 187 [67%] with nilotinib 4

29 2 patients were randomly assigned to receive nilotinib 300 mg twice daily, 281 to receive nilotinib 4

30 with either dose of nilotinib (33 [12%] with nilotinib 300 mg twice daily, 30 [11%] with nilotinib 40

31 d those in the imatinib group (74 [26%] with nilotinib 300 mg twice daily, 59 [21%] with nilotinib 40

32 groups than in the imatinib group (two with nilotinib 300 mg twice daily, five with nilotinib 400 mg

33 % of patients were headache (eight [3%] with nilotinib 300 mg twice daily, four [1%] with nilotinib 4

34 on was low (found in 3, 2, and 3 patients on nilotinib 300 mg twice daily, nilotinib 400 mg twice dai

35 s, 1 of 11, 2 of 11, and 7 of 21 patients on nilotinib 300 mg twice daily, nilotinib 400 mg twice dai

36 Patients (n = 846) received nilotinib 300 mg twice daily, nilotinib 400 mg twice dai

37 s in the second year of the study (four with nilotinib 300 mg twice daily, three with nilotinib 400 m

38 groups than in the imatinib group (five with nilotinib 300 mg twice daily, three with nilotinib 400 m

39 ommon with imatinib than with either dose of nilotinib (33 [12%] with nilotinib 300 mg twice daily, 3

40 :1) to receive nilotinib 300 mg twice a day, nilotinib 400 mg twice a day, or imatinib 400 mg once a

41 0 mg twice daily or 100 mg daily (n=106), or nilotinib 400 mg twice daily (n=108).

42 nib 800 mg/day, and subsequently switched to nilotinib 400 mg twice daily for failing the same target

43 300 mg twice daily vs imatinib, p=0.0004 for nilotinib 400 mg twice daily vs imatinib).

44 300 mg twice daily vs imatinib, p=0.0089 for nilotinib 400 mg twice daily vs imatinib).

45 nts each on nilotinib 300 mg twice daily and nilotinib 400 mg twice daily).

46 nilotinib 300 mg twice daily, 187 [67%] with nilotinib 400 mg twice daily, and 124 [44%] with imatini

47 with nilotinib 300 mg twice daily, five with nilotinib 400 mg twice daily, and 17 with imatinib; p=0.

48 nilotinib 300 mg twice daily, 281 to receive nilotinib 400 mg twice daily, and 283 to receive imatini

49 nilotinib 300 mg twice daily, 59 [21%] with nilotinib 400 mg twice daily, and 29 [10%] with imatinib

50 nilotinib 300 mg twice daily, 30 [11%] with nilotinib 400 mg twice daily, and 59 [21%] with imatinib

51 3 patients on nilotinib 300 mg twice daily, nilotinib 400 mg twice daily, and imatinib, respectively

52 21 patients on nilotinib 300 mg twice daily, nilotinib 400 mg twice daily, and imatinib, respectively

53 ith nilotinib 300 mg twice daily, three with nilotinib 400 mg twice daily, and one with imatinib).

54 ith nilotinib 300 mg twice daily, three with nilotinib 400 mg twice daily, and ten with imatinib).

55 nilotinib 300 mg twice daily, four [1%] with nilotinib 400 mg twice daily, and two [<1%] with imatini

56 846) received nilotinib 300 mg twice daily, nilotinib 400 mg twice daily, or imatinib 400 mg once da

57 eive oral imatinib 400 mg once daily or oral nilotinib 400 mg twice daily.

58 andomly assigned patients (1:1) to switch to nilotinib 400 mg twice per day or an escalation of imati

59 Nilotinib (400 mg twice daily) was approved on the basis

60 er >/=2 years on imatinib were randomized to nilotinib (400 mg twice daily, n = 104) or continued ima

61 BCR-ABL(IS) >10%) on imatinib (33%) than on nilotinib (9%-11%); similarly at 6 months, 16% of patien

62 p (42%, 32-53%; difference 7.9% in favour of nilotinib; 95% CI -6.2 to 22.0, p=0.31).

63 study, we evaluated the in vivo efficacy of nilotinib, a brain penetrant c-Abl inhibitor, in the acu

64 the rate of apoptosis caused by exposure to nilotinib, a drug used therapeutically to treat Ph-posit

65 Nilotinib, a recently approved multitargeted tyrosine ki

66 Treatment using imatinib or nilotinib abolished the aberrant activation of c-Abl and

67 or second-generation TKIs (ie, dasatinib or nilotinib) achieved complete cytogenetic response (58 [8

68 Responses can be achieved with dasatinib or nilotinib after failure of 2 prior tyrosine kinase inhib

69 or with Ph(+) ALL treated with dasatinib or nilotinib after imatinib failure.

70 after imatinib/nilotinib failure and 14 with nilotinib after imatinib/dasatinib failure.

71 ng enhanced the growth-inhibitory effects of nilotinib against 32D/T315I-Bcr-Abl1-derived mouse allog

72 ematologic imatinib intolerance discontinued nilotinib, all because of grade 3/4 thrombocytopenia.

73 resence of imatinib mesylate, dasatinib, and nilotinib, alone and in dual combinations.

74 inhibition using the alternative inhibitor, nilotinib, also resulted in cell death.

75 Therapy with the tyrosine kinase inhibitors nilotinib (AMN107) and dasatinib (BMS-354825) has produc

76 Preclinical in vitro studies have shown that nilotinib (AMN107), a new BCR-ABL tyrosine kinase inhibi

77 The BCR-ABL inhibitor, nilotinib (AMN107), is significantly more potent against

78 bitor of BCR-ABL and Src family kinases) and nilotinib (AMN107, a selective BCR-ABL inhibitor), may p

79 Nilotinib, an orally bioavailable, selective Bcr-Abl tyr

80 ts were enrolled; of whom 324 were allocated nilotinib and 320 were allocated imatinib.

81 unacceptable side effects from dasatinib or nilotinib and 70% of patients with the T315I mutation),

82 96 patients were randomly assigned to nilotinib and 95 patients were randomly assigned to imat

83 tyrosine kinase inhibitors (TKIs), including nilotinib and bosutinib and showed that they reduce the

84 ited high levels of endogenous TDP-43, while nilotinib and bosutinib did not alter TDP-43, underscori

85 The second-line inhibitors nilotinib and dasatinib are effective in patients with i

86 proved ABL tyrosine kinase inhibitors (TKIs) nilotinib and dasatinib, along with investigational TKIs

87 -ABL KD mutant at relevant concentrations of nilotinib and dasatinib, consistent with a central role

88 However, in primary CD34(+) CML cells, nilotinib and IM were equipotent for inhibition of BcrAb

89 = .108) and 22.1% vs 8.7% of patients in the nilotinib and imatinib arms, respectively (P = .0087).

90 s 20.8% and 29.2% vs 3.6% of patients in the nilotinib and imatinib arms, respectively.

91 ts in reversal of the suppressive effects of nilotinib and imatinib mesylate on leukemic progenitor c

92 clinically used tyrosine kinase inhibitors, nilotinib and osimertinib.

93 Recent reports of cardiovascular AEs with nilotinib and particularly ponatinib and of pulmonary ar

94 The effects of nilotinib and PKC412, alone and combined, were investiga

95 persisted and accumulated over 72 hours with nilotinib and remained caspase-3 negative.

96 imatinib (or the chemically related compound nilotinib) and responded; however, selection for compoun

97 atients, 271 received imatinib, 105 received nilotinib, and 107 received dasatinib.

98 ts on imatinib, or second-line dasatinib and nilotinib, and 24 controls.

99 ve percent of patients on bosutinib, 100% on nilotinib, and 33% on imatinib had normal platelet aggre

100 of the tyrosine kinase inhibitors imatinib, nilotinib, and dasatinib on B. malayi adult males, adult

101 15I) mutant is highly resistant to imatinib, nilotinib, and dasatinib, and is frequently detected in

102 ) for front-line treatment of CML: imatinib, nilotinib, and dasatinib.

103 BL mutation mediates resistance to imatinib, nilotinib, and dasatinib.

104 mycophenolate mofetil, rituximab, abatacept, nilotinib, and fresolimumab.

105 The effects of PKC412, nilotinib, and imatinib, alone and in combination, were

106 of 3 tyrosine kinase inhibitors, PKC412 and nilotinib, and imatinib, on 2 GIST-related PDGFRA mutant

107 Conclusions and Relevance: Dasatinib, nilotinib, and ponatinib increase vascular occlusive eve

108 eractions of bosutinib, dasatinib, imatinib, nilotinib, and ponatinib with recombinant hNTs (hENT1, 2

109 irdine, etravirine, felodipine, nicardipine, nilotinib, and sorafenib) or low micromolar range (abira

110 ivity of group 2 ATRT cells to dasatinib and nilotinib, and suggest that these are promising therapie

111 her arterial disorders in patients receiving nilotinib, and venous and arterial vascular occlusive ev

112 A similar risk was also suspected with nilotinib, another BCR-ABL tyrosine kinase inhibitor (TK

113 clinical benefits observed with switching to nilotinib are associated with improved long-term surviva

114 the second-line Abl inhibitors dasatinib and nilotinib are faring in the treatment of imatinib-resist

115 Dasatinib and nilotinib are potent tyrosine kinase inhibitors (TKIs) w

116 BMS-354825 (dasatinib) and AMN107 (nilotinib) are potent alternate Abl inhibitors with acti

117 No patient in the nilotinib arm lost CCyR, vs 3 in the imatinib arm.

118 Adverse events were more common in the nilotinib arm, as expected with the introduction of a ne

119 ents in the imatinib arm vs 3% and 7% in the nilotinib arms had EMR failure.

120 with EMR and found distinct patterns in the nilotinib arms vs the imatinib arm.

121 These results support nilotinib as a first-line treatment option for patients

122 The data also support the use of nilotinib as a treatment option for V561D-PDGFRA-associa

123 y Hh pathway inhibition, in combination with nilotinib, as a potentially effective therapeutic strate

124 nsplant donor, should one offer dasatinib or nilotinib before recommending a transplantation?

125 f the ABCG2 inhibitors Ko143, gefitinib, and nilotinib, but not an ABCB1 inhibitor.

126 the tyrosine kinase inhibitors, imatinib and nilotinib, by BAG956 was demonstrated against BCR-ABL ex

127 Phase 1/2 clinical trials show that nilotinib can induce remissions in patients who have pre

128 -generation inhibitors such as dasatinib and nilotinib can overcome the majority of these mutations b

129 Nilotinib cannot be recommended for broad use to treat f

130 Nilotinib continues to show better efficacy than imatini

131 identify patient subsets for whom first-line nilotinib could be of clinical benefit.

132 nts at diagnosis (n = 21), on TKI (imatinib, nilotinib, dasatinib) before achieving major molecular r

133 The second generation of Bcr-Abl inhibitors nilotinib, dasatinib, and bosutinib developed to overrid

134 ular responses by the second-generation TKIs nilotinib, dasatinib, and bosutinib.

135 of clinically important ABL TKIs (imatinib, nilotinib, dasatinib, ponatinib, and DCC-2036), we inter

136 s and confer varying resistance to imatinib, nilotinib, dasatinib, ponatinib, rebastinib, and bosutin

137 inferior responses previously observed with nilotinib/dasatinib therapy for imatinib-resistant patie

138 Nilotinib decreased soluble and insoluble TDP-43, while

139 inistration of the tyrosine kinase inhibitor nilotinib decreases Abl activity and ameliorates autopha

140 Nilotinib did not induce cellular apoptosis.

141 rt 2 patients failing any target switched to nilotinib directly, as did patients with intolerance or

142 receiving dasatinib, and 27 (25%) receiving nilotinib discontinued treatment for any reason.

143 Both imatinib and nilotinib displayed potent activity in vitro against the

144 inase activity with the c-Abl/Arg inhibitor, nilotinib, dramatically inhibits metastasis in a mouse m

145 developed resistance against vincristine or nilotinib, drugs with distinct cytotoxic mechanisms.

146 ntinued imatinib (n = 103) in the Evaluating Nilotinib Efficacy and Safety in clinical Trials-Complet

147 based on 4 years of follow up in Evaluating Nilotinib Efficacy and Safety in Clinical Trials-Newly D

148 We present data from the Evaluating Nilotinib Efficacy and Safety in clinical Trials-newly d

149 In summary, switching to nilotinib enabled more patients with chronic myeloid leu

150 es in alpha-synuclein expressing brains, but nilotinib enhances protein deposition into the lysosomes

151 ed targeted therapies - imatinib, dasatinib, nilotinib, erlotinib, sunitinib, lapatinib, bortezomib,

152 ith 3 TKIs: 34 with dasatinib after imatinib/nilotinib failure and 14 with nilotinib after imatinib/d

153 in 2006 and 2007, approval of dasatinib and nilotinib followed for use in imatinib-resistant or into

154 sequential treatment with both dasatinib and nilotinib for a total of 146 instances.

155 2 microM for dasatinib, and 81.35 microM for nilotinib; for L3 larvae, 11.27 microM, 13.64 microM, an

156 ths was achieved by 48 of 96 patients in the nilotinib group (50%, 95.18% CI 40-61) and 40 of 95 in t

157 group (59.2% [95% CI 50.9-66.5]) than in the nilotinib group (51.6% [43.0-59.5]; hazard ratio 1.47 [9

158 er crossover, 48 (50%) of 96 patients in the nilotinib group and 34 (36%) of 95 patients in the imati

159 Seven (7%) of 96 patients died in the nilotinib group and five (5%) of 93 patients died in the

160 e reported in 11 (11%) of 96 patients in the nilotinib group and nine (10%) of 93 patients in the ima

161 d elevated lipase level (15; 5%), and in the nilotinib group were anaemia (18; 6%), elevated lipase l

162 1 [4%] in the imatinib group, 14 [4%] in the nilotinib group).

163 tinib group, n=1 [1%]), and QT prolongation (nilotinib group, n=1 [1%]; imatinib group, n=1 [1%, afte

164 matinib group, n=1 [1%]), blast cell crisis (nilotinib group, n=1 [1%]; imatinib group, n=1 [1%]), an

165 ring in more than one patient were headache (nilotinib group, n=2 [2%, including 1 after crossover to

166 Significantly more patients in the nilotinib groups achieved a complete molecular response

167 CML-related deaths had occurred in both the nilotinib groups than in the imatinib group (five with n

168 reatment, including clonal evolution, in the nilotinib groups than in the imatinib group (two with ni

169 BL1 (IS) of > 1% to </= 10% at 3 months with nilotinib had higher cumulative incidence of CCyR by 24

170 Nilotinib has a relatively favorable safety profile and

171 Nilotinib has shown greater efficacy than imatinib in pa

172 Nilotinib has significant efficacy in patients with newl

173 Dasatinib and nilotinib have proven to be highly effective alternate a

174 of phase I and II trials with dasatinib and nilotinib have provided promising data that may reduce d

175 argeted therapies (e.g. imatinib, dasatinib, nilotinib) have been developed to treat Chronic Myeloid

176 t in CML SPCs and endorse the current use of nilotinib in combination with RUX in clinical trials to

177 gated the occurrence of cross-intolerance to nilotinib in imatinib-intolerant patients with CML.

178 The favorable tolerability of nilotinib in patients with imatinib intolerance leads to

179 is known about immune-modulatory effects of nilotinib in vivo, potentially predicting response to th

180 e identified with imatinib mesylate, 10 with nilotinib (including only 1 novel mutation, E292V) and 9

181 Importantly, imatinib and nilotinib increased tyrosine phosphorylation of p130Cas,

182 Nilotinib induced a major cytogenetic response in 66% an

183 ciated protein 1 light chain 3 revealed that nilotinib induced autophagy in a dose- and time-dependen

184 ients on TKI or with imatinib, dasatinib, or nilotinib induced significant and dose-dependent inhibit

185 Our data indicate that nilotinib-induced AMPK activation is mediated by PP2A, a

186 Up-regulating PP2A activity suppressed nilotinib-induced AMPK phosphorylation and autophagy, su

187 dephosphorylation, and enhanced imatinib- or nilotinib-induced growth inhibition in primary CD34(+) m

188 Imatinib and nilotinib-induced tyrosine phosphorylation was dependent

189 Together, our results reveal that nilotinib induces autophagy, but not apoptosis in HCC, a

190 Moreover TNF-alpha inhibition combined with nilotinib induces significantly more apoptosis relative

191 dividually in yeast Saccharomyces cerevisiae Nilotinib inhibited hENT1-mediated uridine transport mos

192 Preventive therapy using imatinib or nilotinib inhibited the development of sclerodermatous c

193 nhibitor, used alone and in combination with nilotinib, inhibited the Hh pathway in CD34(+) CP-CML ce

194 Nilotinib inhibits the tyrosine kinase activity of ABL1/

195 uantification of two TKI drugs (imatinib and nilotinib) inside living cells using hyperspectral stimu

196 Nilotinib is a potent selective inhibitor of the BCR-ABL

197 Nilotinib is an effective option for the initial managem

198 Nilotinib is an orally available receptor tyrosine kinas

199 med that, like IM, the predominant effect of nilotinib is antiproliferative rather than proapoptotic.

200 agnosed CML and those resistant to imatinib, nilotinib is effective and well-tolerated for long-term

201 This study indicates that nilotinib is effective, with a manageable safety profile

202 In summary, nilotinib is highly active and safe in patients with CML

203 rget kinase, the combination of imatinib and nilotinib is highly efficacious in these models, indicat

204 Nilotinib is used for adult leukemia treatment and it en

205 rapy with imatinib (IM), dasatinib (DAS), or nilotinib is very effective in chronic-phase chronic mye

206 mice; however, the combination of ABL001 and nilotinib led to complete disease control and eradicated

207 Overall, nilotinib led to fewer treatment-emergent BCR-ABL mutati

208 of 104 for dasatinib vs 99 [93%] of 107 for nilotinib), major molecular response (51 [76%] vs 171 [8

209 These data suggest that nilotinib may be a therapeutic strategy to degrade alpha

210 ts in metastatic melanoma, and indicate that nilotinib may be useful in preventing metastasis in pati

211 MP2 suggesting that the protective effect of nilotinib may, in part, be parkin-independent or to the

212 842V-PDGFRA probably limits the potential of nilotinib monotherapy for D842V-PDGFRA-associated GIST.

213 alyzed the outcome of 113 patients receiving nilotinib (n = 43) or dasatinib (n = 70) after imatinib

214 ), bosutinib (n = 32), imatinib (n = 19), or nilotinib (n = 9).

215 he ENEST1st clinical study, investigating 52 nilotinib-naive patients with chronic-phase CML.

216 34(+) cells, and in combination with the TKI nilotinib (NIL) significantly enhanced inhibition of pro

217 suggesting that PP2A mediates the effect of nilotinib on AMPK phosphorylation and autophagy.

218 This study investigated the effect of nilotinib on HCC.

219 We investigated the effects of imatinib and nilotinib on human NK cells, monocytes, and macrophages.

220 farction was higher in patients treated with nilotinib or dasatinib (29 and 19 per 1000 person-years,

221 (160 nmol/L) in dual combination with either nilotinib or dasatinib achieved the same zero outgrowth

222 c significance for subsequent treatment with nilotinib or dasatinib as second-line therapy.

223 Equal numbers of patients received nilotinib or dasatinib following imatinib, and 18 receiv

224 Phase III studies comparing imatinib with nilotinib or dasatinib in newly diagnosed CML were publi

225 Combining SGX393 with nilotinib or dasatinib preempted emergence of resistant

226 and F359V/C) predict failure of second-line nilotinib or dasatinib therapy in patients with chronic

227 matinib-resistant patients before they began nilotinib or dasatinib therapy.

228 eloid leukemia in chronic phase treated with nilotinib or imatinib based on 4 years of follow up in E

229 small molecule inhibitors such as imatinib, nilotinib or sunitinib can result in clinical, radiologi

230 unacceptable side effects from dasatinib or nilotinib or who had the BCR-ABL T315I mutation.

231 th dasatinib (OR, 3.86; 95% CI, 1.33-11.18), nilotinib (OR, 3.42; 95% CI, 2.07-5.63), and ponatinib (

232 atients who received 400 or 800 mg imatinib, nilotinib, or dasatinib were analyzed.

233 We recommend as initial treatment imatinib, nilotinib, or dasatinib.

234 cute lymphoblastic leukemia (ALL) to receive nilotinib orally at doses of 50 mg, 100 mg, 200 mg, 400

235 (imatinib 800 mg p=0.029, dasatinib p=0.003, nilotinib p=0.031).

236 18 (imatinib mesylate) and -0.042 +/- 0.015 (nilotinib) per day represents the turnover rate of leuke

237 (imatinib mesylate) and -0.0019 +/- 0.0013 (nilotinib) per day represents the turnover rate of leuke

238 Pharmacological inhibition of ZAK by nilotinib, preventing ZAK-autophosphorylation and thereb

239 When combined, LDE225 + nilotinib reduced CD34(+) CP-CML cell engraftment in NSG

240 pecific and potent tyrosine kinase inhibitor nilotinib, reduced the activity of the JAK2/STAT5 pathwa

241 Our results show that administration of nilotinib reduces c-Abl activation and the levels of the

242 leukemia in chronic phase from the phase II nilotinib registration study with available postbaseline

243 nase inhibitors (TKIs) imatinib mesylate and nilotinib represents a successful application of molecul

244 ncluding those associated with dasatinib and nilotinib resistance, except T315I.

245 We developed an in vitro model of Nilotinib-resistant Ph+ leukemia cells to investigate wh

246 g or the second-generation TKIs dasatinib or nilotinib resulted in superior and deeper responses than

247 riety of BCR-ABL+ cell lines to imatinib and nilotinib results in additive or synergistic cytotoxicit

248 atinib treatment were imatinib-resistant and nilotinib-sensitive.

249 hen combined with either imatinib or PKC412, nilotinib showed no evidence for antagonism and acted in

250 mozide and the kinase inhibitors imatinib or nilotinib shows enhanced effects in inhibiting STAT5 pho

251 activity both strongly reduced imatinib and nilotinib stimulated invasion.

252 nts treated with a novel sequential imatinib/nilotinib strategy aimed at achievement of optimal molec

253 with imatinib and the closely-related drug, nilotinib, strikingly increases tyrosine phosphorylation

254 h the ATP-competitive inhibitors imatinib or nilotinib, suppressed the emergence of resistance mutati

255 e.g., E255K, M351T) or to IM, dasatinib, and nilotinib (T315I) remained fully sensitive to sorafenib.

256 patients had a major molecular response with nilotinib than with imatinib (201 [71%] with nilotinib 3

257 ic and molecular responses with switching to nilotinib than with imatinib dose escalation, although t

258 Nilotinib therapy may induce perifollicular inflammation

259 Augmentation of LDR and Nilotinib therapy seems to be beneficial to control Ph+

260 ly reduced in mice that received imatinib or nilotinib therapy, but not in mice that received prednis

261 At month 6 during nilotinib therapy, CD62L expression returned to levels o

262 ML and a patient cohort receiving first-line nilotinib therapy, we found that successful long-term th

263 lp and body hair within weeks after starting nilotinib therapy.

264 were strongly associated with EMR failure in nilotinib-treated, but not imatinib-treated, patients.

265 eterized by cell viability experiments under Nilotinib treatment and LDR, to explain the cellular res

266 Imatinib and nilotinib treatment increased two dimensional cell migra

267 Imatinib, dasatinib, and nilotinib treatment of scleroderma and normal fibroblast

268 hatase PP2A inactivation were detected after nilotinib treatment.

269 Of 321 patients, 124 (39%) continue on nilotinib treatment.

270 diagnosis and significantly decreased during nilotinib treatment.

271 Moreover, nilotinib up-regulated the phosphryaltion of AMP-activat

272 designed to test the efficacy and safety of nilotinib versus imatinib as first-line therapy for pati

273 gate the safety and efficacy of switching to nilotinib vs imatinib dose escalation for patients with

274 K562, the inhibitory concentration (IC50) of nilotinib was 30 nM versus 600 nM for IM, consistent wit

275 In this phase 2 open-label study, 400 mg nilotinib was administered orally twice daily to 280 pat

276 The safety profile of nilotinib was consistent with other reported studies.

277 Nilotinib was effective in patients harboring BCR-ABL mu

278 cular response and longer-term outcomes with nilotinib was examined.

279 Of note, imatinib and nilotinib were also effective for treatment of experimen

280 eiving first-line or subsequent dasatinib or nilotinib who stopped therapy after at least 3 years of

281 However, a combination of nilotinib with an allosteric type IV inhibitor was recen

282 Furthermore, nilotinib with IM led to further accumulation of this po

283 to evaluate clofarabine with bortezomib and nilotinib with paclitaxel in patients with advanced canc

284 d with imatinib followed by dasatinib and/or nilotinib, with a median follow-up of 28.5 months.