ライフサイエンスコーパス: ruxolitinib

1 interest before, and 72 weeks after starting ruxolitinib.

2 reatment with the janus kinase 1/2 inhibitor ruxolitinib.

3 AT1 GOF mutations were treated in vitro with ruxolitinib.

4 ibrosis is the dual JAK1 and JAK2 inhibitor, ruxolitinib.

5 sponses or haematological toxic effects with ruxolitinib.

6 >/=3 mutations are less likely to respond to ruxolitinib.

7 t drugs, either alone or in combination with ruxolitinib.

8 revented by the Janus kinase (JAK) inhibitor ruxolitinib.

9 introduction of the JAK1 and JAK2 inhibitor ruxolitinib.

10 e treated with a clinically relevant dose of ruxolitinib.

11 t that was abrogated by the JAK1/2 inhibitor ruxolitinib.

12 dependency and sensitizes leukemic cells to ruxolitinib.

13 6 patients with steroid-refractory GVHD with ruxolitinib.

14 d was impaired by the Janus kinase inhibitor ruxolitinib.

15 lar subsets of patients with MF treated with ruxolitinib.

16 018, 71 patients received at least 1 dose of ruxolitinib.

17 toxic concentrations of the JAK1/2 inhibitor ruxolitinib.

18 that is reverted by the JAK1/JAK2 inhibitor ruxolitinib.

19 survival at 2 months from the first dose of ruxolitinib.

20 ibition enhances responsiveness of tumors to ruxolitinib.

21 fter immunosuppressive therapy that included ruxolitinib.

22 Herein the core features of ruxolitinib (1), a marketed JAK1/2 inhibitor, have been

23 ng a validated system to receive either oral ruxolitinib 10 mg twice daily or investigator-selected b

24 al comparing the efficacy and safety of oral ruxolitinib (10 mg twice daily) with the investigator's

25 ith splenomegaly, in a 1:1 ratio, to receive ruxolitinib (110 patients) or standard therapy (112 pati

26 35%) acquired a new mutation while receiving ruxolitinib (14 [61%] in ASXL1).

27 Patients received oral ruxolitinib (15 mg twice a day) on a continuous 28-day c

28 omly assigned 1:1 to the JAK1/JAK2 inhibitor ruxolitinib (15 mg twice daily) plus capecitabine (1,000

29 e 3 or greater anemia was more frequent with ruxolitinib (15.3%; placebo, 1.7%).

30 p of 79 months, 86 patients had discontinued ruxolitinib (30 of whom died while on therapy).

31 were observed with similar frequency in the ruxolitinib (74.6%) and placebo (81.7%) groups.

32 Ruxolitinib, a JAK 1 and JAK 2 inhibitor, showed superio

33 imed to determine the activity and safety of ruxolitinib, a JAK inhibitor, in adults with secondary h

34 ranscription (JAK-STAT) signaling pathway by ruxolitinib, a JAK-STAT-specific inhibitor.

35 Importantly, Ruxolitinib, a JAK1 inhibitor, could rescue the phenotyp

36 Of note, ruxolitinib, a JAK1/2 inhibitor approved for the treatme

37 Finally, ruxolitinib, a JAK1/2 inhibitor, was effective in vivo i

38 Ruxolitinib, a Janus kinase (JAK) 1 and 2 inhibitor, was

39 In the pivotal RESPONSE study, ruxolitinib, a Janus kinase (JAK)1 and JAK2 inhibitor, w

40 nt with C188-9, a STAT3/5 inhibitor, or with ruxolitinib, a Janus kinase 1/2 (JAK1/2) inhibitor.

41 Ruxolitinib, a selective inhibitor of Janus kinase 1 and

42 In a phase 2 trial, ruxolitinib, a selective Janus kinase (JAK1 and JAK2) in

43 th a smaller number of infused cells; Epo or ruxolitinib administration could be used to adjust their

44 Here we investigated whether ruxolitinib affects dendritic cell (DC) biology.

45 g best available therapy could cross over to ruxolitinib after week 32.

46 As predicted, ruxolitinib alone had no significant antileukemic effect

47 d reduced bone marrow fibrosis compared with ruxolitinib alone.

48 Eight weeks-treatment with ruxolitinib, an FDA-approved JAK1/2 inhibitor, reduced c

49 Moreover, ruxolitinib, an inhibitor of IFN-triggered Janus kinase/

50 Notably, three patients treated with oral ruxolitinib, an inhibitor of JAK1 and JAK2, achieved nea

51 of differing hydrophilicities, acarbose and ruxolitinib and 16 ILs, the dependence of skin penetrati

52 ol was achieved in 60% of patients receiving ruxolitinib and 20% of those receiving standard therapy;

53 4 patients were randomly assigned to receive ruxolitinib and 75 to receive best available therapy.

54 r 100 patient-years of exposure were 8.0 for ruxolitinib and 8.2 for the crossover population).

55 r 100 patient-years of exposure were 8.9 for ruxolitinib and 8.8 for the crossover population), thoug

56 In both models, ruxolitinib and alphaIFN-gamma reduced inflammation-asso

57 day 28, 24 (55.8%) of 43 patients receiving ruxolitinib and corticosteroids had a 50% or greater cor

58 lic events occurred in one patient receiving ruxolitinib and in six patients receiving standard thera

59 JAK1/2 inhibitors (such as ruxolitinib and JAK inhibitor I) strongly stimulate VSV

60 val, some have disease that is refractory to ruxolitinib and many lose their response over time.

61 st available therapy crossed over to receive ruxolitinib and no patient remained on best available th

62 that novel combinations of JAK2 inhibitors (ruxolitinib and pacritinib) with SMO inhibitors (vismode

63 Moreover, combining VSV with ruxolitinib and Polybrene or DEAE-dextran successfully b

64 ithm is uncertain, given the availability of ruxolitinib and renewed interest in interferons.

65 profile was consistent with expectations for ruxolitinib and this patient population.

66 JAK inhibitors (ruxolitinib and tofacitinib) inhibited the growth of pro

67 inhibition of JAK2/STAT3 and MEK/ERK/1/2 by ruxolitinib and trametinib potentiated tumor response to

68 tumor-bearing mice, whereas BV combined with ruxolitinib and/or with Navitoclax resulted in a sustain

69 fety and efficacy of JAK inhibitors, such as ruxolitinib, and evaluate their role in the context of o

70 Moreover, the combination of BMN673, ruxolitinib, and hydroxyurea was highly effective in viv

71 The combination of dasatinib, ruxolitinib, and the corticosteroid dexamethasone yielde

72 OR and JAK2 rearrangements were sensitive to ruxolitinib, and the ETV6-NTRK3 fusion was sensitive to

73 symptoms, as well as the risk of developing ruxolitinib-associated anemia and thrombocytopenia, occu

74 s who had a grade >=3 treatment-emergent and ruxolitinib-attributed adverse event that did not resolv

75 fter at least 5 to 10 days of treatment with ruxolitinib, based either on objective increase in stage

76 d efficacy of ruxolitinib, it is likely that ruxolitinib-based combinations will be a major way forwa

77 Momelotinib but not ruxolitinib blocked cytokine-induced proliferation of CL

78 ion (CDH1, SNAI2, TWIST1, and beta catenin); ruxolitinib blocked these effects.

79 tion by hydroxyurea and JAK1/2 inhibition by ruxolitinib, both of which are not curative.

80 gnificantly reduced following treatment with ruxolitinib, but they remained unchanged or were increas

81 00 mg once a day or BAT (which could include ruxolitinib, chemotherapy, steroids, no treatment, or ot

82 Either ruxolitinib combined with Navitoclax or BV alone prolong

83 maintained ERK activation in the presence of ruxolitinib, consistent with its function as a ligand-in

84 The findings of this study indicate that ruxolitinib could be considered a standard of care for s

85 r very good partial response at day 28 after ruxolitinib could be considered as an eligibility criter

86 active response technology system to receive ruxolitinib cream (1.5% twice daily, 1.5% once daily, 0.

87 t-related adverse event among patients given ruxolitinib cream (one [3%] of 33 in the 1.5% twice dail

88 ent in 13 (10%) of 125 patients who received ruxolitinib cream and one (3%) of 32 patients who receiv

89 reached by significantly more patients given ruxolitinib cream at 1.5% twice daily (15 [45%] of 33) a

90 24 were re-randomised to one of three higher ruxolitinib cream doses (0.5% once daily, 1.5% once dail

91 We investigated the therapeutic potential of ruxolitinib cream in patients with vitiligo and report t

92 These data suggest that ruxolitinib cream might be an effective treatment option

93 Treatment with ruxolitinib cream was associated with substantial repigm

94 eviously, we reported that the JAK inhibitor ruxolitinib dampens T-cell activation and lessens inflam

95 In mice, ruxolitinib decreased basal and GH-stimulated STAT5 phos

96 on of STAT3 activity using the JAK inhibitor ruxolitinib decreases breast cancer invasion in vivo.

97 e considered as refractory to ruxolitinib vs ruxolitinib dependent.

98 The median follow-up after ruxolitinib discontinuation for the remaining 56 patient

99 Here we describe outcomes after ruxolitinib discontinuation in MF patients enrolled in a

100 In vivo, ruxolitinib displayed activity in 6 of 6 patient-derived

101 od cell transfusions while on ruxolitinib or ruxolitinib dose reduction to less than 20 mg twice a da

102 LKB1-defcient mice with the JAK1/2 inhibitor ruxolitinib dramatically decreased polyposis.

103 singly, both JAK/STAT pathway activation and ruxolitinib efficacy were independent of the presence of

104 an adenoviral infection model, we show that ruxolitinib-exposed mice exhibit delayed adenoviral clea

105 After ruxolitinib failure, however, there are few therapeutic

106 atabase of patients who began treatment with ruxolitinib for MPNs from January 2010 to March 2017.

107 nduced murine model of CP, administration of ruxolitinib for one week significantly reduced biomarker

108 the dual Janus kinase 1/2 (JAK1/2) inhibitor ruxolitinib for the treatment of myeloproliferative neop

109 ection was reported in 6% of patients in the ruxolitinib group and 0% of those in the standard-therap

110 omization; 154 patients were assigned to the ruxolitinib group and 155 to the control group.

111 ytopenia (in 50 of 152 patients [33%] in the ruxolitinib group and 27 of 150 [18%] in the control gro

112 loss of response at 6 months was 10% in the ruxolitinib group and 39% in the control group.

113 dian overall survival was 11.1 months in the ruxolitinib group and 6.5 months in the control group (h

114 ssion was achieved in 24% of patients in the ruxolitinib group and 9% of those in the standard-therap

115 iagnosis was 8.2 years (IQR 3.9-12.3) in the ruxolitinib group and 9.3 years (4.9-13.8) in the best a

116 Patients randomly assigned to the ruxolitinib group received the drug orally at a starting

117 overall response at day 56 was higher in the ruxolitinib group than in the control group (40% [61 pat

118 Overall response at day 28 was higher in the ruxolitinib group than in the control group (62% [96 pat

119 Thromboembolic events were lower in the ruxolitinib group than the best available therapy group.

120 t was achieved in 21% of the patients in the ruxolitinib group versus 1% of those in the standard-the

121 ) and angina pectoris (two [3%] of 74 in the ruxolitinib group vs none in the best available therapy

122 ause, included thrombocytopenia (none in the ruxolitinib group vs two [3%] of 75 in the best availabl

123 y grade were anaemia (ten [14%] of 74 in the ruxolitinib group vs two [3%] of 75 in the best availabl

124 In the ruxolitinib group, grade 3 or 4 anemia occurred in 2% of

125 Among 25 primary responders in the ruxolitinib group, six had progressed at the time of fin

126 There were two on-treatment deaths in the ruxolitinib group.

127 Patients treated with ruxolitinib had a higher systolic blood pressure, serum

128 Patients receiving ruxolitinib had longer survival (5 years, 95% confidence

129 However, although ruxolitinib has changed the therapeutic scenario of MF,

130 011, the Janus kinase 1/2 (JAK1/2) inhibitor ruxolitinib has evolved to become the centerpiece of the

131 Ruxolitinib has shown success in alleviating the symptom

132 ological blockade of Jak-Stat signaling with ruxolitinib has significant antileukemic activity in thi

133 anus kinase 1/2 (JAK1/2) inhibitors, such as ruxolitinib, have been developed as immunosuppressive ag

134 Mechanistically, we could show that ruxolitinib impaired differentiation of CD4(+) T cells i

135 our findings offer compelling evidence that ruxolitinib impairs NK cell function in MPN patients, of

136 Ruxolitinib improved survival independent of mutation pr

137 tes JAK2 in CLL cells and the JAK2 inhibitor ruxolitinib improves symptoms in patients with myelofibr

138 We conducted a phase II study of ruxolitinib in 44 patients (21 CNL and 23 aCML).

139 BAT was ruxolitinib in 46 (89%) of 52 patients.

140 rt of patients with MF who were treated with ruxolitinib in a phase 1/2 study.

141 an open-label, single-centre, pilot study of ruxolitinib in adults with secondary haemophagocytic lym

142 58-71% of patients treated with ruxolitinib in clinical trials so far have not achieved

143 studies to test the therapeutic efficacy of ruxolitinib in CLL are warranted.

144 tudy, we assessed the efficacy and safety of ruxolitinib in controlling disease in patients with poly

145 ossibility that the therapeutic potential of ruxolitinib in ETP-ALL extends beyond those cases with J

146 stablish the preclinical in vivo efficacy of ruxolitinib in ETP-ALL, a biologically distinct subtype

147 e of the Janus kinase 1/2 (JAK1/2) inhibitor ruxolitinib in murine models of hemophagocytic lymphohis

148 ative neoplasms (MPNs) has led to studies of ruxolitinib in other clinical contexts, including JAK-mu

149 safety and efficacy of the JAK1/2 inhibitor ruxolitinib in patients with CNL and aCML, irrespective

150 clinical trial to evaluate BV combined with ruxolitinib in select patients with HL.

151 to investigate the therapeutic potential of ruxolitinib in treating autoimmunity secondary to STAT1

152 he small-molecule Janus kinase 1/2 inhibitor ruxolitinib in vitro and in vivo restored perforin expre

153 ed sensitivity of JAK2-mutant progenitors to ruxolitinib in vitro.

154 ects were additive with the JAK1/2 inhibitor ruxolitinib in vivo and in vitro.

155 of mammary tumors to the JAK/STAT inhibitor ruxolitinib in vivo and that ruxolitinib-treated macroph

156 -acid substitutions conferring resistance to ruxolitinib (INCB018424) and cross-resistance to the JAK

157 b also reduced BCR signaling, in contrast to ruxolitinib, indicating that these JAK inhibitors in fac

158 In conclusion, we postulate that ruxolitinib-induced deficiencies in DSB repair pathways

159 Ruxolitinib inhibited 2 major DSB repair mechanisms, BRC

160 ation of CLL cells with the JAK1/2 inhibitor ruxolitinib inhibited IgM-induced STAT3 phosphorylation

161 ic studies revealed that in vivo exposure to ruxolitinib inhibited signal transducer and activation o

162 Ruxolitinib inhibits signaling downstream of IFN-gamma,

163 the incorporation of JAK inhibitors such as ruxolitinib into future clinical trials for patients wit

164 that patients with ruxolitinib-resistant or ruxolitinib-intolerant myelofibrosis might achieve signi

165 r, in patients with ruxolitinib-resistant or ruxolitinib-intolerant myelofibrosis.

166 We showed that ruxolitinib is a safe and effective long-term treatment

167 Ruxolitinib is a small-molecule inhibitor of the JAK kin

168 These preliminary data suggest that ruxolitinib is active, well tolerated, and manageable in

169 Ruxolitinib is an FDA approved janus kinase (JAK)1/2 inh

170 tion of increased STAT1 phosphorylation with ruxolitinib is an important option for therapeutic inter

171 Ruxolitinib is in late-phase clinical trials in essentia

172 The MAJIC-ET trial suggests that ruxolitinib is not superior to current second-line treat

173 The Janus kinase (JAK) inhibitor ruxolitinib is the only approved therapy for patients wi

174 -positive and JAK2-negative MF; one of them, ruxolitinib, is the current best available therapy for M

175 Given the proven safety and efficacy of ruxolitinib, it is likely that ruxolitinib-based combina

176 h AXL and JAK1 were sensitive to TP-0903 and ruxolitinib (JAK inhibitor) treatments, supporting the C

177 MAJIC is a randomized phase 2 trial of ruxolitinib (JAK1/2 inhibitor) vs best available therapy

178 Notably, despite discontinuation of ruxolitinib, LCMV-infected Prf1 (-/-) mice exhibited enh

179 This observation suggests that ruxolitinib may modify the natural history of PMF.

180 owed reduction of mutated allele burden, and ruxolitinib might extend survival of patients with highe

181 DM1 null tumours with the JAK/STAT inhibitor ruxolitinib mimics CADM1 gene restoration in preventing

182 s with myelofibrosis previously treated with ruxolitinib, momelotinib was not superior to BAT for the

183 tent inhibition of downstream signaling than ruxolitinib monotherapy.

184 2 patients were randomly assigned to receive ruxolitinib (n=110, 50%) or best available therapy (n=11

185 In the intent-to-treat population (ruxolitinib, n = 64; placebo, n = 63), the hazard ratio

186 in these studies, we analyzed the cohort of ruxolitinib-naive patients used for developing the dynam

187 ned, and it provides the highest delivery of ruxolitinib of all ILs tested here.

188 We also examined the effects of ruxolitinib on adipose tissue JAK/STAT signaling in a mo

189 -4 anaemia or thrombocytopenia occurred with ruxolitinib; one patient (1%) reported grade 3-4 anaemia

190 lammation-associated anemia, indicating that ruxolitinib operates in an IFN-gamma-dependent manner to

191 Thus, ruxolitinib operates through IFN-gamma-dependent and -in

192 ded 58 and 52 patients randomized to receive ruxolitinib or BAT, respectively.

193 were randomly assigned 1:1 to receive either ruxolitinib or best available therapy.

194 fficiently blocked by JAK inhibitors such as ruxolitinib or CMP6 in short-term assays.

195 e use of the two-agent combination of either ruxolitinib or Navitoclax with BV or the three-agent com

196 Treatment with ruxolitinib or PU-H71 improved survival of mice engrafte

197 equired red blood cell transfusions while on ruxolitinib or ruxolitinib dose reduction to less than 2

198 ducer and activator of transcription (STAT) (ruxolitinib) or mitogen-activated protein kinase kinase

199 ensitive to decitabine, the JAK1/2 inhibitor ruxolitinib, or the heat shock protein 90 inhibitor 8-(6

200 h baseline after >=14 days of treatment with ruxolitinib; or (3) loss of response, defined as objecti

201 Participants were given 10 mg ruxolitinib orally twice a day.

202 id-refractory aGVHD were eligible to receive ruxolitinib orally, starting at 5 mg twice daily plus co

203 IPSS risk have shown a survival advantage of ruxolitinib over placebo (COMFORT-1) or best available t

204 n mice were treated with the JAK-2 inhibitor ruxolitinib (P < 0.0001).

205 d PRO-related labeling (abiraterone acetate, ruxolitinib phosphate, and crizotinib).

206 Ruxolitinib plus capecitabine was generally well tolerat

207 Emerging concepts include the use of ruxolitinib pretransplant, optimizing MAC to decrease to

208 Ruxolitinib produced durable responses and encouraging s

209 The JAK1/JAK2 inhibitor ruxolitinib produced significant reductions in splenomeg

210 Although the Janus kinase inhibitor ruxolitinib provides symptomatic relief, it does not red

211 t common adverse event in patients receiving ruxolitinib (rates per 100 patient-years of exposure wer

212 lipopolysaccharide-induced maturation step, ruxolitinib reduced DC activation as demonstrated by dec

213 , melanocytes treated with the JAK inhibitor ruxolitinib reduced expression of HMGB1 and MX1 as well

214 reatment with the Janus kinase 1/2 inhibitor ruxolitinib reduced hyperresponsiveness to type I and II

215 In the present study the JAK1/2 inhibitor ruxolitinib reduced phosphorylation of STAT3 and STAT6 a

216 nt of cultured PSC with the Jak1/2 inhibitor ruxolitinib reduced STAT3 phosphorylation, cell prolifer

217 In vivo treatment with the Jak1/2 inhibitor ruxolitinib reduced the severity of experimental CP, sug

218 hock protein 90 (HSP90) inhibitor PU-H71 and ruxolitinib reduced total and phospho-JAK2 and achieved

219 Here, we propose to define ruxolitinib-refractory acute GVHD as disease that shows:

220 ated symptoms improved in patients receiving ruxolitinib relative to BAT.

221 In summary, ruxolitinib represents a novel targeted approach in GVHD

222 thrombocythaemia myelofibrosis, found to be ruxolitinib resistant or intolerant after at least 14 da

223 mary endpoint, suggesting that patients with ruxolitinib-resistant or ruxolitinib-intolerant myelofib

224 a JAK2-selective inhibitor, in patients with ruxolitinib-resistant or ruxolitinib-intolerant myelofib

225 and Janus kinase 2 (JAK2) with dasatinib and ruxolitinib, respectively.

226 Moreover, the JAK1/2 inhibitor ruxolitinib restored sensitivity to the BCL2 inhibitor v

227 ought to evaluate the efficacy and safety of ruxolitinib (RUX) cream in adults with AD.

228 e JAK/STAT pathway, and the JAK1/2 inhibitor ruxolitinib (RUX) has shown efficacy in murine HLH model

229 C-ET is a randomized phase 2 study comparing ruxolitinib (RUX) to best available therapy (BAT) in HC-

230 Similar observations were made with Ruxolitinib (Rux), a JAK-specific inhibitor.

231 Unexpectedly, another JAK inhibitor, ruxolitinib (RUX), was ineffective in 8 of 10 FED-respon

232 cells were treated with the JAK1/2 inhibitor ruxolitinib (RUX).

233 le of this pathway using the JAK2 inhibitor, ruxolitinib (RUX).

234 if some patients treated with interferon and ruxolitinib showed reduction of mutated allele burden, a

235 Our results demonstrate that ruxolitinib significantly affects DC differentiation and

236 models, treatment with the JAK1/2 inhibitor ruxolitinib significantly lessened the clinical and labo

237 with myelofibrosis (MF) derive benefit from ruxolitinib, some are refractory, have a suboptimal resp

238 cally relevant doses of the JAK1/2 inhibitor ruxolitinib suppresses the harmful consequences of macro

239 e-free survival was considerably longer with ruxolitinib than with control (5.0 months vs. 1.0 month;

240 13 mg/L), OS was significantly greater with ruxolitinib than with placebo (hazard ratio, 0.47; 95% C

241 re much more sensitive to the JAK inhibitor, ruxolitinib, than JAK2V617F-expressers, suggesting that

242 cts of the JAK1/2 inhibitors momelotinib and ruxolitinib, the BTK inhibitors ibrutinib and tirabrutin

243 analysis was performed to determine whether ruxolitinib therapy altered the JAK2p.V617F allele burde

244 rvival at 5 years was 91.9% (84.4-95.9) with ruxolitinib therapy and 91.0% (82.8-95.4) with best avai

245 Ruxolitinib therapy led to significant improvements in e

246 tors, and deletion of Jak2 following chronic ruxolitinib therapy markedly reduced mutant allele burde

247 ution or decreasing platelet counts while on ruxolitinib therapy may be markers of poor prognosis.

248 tem involvement was significantly reduced by ruxolitinib therapy.

249 ted by dual blockade with the JAK2 inhibitor ruxolitinib to a much greater extent than treatment with

250 We did a phase 2 trial of ruxolitinib to test this hypothesis.

251 /STAT inhibitor ruxolitinib in vivo and that ruxolitinib-treated macrophages produce soluble factors

252 We found a reduction in NK cell numbers in ruxolitinib-treated patients that was linked to the appe

253 ocrit control was achieved in 46 (62%) of 74 ruxolitinib-treated patients versus 14 (19%) of 75 patie

254 reased infection rates have been reported in ruxolitinib-treated patients, and natural killer (NK) ce

255 partial molecular response in CALR-positive ruxolitinib-treated patients.

256 Ruxolitinib-treated tumors in both the immunocompromised

257 rmore, more than 50% of patients discontinue ruxolitinib treatment after 3-5 years.

258 Ruxolitinib treatment also improves survival in the immu

259 Importantly, ruxolitinib treatment also significantly improved the su

260 a cohort of 28 MPN patients with or without ruxolitinib treatment and 24 healthy individuals.

261 Ruxolitinib treatment decreased peripheral blast counts

262 Patients who had myelofibrosis and previous ruxolitinib treatment for at least 28 days who either re

263 Conversely, ruxolitinib treatment in allo-HCT recipients increased F

264 d to determine the metabolic consequences of ruxolitinib treatment in patients with MPNs.

265 Combined gedatolisib and ruxolitinib treatment of CRLF2/JAK-mutant models more ef

266 Taken together, ruxolitinib treatment offers the first widely approved t

267 In vivo, ruxolitinib treatment suppressed signal transducer and a

268 e events were generally lower with long-term ruxolitinib treatment than with best available therapy.

269 ductions in allele burden from baseline with ruxolitinib treatment that correlated with spleen volume

270 Whether ruxolitinib treatment would benefit patients with CLL re

271 During ruxolitinib treatment, liver tissue damage receded conco

272 sible long-term side effects associated with ruxolitinib treatment.

273 of NK cells in MPN was further aggravated by ruxolitinib treatment.

274 s assessed by the investigator as related to ruxolitinib treatment.

275 omised, open-label, phase 3b study assessing ruxolitinib versus best available therapy in patients wi

276 study to evaluate the efficacy and safety of ruxolitinib versus standard therapy in patients with pol

277 ade 3 and 4 anemia occurred in 19% and 0% of ruxolitinib vs 0% (both grades) in the BAT arm, and grad

278 3 and 4 thrombocytopenia in 5.2% and 1.7% of ruxolitinib vs 0% (both grades) of BAT-treated patients.

279 reported in 27 (46.6%) patients treated with ruxolitinib vs 23 (44.2%) with BAT (P = .40).

280 lenomegaly and improvements in symptoms with ruxolitinib vs placebo at week 24.

281 hat would now be considered as refractory to ruxolitinib vs ruxolitinib dependent.

282 INTERPRETATION: In patients with CLL, ruxolitinib was associated with significant improvements

283 sis of a matrix screen of drug combinations, ruxolitinib was combined with the Bcl-2/Bcl-xL inhibitor

284 s a consequence, it remained unclear whether ruxolitinib was exerting its beneficial effects in HLH b

285 Treatment with ruxolitinib was followed by a prompt and sustained recov

286 Ruxolitinib was recently approved for the treatment of c

287 Although the JAK inhibitor ruxolitinib was recently approved for use in hydroxyurea

288 unacceptable side effects from hydroxyurea, ruxolitinib was superior to standard therapy in controll

289 Ruxolitinib was well tolerated and demonstrated an estim

290 identify genes that may predict response to ruxolitinib, we performed targeted next-generation seque

291 No serious adverse events attributed to ruxolitinib were observed.

292 ree compounds, roflumilast, tofacitinib, and ruxolitinib, were topically administered to the mouse ea

293 Moreover, combining VSV with polycations and ruxolitinib (which inhibits antiviral signaling) success

294 Food and Drug Administration (dasatinib and ruxolitinib, which inhibit BCR-ABL and Janus kinases, re

295 Moreover, ruxolitinib, which preferentially blocks JAK1 and JAK2,

296 compare the long-term safety and efficacy of ruxolitinib with best available therapy in patients with

297 ss this question, we compared the effects of ruxolitinib with those obtained using an IFN-gamma-neutr

298 from diagnosis of 100 PMF patients receiving ruxolitinib within COMFORT-2 with that of 350 patients o

299 ients with myelofibrosis, we postulated that ruxolitinib would improve disease-related symptoms in pa

300 d not resolve within 7 days of discontinuing ruxolitinib would serve as a clinical indication for add