ライフサイエンスコーパス: tofacitinib

1 erate to severe ulcerative colitis receiving tofacitinib.

2 quality of life and patient preferences for tofacitinib.

3 ion of germinal centers of mice treated with tofacitinib.

4 synthesis of the Janus kinase inhibitor (R)-tofacitinib.

5 second structurally unrelated Jak inhibitor, Tofacitinib.

6 patients with severe GA and is mitigated by tofacitinib.

7 developed in six patients who were receiving tofacitinib.

8 nd 58.3% had received >= 1 biologic prior to tofacitinib.

9 ependent manner, which was not observed with tofacitinib.

10 tocilizumab, and 1.47 (95% CI 0.54-3.27) for tofacitinib.

11 month follow-up, 84.9% of patients continued tofacitinib.

12 tient record forms for patients treated with tofacitinib.

13 ts with UC, including 642 patients receiving tofacitinib.

14 and tapinarof and the Janus kinase inhibitor tofacitinib.

15 in patients who received placebo followed by tofacitinib.

16 greater response rates were observed in the tofacitinib 0.001% twice daily (27.3%), 0.005% twice dai

17 ring (CCC; 100%) at week 8 was greatest with tofacitinib 0.005% once daily (15.9%) versus vehicle (6.

18 The tofacitinib 0.005% once daily group showed significant i

19 HLA-DR was observed in patients treated with tofacitinib 0.005% QD and 0.003% BID: 71% and 67% of bas

20 n tears was 36% of baseline (P=0.053) in the tofacitinib 0.005% QD group and 95% of baseline (P > 0.2

21 , and IL-12p70, were markedly reduced in the tofacitinib 0.005% QD group but not the vehicle group.

22 at week 8 (40% of baseline, P=0.035) in the tofacitinib 0.005% QD group, whereas the vehicle group s

23 domized in a 2:2:2:3:3 ratio to receive oral tofacitinib 0.5 mg, 3 mg, 10 mg, or 15 mg, or placebo tw

24 Tofacitinib (0.0003% twice daily, n = 46; 0.001% in both

25 Patients received 1 of 5 doses of tofacitinib (0.0003%, 0.001%, 0.003%, or 0.005% twice da

26 ients were assigned randomly to groups given tofacitinib (0.5, 3, 10, or 15 mg twice daily) or placeb

27 r endoscopic remission during induction with tofacitinib 10 mg BID may allow successful maintenance w

28 mg twice daily [BID] and 75.0% vs. 54.2% for tofacitinib 10 mg BID).

29 facitinib 5 mg group, ten (3%) of 330 in the tofacitinib 10 mg group, 11 (3%) of 335 in the etanercep

30 itinib 5 mg group, 210 (63.6%) of 330 in the tofacitinib 10 mg group, 197 (58.8%) of 335 in the etane

31 itinib 5 mg group, 225 (68.2%) of 330 in the tofacitinib 10 mg group, 222 (66.3%) of 335 in the etane

32 329 in the tofactinib 5 mg group, 330 in the tofacitinib 10 mg group, 335 in the etanercept group, an

33 acitinib 5 mg group, five (2%) of 330 in the tofacitinib 10 mg group, seven (2%) of 335 in the etaner

34 (330 to tofacitinib 5 mg twice daily, 332 to tofacitinib 10 mg twice daily, 336 to etanercept 50 mg t

35 65,050, $579,622, $750,200, and $787,998 for tofacitinib 10 mg, tofacitinib 5 mg, infliximab, vedoliz

36 y assigned to receive induction therapy with tofacitinib (10 mg twice daily) or placebo for 8 weeks.

37 r 1 month of treatment were compared between tofacitinib (10 mg two times a day) and etanercept (50 m

38 s adverse events for patients receiving 5-mg tofacitinib, 10-mg tofacitinib, or placebo were 6.9, 7.3

39 ne was significantly greater (P = 0.001) for tofacitinib 15 mg BID versus placebo.

40 For tofacitinib 15 mg BID, most patients reported satisfacti

41 4 patients), tocilizumab (2548 patients), or tofacitinib (1565 patients).

42 = 507) were randomized to receive placebo or tofacitinib (20 mg/day, 1 mg twice daily, 3 mg twice dai

43 rate by week 44 was significantly lower with tofacitinib (21 [29%] of 72 patients) than with placebo

44 mg BID may allow successful maintenance with tofacitinib 5 mg BID.

45 corded in 130 (39.5%) of 329 patients in the tofacitinib 5 mg group, 210 (63.6%) of 330 in the tofaci

46 hieved by 155 (47.1%) of 329 patients in the tofacitinib 5 mg group, 225 (68.2%) of 330 in the tofaci

47 curring in seven (2%) of 329 patients in the tofacitinib 5 mg group, five (2%) of 330 in the tofaciti

48 Three (1%) of 329 patients in the tofacitinib 5 mg group, ten (3%) of 330 in the tofacitin

49 domly assigned in a 3:3:3:1 ratio to receive tofacitinib 5 mg or 10 mg twice daily at about 12 h inte

50 eline MES of 0 versus 1 (61.9% vs. 36.5% for tofacitinib 5 mg twice daily [BID] and 75.0% vs. 54.2% f

51 ed them to the four treatment groups (330 to tofacitinib 5 mg twice daily, 332 to tofacitinib 10 mg t

52 750,200, and $787,998 for tofacitinib 10 mg, tofacitinib 5 mg, infliximab, vedolizumab, golimumab, ad

53 re randomly assigned (1:1:1) to receive oral tofacitinib (5 mg twice daily) monotherapy, oral tofacit

54 citinib (5 mg twice daily) monotherapy, oral tofacitinib (5 mg twice daily) plus methotrexate, or sub

55 ients were randomly assigned 4:4:1:1 to oral tofacitinib, 5 mg or 10 mg twice daily, or placebo advan

56 or 10 mg twice daily, or placebo advanced to tofacitinib, 5 mg or 10 mg twice daily.

57 er among patients receiving 5 mg or 10 mg of tofacitinib (51.5% and 52.6%, respectively) and among th

58 sis of GA and also evaluated the efficacy of tofacitinib (a Janus kinase 1/3 inhibitor) in 5 patients

59 pathway in malignant T cells, and blocked by tofacitinib, a clinical-grade JAK3 inhibitor.

60 ound with strong JAK2 inhibitor activity, or Tofacitinib, a clinically used selective JAK small molec

61 these results, the patient was treated with tofacitinib, a JAK inhibitor, leading to the rapid resol

62 ensitive to the cytokine-signaling inhibitor tofacitinib, a Janus kinase (JAK) inhibitor targeting JA

63 with cutaneous sarcoidosis are treated with tofacitinib, a Janus kinase inhibitor.

64 Tofacitinib, a novel, oral Janus kinase inhibitor, demon

65 n a 2:2:1:1 ratio, to four regimens: 5 mg of tofacitinib administered orally twice daily (132 patient

66 progressively reduced after days 1 and 3 of tofacitinib administration, respectively (eg, KRT16 decr

67 tofacitinib, and definite willingness to use tofacitinib again on the IBD PRTI at week 8.

68 Tofacitinib also inhibited the expression of IFN-gamma-i

69 erate to severe ulcerative colitis receiving tofacitinib, although at an individual level the agreeme

70 Tofacitinib, an oral Janus kinase inhibitor that targets

71 Tofacitinib, an oral Janus kinase inhibitor, is being in

72 Tofacitinib, an oral, small-molecule Janus kinase inhibi

73 CR20 response were 50% with the 5-mg dose of tofacitinib and 47% with the 10-mg dose, as compared wit

74 ccurred in 68 (77%) of 88 patients receiving tofacitinib and 63 (74%) of 85 in the placebo group.

75 cohort design compared patients treated with tofacitinib and adalimumab.

76 Tofacitinib and etanercept commonly reduced IL-6, CCL20,

77 se archived from a phase 3 clinical trial of tofacitinib and etanercept in adults with moderate-to-se

78 e event rates over 12 weeks were similar for tofacitinib and etanercept.

79 ascular events occurred in five who received tofacitinib and in none who received placebo; as compare

80 ancer occurred in five patients who received tofacitinib and in one who received placebo, and adjudic

81 Efficacy has been shown in phase III with tofacitinib and in phase II with fostamatinib and VX-509

82 alimumab and methotrexate (-6 [-14 to 3]) or tofacitinib and methotrexate (-8 [-16 to 1]).

83 INTERPRETATION: Tofacitinib and methotrexate combination therapy was non

84 Non-inferiority was declared for tofacitinib and methotrexate versus adalimumab and metho

85 monotherapy, 173 (46%) of 376 patients with tofacitinib and methotrexate, and 169 (44%) of 386 patie

86 nt (384 had tofacitinib monotherapy; 376 had tofacitinib and methotrexate; and 386 had adalimumab and

87 The results suggest that tofacitinib and other Janus kinase inhibitors may be eff

88 te a powerful synergism between CTLA4-Ig and tofacitinib and suggest their combined use is a promisin

89 X-509 and fostamatinib; lipid elevation with tofacitinib and VX-509; creatinine elevation and anemia

90 e series of 4 patients with PEM treated with tofacitinib and/or upadacitinib in 2015 to 2021 at the d

91 The JAK inhibitors CP-690,550 (tofacitinib) and INCB018424 (ruxolitinib) have demonstra

92 tacrolimus, mycophenolate (MPA), sirolimus, tofacitinib, and belatacept.

93 xtreme satisfaction, definite preference for tofacitinib, and definite willingness to use tofacitinib

94 VX-509; creatinine elevation and anemia with tofacitinib, and hypertension and diarrhea with fostamat

95 The three compounds, roflumilast, tofacitinib, and ruxolitinib, were topically administere

96 trametinib, the Janus kinase-STAT inhibitor tofacitinib, and the STAT5 inhibitor pimozide reversed s

97 with prior biologic exposure, upadacitinib, tofacitinib, and ustekinumab were ranked highest for ach

98 ted to autoimmune disorders and that topical tofacitinib application should be considered a strategy

99 We further evaluated the efficacy of tofacitinib as induction and maintenance therapy.

100 Tofacitinib, as well as antiviral agents, suppressed cul

101 n = 384) were randomized to receive placebo, tofacitinib at 1, 3, 5, 10, or 15 mg administered orally

102 eks (total of 6 injections) followed by oral tofacitinib at 5 mg twice a day for 12 weeks.

103 ose taken orally twice daily (107 patients), tofacitinib at a 10-mg dose taken orally twice daily (10

104 io to receive one of the following regimens: tofacitinib at a 5-mg dose taken orally twice daily (107

105 to MTX has been inadequate, the addition of tofacitinib at a dosage >/=3 mg twice daily showed susta

106 Treatment with tofacitinib at a dose of >/=3 mg twice a day resulted in

107 32%, 48%, 61%, and 78% of patients receiving tofacitinib at a dose of 0.5 mg (P=0.39), 3 mg (P=0.55),

108 13%, 33%, 48%, and 41% of patients receiving tofacitinib at a dose of 0.5 mg (P=0.76), 3 mg (P=0.01),

109 Patients were randomly assigned to receive tofacitinib at a dose of 0.5 mg, 3 mg, 10 mg, or 15 mg o

110 About one-third of patients (31.7%) stopped tofacitinib at one year, primarily for lack of efficacy

111 eased at baseline but reduced after 1 day of tofacitinib (baseline, median of 1290 pSTAT1(+) cells/mu

112 kidney transplantation patients treated with tofacitinib/basiliximab (n=5), calcineurin inhibitor (CN

113 nsplantation patients, 7 days after starting tofacitinib/basiliximab treatment, cytokine-induced P-ST

114 Short-term treatment with tofacitinib BID was associated with dose-dependent impro

115 eneralized vitiligo for which treatment with tofacitinib citrate, an oral Janus kinase 1/3 inhibitor,

116 reduced risk of ILD in patients treated with tofacitinib compared with patients treated with adalimum

117 High tofacitinib concentrations were independently associated

118 f the patients who received the 5-mg dose of tofacitinib continuously and in 6% who received the 10-m

119 range occurred in more patients who received tofacitinib continuously than in patients who received p

120 hemic stroke among the patients who received tofacitinib continuously.

121 This study indicates that in the future tofacitinib could provide a convenient and well-tolerate

122 nsive (MI) or less intensive (LI) regimen of tofacitinib (CP-690, 550), an oral Janus kinase inhibito

123 stigate how selective inhibition of JAK with tofacitinib (CP-690,550) affects osteoclast-mediated bon

124 gs targeting this pathway, the JAK inhibitor tofacitinib (CP-690,550) and the anti-interleukin (IL)-2

125 Tofacitinib (CP-690,550) is a novel oral Janus kinase in

126 Tofacitinib (CP-690,550) is a novel oral Janus kinase in

127 his study, we examined the mode of action of tofacitinib (CP-690,550) on JAK/STAT signaling pathways

128 One additional treatment may be tofacitinib (CP-690,550), an oral inhibitor of Janus kin

129 A new Janus kinase inhibitor, tofacitinib (CP-690550), has shown promising results for

130 This phase 1/2 study of tofacitinib demonstrated a trend for improving both sign

131 rom baseline for all tofacitinib groups, and tofacitinib demonstrated greater improvements than cyclo

132 Tofacitinib did not impact human osteoclast differentiat

133 Tofacitinib diminished the expansion and activation of m

134 cells with the Janus kinase (JAK) inhibitor tofacitinib disproportionately altered the expression of

135 Tofacitinib disrupted adventitial microvascular angiogen

136 20 response rates for patients receiving all tofacitinib dosages >/=3 mg twice daily (52.9% for 3 mg

137 ), placebo with a blinded switch to the 5-mg tofacitinib dose at 3 months (52), or placebo with a bli

138 r placebo with a blinded switch to the 10-mg tofacitinib dose at 3 months (53).

139 the placebo group that switched to the 5-mg tofacitinib dose, and 64% in the placebo group that swit

140 the placebo group that switched to the 10-mg tofacitinib dose.

141 eduction) from baseline was observed for all tofacitinib doses (-0.9 to -1.9) and vehicle (-2.0), but

142 tically significant (P<0.2, 2-sided) for all tofacitinib doses (1.7-3.1 mm), cyclosporine (3.9 mm), a

143 All tofacitinib doses were well tolerated, exhibiting better

144 In this study, we aimed to compare two tofacitinib doses with high-dose etanercept or placebo i

145 ing the inhibitor 1400W or the JAK inhibitor tofacitinib dramatically improved the in vitro HI phenot

146 es of herpes zoster in patients who received tofacitinib during the trial.

147 th predominantly biologically refractory UC, tofacitinib effectively induced clinical remission and e

148 Tofacitinib effectively suppressed innate and adaptive i

149 The JAK inhibitor tofacitinib effectively suppresses tissue-resident memor

150 assigned to receive maintenance therapy with tofacitinib (either 5 mg or 10 mg twice daily) or placeb

151 Intervention via tofacitinib enabled disease control and tapering of othe

152 All doses of tofacitinib exhibited a reasonable safety profile and we

153 In the entire tofacitinib exposure period, 107 (48%) of 225 patients h

154 cacy medication (eg, golimumab, ustekinumab, tofacitinib, filgotinib, and mirikizumab) rather than a

155 oral compounds including kinase inhibitors (tofacitinib, fostamatinib, VX-509), an S1P lyase inhibit

156 ge in the HAQ-DI score was -0.35 in the 5-mg tofacitinib group and -0.40 in the 10-mg tofacitinib gro

157 .0001), and 71.9% (15 mg; P < 0.0001) in the tofacitinib group and 35.9% of patients in the adalimuma

158 ccurred in 34.3% of the patients in the 5-mg tofacitinib group and 40.6% in the 10-mg tofacitinib gro

159 sponse rates at month 3 were 50% in the 5-mg tofacitinib group and 61% in the 10-mg tofacitinib group

160 ia for an ACR 20 response (59.8% in the 5-mg tofacitinib group and 65.7% in the 10-mg tofacitinib gro

161 y 28 occurred in 2.8% of the patients in the tofacitinib group and in 5.5% of those in the placebo gr

162 -mg tofacitinib group and 40.6% in the 10-mg tofacitinib group versus 11.1% in the placebo group (P<0

163 eks occurred in 18.5% of the patients in the tofacitinib group versus 8.2% in the placebo group (P=0.

164 -mg tofacitinib group and 65.7% in the 10-mg tofacitinib group vs. 26.7% in the combined placebo grou

165 events occurring in >10% of patients in any tofacitinib group were diarrhea, upper respiratory tract

166 events through month 12 was 66% in the 5-mg tofacitinib group, 71% in the 10-mg tofacitinib group, 7

167 the 5-mg tofacitinib group, 71% in the 10-mg tofacitinib group, 72% in the adalimumab group, 69% in t

168 -mg tofacitinib group and -0.40 in the 10-mg tofacitinib group, as compared with -0.18 in the placebo

169 5-mg tofacitinib group and 61% in the 10-mg tofacitinib group, as compared with 33% in the placebo g

170 losis developed in two patients in the 10-mg tofacitinib group.

171 ponse rates (month 6) for the 5-mg and 10-mg tofacitinib groups compared with the combined placebo gr

172 DI scores were greater in the 5-mg and 10-mg tofacitinib groups than in the placebo groups (-0.50 and

173 th 3, a higher percentage of patients in the tofacitinib groups than in the placebo groups met the cr

174 se rates (month 6) were also superior in the tofacitinib groups versus placebo.

175 In the tofacitinib groups, 2 cases of tuberculosis, 2 cases of

176 gnificant improvements from baseline for all tofacitinib groups, and tofacitinib demonstrated greater

177 placebo (5.6% and 8.7% in the 5-mg and 10-mg tofacitinib groups, respectively, and 4.4% with placebo;

178 creatinine levels had small increases in the tofacitinib groups.

179 -user cohort analysis, patients treated with tofacitinib had 68% reduced risk of ILD compared with ad

180 eated with adalimumab, patients treated with tofacitinib had a lower risk of ILD (adjusted hazard rat

181 Three patients treated with tofacitinib had an absolute neutrophil count of less tha

182 The remaining agents (MPA, belatacept, and tofacitinib) had less apparent dose-dependent effects on

183 Tofacitinib has a multitiered response in patients with

184 Tofacitinib improved disease control in patients with ac

185 mal models, the Janus kinase (JAK) inhibitor tofacitinib improves clinical features, immune dysregula

186 phase 2 trial, we evaluated the efficacy of tofacitinib in 194 adults with moderately to severely ac

187 nts still receiving placebo were switched to tofacitinib in a blinded fashion.

188 Herein we report the effects of tofacitinib in a murine model of GVHD.

189 We evaluated tofacitinib in patients with active psoriatic arthritis

190 We evaluated tofacitinib in patients with active psoriatic arthritis

191 chanisms underlying the clinical efficacy of tofacitinib in patients with psoriasis.

192 ment of 5 patients with recalcitrant GA with tofacitinib inhibited IFN-gamma and oncostatin M, as wel

193 tralizing antibody and Jak family kinases by tofacitinib inhibited STAT3 signaling, peritumoral angio

194 JAK inhibitors (ruxolitinib and tofacitinib) inhibited the growth of pro-B1 ALL cell lin

195 ve, 1 or >= 2; minimum of 12 months prior to tofacitinib initiation).

196 In the 6 months prior to tofacitinib initiation, 65.8% of patients had received o

197 Tofacitinib is a novel, oral, Janus kinase inhibitor tha

198 Tofacitinib is an oral Janus kinase inhibitor being inve

199 Tofacitinib is an oral Janus kinase inhibitor for the tr

200 Tofacitinib is an oral Janus kinase inhibitor that is un

201 Tofacitinib is effective in treatment of ulcerative coli

202 tients hospitalized with Covid-19 pneumonia, tofacitinib led to a lower risk of death or respiratory

203 Topical ophthalmic tofacitinib may act as an immunomodulator in patients wi

204 Tofacitinib may be an effective drug for treatment again

205 Tofacitinib may carry a significant risk for LTBI reacti

206 cause the increase of viral infections under tofacitinib may have been influenced by overlapping toxi

207 ies are needed to better understand the role tofacitinib may play in preventing ILD in patients with

208 r biologic agents, vedolizumab, ustekinumab, tofacitinib, methotrexate, and corticosteroid use.

209 Tofacitinib monotherapy at >/=3 mg twice a day was effic

210 Two (1%) of the 384 patients receiving tofacitinib monotherapy died.

211 ference 2% [98.34% CI -6 to 11]) but not for tofacitinib monotherapy versus either adalimumab and met

212 n patients with active rheumatoid arthritis, tofacitinib monotherapy was associated with reductions i

213 Tofacitinib monotherapy was not shown to be non-inferior

214 s attained in 147 (38%) of 384 patients with tofacitinib monotherapy, 173 (46%) of 376 patients with

215 In total, 23 (6%) of 384 patients receiving tofacitinib monotherapy, 26 (7%) of 376 patients receivi

216 aimed to assess the comparative efficacy of tofacitinib monotherapy, tofacitinib plus methotrexate,

217 1146 patients received treatment (384 had tofacitinib monotherapy; 376 had tofacitinib and methotr

218 Among patients initiating tofacitinib (N = 225), mean age was 45.6 (SD 16.5) years

219 th polyarticular course JIA were assigned to tofacitinib (n=72) or placebo (n=70).

220 Although new safety signals have emerged for tofacitinib, namely malignancy and cardiovascular diseas

221 Our goal was to characterize the impact of tofacitinib on LTBI using a mouse model of contained tub

222 current study was to determine the effect of tofacitinib on patient-reported outcomes (PROs).

223 is were randomized (3:1) to receive 10 mg of tofacitinib or placebo twice daily for 12 weeks.

224 ng inflamed human arteries were treated with tofacitinib or vehicle.

225 (JAK) signaling via STAT1 (glucocorticoids, tofacitinib, or filgotinib) reduced expression of protei

226 r patients receiving 5-mg tofacitinib, 10-mg tofacitinib, or placebo were 6.9, 7.3, or 10.9 events pe

227 inhibition of the second wave with CP690550 (tofacitinib) over a 2-week period enduringly suppressed

228 score-matched patient pairs, including 4224 tofacitinib pairs (mean [SD] age 72.19 [5.65] years; 694

229 ility to assess drug combinations other than tofacitinib plus methotrexate was limited.

230 notherapy, 26 (7%) of 376 patients receiving tofacitinib plus methotrexate, and 36 (9%) of 386 patien

231 arative efficacy of tofacitinib monotherapy, tofacitinib plus methotrexate, and adalimumab plus metho

232 Oral administration of tofacitinib prevented GVHD-like disease manifested by we

233 Furthermore, tofacitinib promoted M2 anti-inflammatory phenotype of m

234 in vivo systemic and topical treatment, with tofacitinib protecting mice from developing severe cutan

235 We found that tofacitinib reduced the expression of granzyme B by CD8

236 kemic mice with the JAK3 selective inhibitor tofacitinib reduced the white blood cell count and cause

237 reatment of mice with the pan-Jak inhibitor, tofacitinib, reduced psoriasis-like dermatitis and epide

238 Our data indicate that tofacitinib reduces host containment of Mycobacterium tu

239 cular proteins significantly reduced only in tofacitinib responders.

240 ession, whereas the Janus kinase 3 inhibitor tofacitinib's success in the treatment of rheumatoid art

241 Compared with etanercept, tofacitinib showed a wider spectrum of cardiovascular bl

242 These results suggest that the JAK inhibitor tofacitinib suppresses osteoclast-mediated structural da

243 lobulin, basiliximab, rituximab, eculizumab, tofacitinib, tacrolimus, mycophenolate mofetil and taper

244 s than 2.6 was not significantly higher with tofacitinib than with placebo (5.6% and 8.7% in the 5-mg

245 Adverse events occurred more frequently with tofacitinib than with placebo, and pulmonary tuberculosi

246 Adverse events were more frequent with tofacitinib than with placebo.

247 and herpes zoster infection were higher with tofacitinib than with placebo.

248 ction and serious infection were higher with tofacitinib than with placebo.

249 cle, we report that monotherapy of mice with tofacitinib (the JAK inhibitor) quells Ab responses to a

250 Among patients with UC initiating tofacitinib, the majority had prior biologic use.

251 ition, since the approval of ruxolitinib and tofacitinib, the therapeutic use of JAK inhibitors (jaki

252 , double-blind, placebo-controlled trials of tofacitinib therapy in adults with ulcerative colitis.

253 Tofacitinib therapy strongly inhibits gamma(c) cytokine-

254 Like tofacitinib, tocilizumab, a biologic targeting the IL-6

255 Adalimumab (ADA) and tofacitinib (TOF) were shown to be equivalent in patient

256 Sustain, a numerically higher proportion of tofacitinib-treated patients achieved remission with OCT

257 adverse events (AEs) in patients across all tofacitinib treatment arms (n = 272) were urinary tract

258 Importantly, tofacitinib treatment did not alter T helper type 1 resp

259 Mechanistic investigations revealed that tofacitinib treatment led to reduced numbers of CD127+ p

260 irst 10 participants to complete 16 weeks of tofacitinib treatment shows a good safety profile and no

261 Tofacitinib treatment was associated with elevations in

262 C (endoscopic Mayo score [EMS] >=2) starting tofacitinib treatment were included.

263 e normal Ig levels were still present during tofacitinib treatment, this agent specifically reduced a

264 orally twice daily (132 patients); 10 mg of tofacitinib twice daily (132 patients); placebo, with a

265 ents); or placebo, with a switch to 10 mg of tofacitinib twice daily at 3 months (65 patients).

266 patients); placebo, with a switch to 5 mg of tofacitinib twice daily at 3 months (66 patients); or pl

267 thotrexate were randomly assigned to 5 mg of tofacitinib twice daily, 10 mg of tofacitinib twice dail

268 mly assigned, in a 4:4:1:1 ratio, to 5 mg of tofacitinib twice daily, 10 mg of tofacitinib twice dail

269 to 5 mg of tofacitinib twice daily, 10 mg of tofacitinib twice daily, 40 mg of adalimumab once every

270 ly, placebo for 3 months followed by 5 mg of tofacitinib twice daily, or placebo for 3 months followe

271 to 5 mg of tofacitinib twice daily, 10 mg of tofacitinib twice daily, placebo for 3 months followed b

272 or placebo for 3 months followed by 10 mg of tofacitinib twice daily.

273 a blinded fashion to either 5 mg or 10 mg of tofacitinib twice daily; at month 6, all patients still

274 ests using a higher-efficacy medication (eg, tofacitinib, upadacitinib, and ustekinumab) or an interm

275 nalysis to investigate the safety profile of tofacitinib, upadacitinib, filgotinib, and baricitinib i

276 e use of infliximab, golimumab, vedolizumab, tofacitinib, upadacitinib, ustekinumab, ozanimod, etrasi

277 TNF-alpha therapy are urgently required, and tofacitinib, vedolizumab and ustekinumab appear to be th

278 al characteristics of patients who initiated tofacitinib, vedolizumab or TNFi were described.

279 test elevation and neutropenia occurred with tofacitinib, VX-509 and fostamatinib; lipid elevation wi

280 More importantly, tofacitinib was also effective in reversing established

281 Tofacitinib was associated with an increase in both low-

282 received placebo; as compared with placebo, tofacitinib was associated with increased lipid levels.

283 phosphorylated STAT (P-STAT) 5 inhibition by tofacitinib was determined in cytokine-activated CD4(+)

284 Tofacitinib was equivalent to CsA in preventing acute re

285 ately to severely active ulcerative colitis, tofacitinib was more effective as induction and maintena

286 ad an inadequate response to TNF inhibitors, tofacitinib was more effective than placebo over 3 month

287 que psoriasis, the 10 mg twice daily dose of tofacitinib was non-inferior to etanercept 50 mg twice w

288 iting the JAK/STAT inflammatory pathway with tofacitinib was not renoprotective.

289 However, the safety profile of tofacitinib was poor, including increased incidences of

290 arthritis receiving background methotrexate, tofacitinib was significantly superior to placebo and wa

291 of age with >=1 cardiovascular risk factor, tofacitinib was statistically inferior to TNF inhibitors

292 The efficacy of tofacitinib was superior to that of placebo at month 3 i

293 first such drug (the JAK inhibitor Xeljanz, tofacitinib) was approved by the FDA in November 2012 fo

294 the study, patients received oral open-label tofacitinib (weight-based doses; 5 mg twice daily or low

295 erely active ulcerative colitis treated with tofacitinib were more likely to have clinical response a

296 uction, but the protein reduction effects of tofacitinib were strictly confined to treatment responde

297 nistration of the Janus kinase 2/3 inhibitor tofacitinib, which blocks IL-15 signaling.

298 Here we tested whether tofacitinib, which inhibits IL-15 signaling by blocking

299 Lesional T cells responded to tofacitinib with reduced proliferation rates (<10%) and

300 ombination of JAK inhibitors, ruxolitinib or tofacitinib, with dasatinib elicited strong and specific