ライフサイエンスコーパス: adalimumab

1 ated antibodies against mouse and human TNF (adalimumab).

2 received her bimonthly dose of subcutaneous adalimumab.

3 ightly adalimumab with thiopurine, or weekly adalimumab.

4 ltrates following subcutaneous injections of adalimumab.

5 followed by remission, off medication, than adalimumab.

6 fliximab, etanercept, and in a lesser extent adalimumab.

7 nt modalities, was successfully treated with adalimumab.

8 derived monoclonal antibodies for binding to adalimumab.

9 ith TNF as well as each other for binding to adalimumab.

10 ly diverse and involves multiple epitopes on adalimumab.

11 [95% credible interval, 1.13 to 3.59]) than adalimumab.

12 mmaRIIIa with a higher affinity than control adalimumab.

13 in carotids after 52 weeks of treatment with adalimumab.

14 reduced, compared with addition of a control adalimumab.

15 lammation in psoriasis patients treated with adalimumab.

16 th hidradenitis suppurativa not eligible for adalimumab.

17 tive use of TDM in IBD patients treated with adalimumab.

18 mly assigned to adalimumab 0.8 mg/kg (n=38), adalimumab 0.4 mg/kg (n=39) or methotrexate (n=37).

19 In the adalimumab 0.4 mg/kg group, 17 (44%) of 39 patients achi

20 events were reported, all in patients in the adalimumab 0.4 mg/kg group, and were not judged to be re

21 ing initial treatment; 22 [56%] of 39 in the adalimumab 0.4 mg/kg group; 21 [57%] of 37 in the methot

22 2015, 114 patients were randomly assigned to adalimumab 0.8 mg/kg (n=38), adalimumab 0.4 mg/kg (n=39)

23 23 (61%) of 38 patients in the adalimumab 0.8 mg/kg group and 15 (41%) of 37 in the met

24 s achieved in 22 (58%) of 38 patients in the adalimumab 0.8 mg/kg group compared with 12 (32%) of 37

25 vents were infections (17 [45%] of 38 in the adalimumab 0.8 mg/kg group during initial treatment; 22

26 INTERPRETATION: Treatment with adalimumab 0.8 mg/kg in children and adolescents with se

27 ce or web-response system (1:1:1) to receive adalimumab 0.8 mg/kg or 0.4 mg/kg subcutaneously at week

28 assessment (PGA) score at week 16, comparing adalimumab 0.8 mg/kg with methotrexate.

29 methotrexate, 3; fumaric acid esters, 2; and adalimumab, 1), but methotrexate and biologic agents wer

30 more frequently among patients who received adalimumab (1052.4 vs. 971.7 adverse events and 28.8 vs.

31 A total of 217 patients (110 adalimumab, 107 placebo) in VISUAL-1 and 226 patients (1

32 7 placebo) in VISUAL-1 and 226 patients (115 adalimumab, 111 placebo) in VISUAL-2 were studied using

33 2 (11.5-17.4); etanercept, 15.3 (11.6-20.1); adalimumab, 13.9 (11.4-16.6); and ustekinumab, 15.1 (10.

34 icentre prospective cohort (160 treated with adalimumab, 171 etanercept).

35 herent compared to those using etanercept or adalimumab (29.2% vs. 16.4%; P </= 0.001).

36 A 16-week course of subcutaneous adalimumab (40 mg every 2 weeks after a loading dose) or

37 system, in a 1:1 ratio, block size four) to adalimumab (40 mg every other week) plus methotrexate (i

38 ce daily) plus methotrexate, or subcutaneous adalimumab (40 mg every other week) plus methotrexate at

39 R] >3.2; rituximab group) or a TNF inhibitor-adalimumab (40 mg subcutaneously every other week) or et

40 Treatment with adalimumab (40 mg weekly), as compared with placebo, res

41 835 serial samples were tested (414 adalimumab, 421 etanercept).

42 ISUAL-2, patients were randomized to receive adalimumab, 80-mg, subcutaneous loading dose followed by

43 drug clearance in infants was 4.0 months for adalimumab (95% CI, 2.9-5.0) and 7.3 months for inflixim

44 her drug concentration at birth was 1.21 for adalimumab (95% confidence interval [CI], 0.94-1.49) and

45 randomly assigned in a 1:1 ratio to receive adalimumab (a loading dose of 80 mg followed by a dose o

46 Adalimumab, a fully human anti-tumor necrosis factor alp

47 rum trough adalimumab and antibodies against adalimumab (AAA) levels and class II HLA typing.

48 research has shown that new anti-TNF agents, adalimumab (ADA) and golimumab, are effective in inducti

49 study data of low quality suggests that only adalimumab (adjusted hazard ratio [adjHR] = 2.52, 95% co

50 weekly adalimumab and azathioprine or weekly adalimumab alone if failure criteria were not met.

51 were injected once with either infliximab or adalimumab, alone or preincubated with TNF-alpha.

52 In a phase 2 trial, adalimumab, an antibody against tumor necrosis factor al

53 re to best score in NEI VFQ-25 was -1.30 for adalimumab and -5.50 for placebo-a difference of 4.20 (9

54 change from baseline NEI VFQ-25 was 3.36 for adalimumab and 1.24 for placebo-a difference of 2.12 (95

55 ease) occurred in 1.3% of patients receiving adalimumab and 1.3% of those receiving placebo in PIONEE

56 arch 2012 through November 2014: 36 received adalimumab and 44 received infliximab; 39 received conco

57 nders to certolizumab pegol were switched to adalimumab and 57 non-responders to adalimumab were swit

58 assessed, blood samples were collected, and adalimumab and ADA concentrations was determined at base

59 Adalimumab and ADA concentrations, clinical response and

60 Patient PASI and adalimumab and ADA concentrations.

61 aluation included assessment of serum trough adalimumab and antibodies against adalimumab (AAA) level

62 n was possible for patients receiving weekly adalimumab and azathioprine or weekly adalimumab alone i

63 imumab every week, and lastly to both weekly adalimumab and daily azathioprine.

64 opecia universalis successfully treated with adalimumab and discuss the possible mechanism.OBSERVATIO

65 In the combined GEE model including adalimumab and etanercept, a body-mass index of 30 kg/m(

66 sk of malignancy associated with combination adalimumab and immunomodulator therapy with that of adal

67 ts before (PP) and after treatment (PT) with adalimumab and in normal skin from healthy individuals (

68 Based on a network meta-analysis, adalimumab and infliximab + azathioprine are the most ef

69 Adalimumab and infliximab + azathioprine were superior t

70 est a higher risk of serious infections with adalimumab and infliximab compared with nonmethotrexate

71 We investigated the concentrations of adalimumab and infliximab in umbilical cord blood of new

72 ot for tofacitinib monotherapy versus either adalimumab and methotrexate (-6 [-14 to 3]) or tofacitin

73 ared for tofacitinib and methotrexate versus adalimumab and methotrexate (difference 2% [98.34% CI -6

74 xate combination therapy was non-inferior to adalimumab and methotrexate combination therapy in the t

75 RNA downregulation at study completion among adalimumab and methotrexate responders suggest a disease

76 Between adalimumab and methotrexate responders, we found no sign

77 (P = .03) and IL22 (P = .006) mRNA comparing adalimumab and methotrexate responders.

78 Adalimumab and methotrexate responses are differentiated

79 ad tofacitinib and methotrexate; and 386 had adalimumab and methotrexate).

80 otrexate, and 169 (44%) of 386 patients with adalimumab and methotrexate.

81 significant difference in NEI VFQ-25 between adalimumab and placebo of 3.07 (95% CI, 2.09 to 4.06; P

82 The temporal effects of adalimumab and placebo on NEI VFQ-25 were investigated u

83 .019 to 0.055; P = 0.629) at week 16 between adalimumab and placebo.

84 level of 3 anti-TNFalpha drugs (infliximab, adalimumab, and certolizumab) was measured, with >/= 0.9

85 s factor (TNF) agents such as infliximab and adalimumab, and etanercept is not effective for treatmen

86 Infliximab, adalimumab, and etanercept were incubated with mucosal h

87 MMP3 and MMP12 cleaved infliximab, adalimumab, and etanercept, releasing a 32-kilodalton Fc

88 containing the biopharmaceuticals Rituximab, Adalimumab, and Etanercept, respectively.

89 ed the integrity and function of infliximab, adalimumab, and etanercept.

90 atient-years in the ustekinumab, etanercept, adalimumab, and infliximab cohorts, respectively, and 1.

91 our specific drugs: etanercept, ustekinumab, adalimumab, and methotrexate.

92 non-biologic systemic therapies, etanercept, adalimumab, and ustekinumab for the treatment of psorias

93 nd azathioprine (infliximab + azathioprine), adalimumab, and vedolizumab were superior to placebo for

94 We conclude that although all anti-adalimumab antibodies compete for binding to TNF, the re

95 Anti-adalimumab antibodies were detected in 31 (24.8%) of 125

96 , or from immune-complex deposition via anti-adalimumab antibodies.

97 iologic agents (in particular infliximab and adalimumab) are effective in the treatment of severe ocu

98 a trial to assess the efficacy and safety of adalimumab as a glucocorticoid-sparing agent for the tre

99 a 10-mg dose taken orally twice daily (104), adalimumab at a 40-mg dose administered subcutaneously o

100 In period 2, patients were reassigned to adalimumab at a weekly or every-other-week dose or to pl

101 ly assigned in a 2:1 ratio to receive either adalimumab (at a dose of 20 mg or 40 mg, according to bo

102 A hypo-fucosylated form of adalimumab bound human FcgammaRIIIa with a higher affini

103 Adalimumab bound to monocyte membrane TNF from RA patien

104 show that the therapeutic anti-TNF antibody adalimumab, but not the soluble TNF receptor etanercept,

105 Infliximab and adalimumab can be considered as first-line immunomodulat

106 Infliximab and adalimumab can be considered as potential second-line im

107 Infliximab and adalimumab can be considered as second-line immunomodula

108 Infliximab and adalimumab can be considered in these patients in prefer

109 , azathioprine/6-mercaptopurine, infliximab, adalimumab, certolizumab, vedolizumab, or combined thera

110 th CD who participated in clinical trials of adalimumab (CLASSIC I and II, CHARM, GAIN, EXTEND, and A

111 phy indices also improved significantly with adalimumab compared with controls in the ascending aorta

112 % CI, 1.04 to 7.36; P = .01) associated with adalimumab compared with placebo.

113 clinical response and ADA concentration, and adalimumab concentration and clinical response had corre

114 presence of ADA is strongly correlated with adalimumab concentration and greatly influences clinical

115 Adalimumab concentration was the most significant indepe

116 ti-drug antibodies was associated with lower adalimumab concentrations (Spearman r=-0.66, p=0.0041).

117 hs, presence of anti-drug antibodies and low adalimumab concentrations are a significant predictor fo

118 months, anti-drug antibody formation and low adalimumab concentrations were significant predictors of

119 n from baseline to week 78, compared between adalimumab-continuation and methotrexate-monotherapy.

120 nctional, and structural outcomes, with both adalimumab-continuation and methotrexate-monotherapy.

121 73 of 105 (70%) patients in the adalimumab-continuation group and 61 of 112 (54%) patien

122 ]<3.2 at weeks 22 and 26) were randomised to adalimumab-continuation or adalimumab-withdrawal for an

123 ity target, of whom 105 were rerandomised to adalimumab-continuation.

124 Adalimumab cross-reacts with murine TNF-alpha whereas in

125 Adalimumab did not affect plasma SIV RNA levels or measu

126 The adalimumab dose interval was shortened because of lack o

127 When injected alone, only adalimumab elicited a humoral response.

128 cohorts, including ustekinumab, infliximab, adalimumab, etanercept, and nonbiologics (with or withou

129 ents with significant skin and nail disease, adalimumab, etanercept, and ustekinumab are strongly rec

130 Adalimumab, etanercept, infliximab and tocilizumab all s

131 alen, methotrexate, cyclosporine, acitretin, adalimumab, etanercept, infliximab, or ustekinumab or ph

132 : Biological therapy approved for psoriasis (adalimumab, etanercept, infliximab, ustekinumab) with th

133 m topical therapy has failed, treatment with adalimumab, etanercept, intralesional corticosteroids, u

134 h significant nail, skin, and joint disease, adalimumab, etanercept, ustekinumab, infliximab, methotr

135 eatment, to adalimumab induction followed by adalimumab every other week, adalimumab every week, and

136 All patients received 40 mg adalimumab every other week.

137 ion followed by adalimumab every other week, adalimumab every week, and lastly to both weekly adalimu

138 As a consequence, adalimumab expanded functional Foxp3(+) T reg cells equi

139 infection history, infliximab exposure, and adalimumab exposure were each associated with an increas

140 07 patients were randomized (1:1) to receive adalimumab for 52 weeks or placebo for 16 weeks followed

141 52 weeks or placebo for 16 weeks followed by adalimumab for 52 weeks.

142 arly designed, phase 3 multicenter trials of adalimumab for hidradenitis suppurativa, with two double

143 ised 73 patients who were being treated with adalimumab for more than 24 weeks until 401 weeks.

144 cohorts included adult patients treated with adalimumab for plaque-type psoriasis.

145 For 80 patients treated with adalimumab for psoriasis, disease severity (PASI) was as

146 ent (for up to 36 weeks) and re-treated with adalimumab (for 16 weeks) if disease became uncontrolled

147 Infliximab was cleared more slowly than adalimumab from the infants.

148 After MMP degradation, infliximab and adalimumab functioned as F(ab')2 fragments, whereas clea

149 A set of four allotype variants of adalimumab (G1m17,1; G1m17,-1; G1m3,1; and G1m3,-1) was

150 ere is high-quality evidence of benefit from adalimumab given weekly, while every other week dosing i

151 bias and showed that all biological agents (adalimumab, golimumab, infliximab, and vedolizumab) resu

152 mg, and 200-mg guselkumab groups than in the adalimumab group (58%) (P<0.05 for all comparisons).

153 mg, and 200-mg guselkumab groups than in the adalimumab group (71%, 77%, and 81%, respectively, vs. 4

154 ime to treatment failure was 24 weeks in the adalimumab group and 13 weeks in the placebo group.

155 nt failure was significantly improved in the adalimumab group compared with the placebo group (median

156 lacebo group whereas one (1%) patient in the adalimumab group reported non-serious squamous cell carc

157 ual acuity) were significantly better in the adalimumab group than in the placebo group.

158 eatment failures in 60 patients (27%) in the adalimumab group versus 18 treatment failures in 30 pati

159 e placebo group and 27 [23%] patients in the adalimumab group), nasopharyngitis (16 [17%] and eight [

160 % in the 10-mg tofacitinib group, 72% in the adalimumab group, 69% in the placebo group that switched

161 atients in the guselkumab groups, 12% in the adalimumab group, and 14% in the placebo group.

162 ompared with 45 (39%) of 115 patients in the adalimumab group.

163 in the placebo group and 10.2 months in the adalimumab group.

164 placebo group and 245 days (119-564) in the adalimumab group.

165 dose with placebo); the rate was 52% in the adalimumab group.

166 placebo); the score change was -0.38 in the adalimumab group.

167 Patients who received adalimumab had a much higher incidence of adverse events

168 Patients receiving adalimumab had significantly greater improvement than th

169 Adalimumab has proven to be effective in suppressing pso

170 zard ratio [HR] = 1.10, 95% CI = 0.75-1.60), adalimumab (HR = 0.93, 95% CI = 0.69-1.26), or ustekinum

171 (etanercept: HR = 1.47, 95% CI = 0.95-2.28; adalimumab: HR = 1.26, 95% CI = 0.86-1.84; ustekinumab:

172 Adalimumab (Humira(R)), a fully human recombinant antibo

173 e treated for 12 weeks in a pilot study with adalimumab (Humira), a human anti-TNF monoclonal antibod

174 of recurrence also received a thiopurine, or adalimumab if they were intolerant to thiopurines.

175 ession did not show any protective effect on adalimumab immunogenicity in our cohort.

176 The production of antibodies to adalimumab in autoimmune patients treated with adalimuma

177 rial, we assessed the efficacy and safety of adalimumab in children and adolescents 2 years of age or

178 We assessed the efficacy and safety of adalimumab in children and adolescents with severe plaqu

179 e aimed to assess the efficacy and safety of adalimumab in patients with inactive, non-infectious uve

180 nti-interleukin-23 monoclonal antibody, with adalimumab in patients with moderate-to-severe plaque ps

181 ongoing to provide long-term safety data for adalimumab in patients with non-infectious uveitis.

182 We tested the efficacy of adalimumab in the treatment of JIA-associated uveitis.

183 d herein, a recombinant monoclonal antibody (adalimumab) in cell culture was covalently modified by x

184 We assessed whether adalimumab, in addition to standard UC therapy, reduced

185 Hypo-fucosylated adalimumab increased the number of CD206(+) macrophages

186 inding to a panel of single-point mutants of adalimumab indicates markedly different fine specificiti

187 in a stepwise manner, from no treatment, to adalimumab induction followed by adalimumab every other

188 Adalimumab, infliximab, and infliximab + azathioprine we

189 ticosteroid therapy, but recurred after each adalimumab injection over the following weeks.

190 The immunogenicity of infliximab and adalimumab is a major concern because patients may devel

191 Treatment of noninfectious uveitis with adalimumab is associated with high rates of favorable cl

192 This post hoc analysis suggests that adalimumab is associated with statistically significant

193 es suggests that the immune response against adalimumab is broad, involving multiple B-cell clones ea

194 Adalimumab is effective for induction and maintenance of

195 Adalimumab is effective in a significant proportion of p

196 Adalimumab is indicated for the treatment of moderate to

197 alimumab in autoimmune patients treated with adalimumab is shown to diminish treatment efficacy.

198 These findings suggest that adalimumab is well tolerated and could be an effective t

199 alpha have been studied most often, and one, adalimumab, is U.S. Food and Drug Administration approve

200 AAA was associated with undetectable trough adalimumab levels and worse uveitis outcome.

201 In all patients with permanent AAA+, trough adalimumab levels became undetectable (P < 0.001).

202 size of four, to receive either subcutaneous adalimumab (loading dose 80 mg; biweekly dose 40 mg) or

203 Although adalimumab may reduce vascular inflammation in patients

204 , exposure to corticosteroids, infliximab or adalimumab, metronidazole, hospitalizations, higher ambu

205 h the general population, patients receiving adalimumab monotherapy did not have a greater than expec

206 ts with CD, the incidence of malignancy with adalimumab monotherapy was not greater than that of the

207 malignancy in patients with CD who received adalimumab monotherapy, compared with the general popula

208 Compared with patients receiving adalimumab monotherapy, those patients receiving combina

209 mab and immunomodulator therapy with that of adalimumab monotherapy.

210 on adalimumab plus methotrexate who withdrew adalimumab mostly maintained their good responses.

211 Data for patients on adalimumab (n=1,879), etanercept (n=1,098), infliximab (

212 d 229 patients to receive placebo (n=114) or adalimumab (n=115); 226 patients comprised the intention

213 enter pharmacovigilance registry (n = 1,239; adalimumab, n = 538; etanercept, n = 104; ustekinumab, n

214 To assess the effect of adalimumab on the visual functioning and quality of life

215 ts of tumor necrosis factor-alpha antagonist adalimumab on vascular inflammation in patients with pso

216 zed in a 1:1 fashion to receive subcutaneous adalimumab or oral methotrexate.

217 Patients were randomized to receive adalimumab or placebo and underwent a protocol-defined m

218 e not aware of the presence of antibodies to adalimumab or the adalimumab serum concentration when as

219 azathioprine (OR, 3.1; 95% CrI, 1.4-7.7) and adalimumab (OR, 2.1; 95% CrI, 1.0-4.6) were superior to

220 azathioprine were superior to certolizumab: adalimumab (OR, 2.5; 95% CrI, 1.4-4.6) and infliximab +

221 e superior to azathioprine/6-mercaptopurine: adalimumab (OR, 2.9; 95% CrI, 1.6-5.1), infliximab (OR,

222 (a 160-mg dose followed by an 80-mg dose of adalimumab) or placebo in 2 trials (ULTRA 1 and ULTRA 2;

223 As compared with adalimumab, patients on etanercept (HR 1.63; 95% CI: 1.4

224 Compared to adalimumab, patients receiving etanercept were more like

225 proportion of patients treated with initial adalimumab plus methotrexate achieved the low disease ac

226 exate, and 36 (9%) of 386 patients receiving adalimumab plus methotrexate discontinued due to adverse

227 otherapy, tofacitinib plus methotrexate, and adalimumab plus methotrexate for the treatment of rheuma

228 466 patients in the adalimumab plus methotrexate group completed period 1; 2

229 Patients in the adalimumab plus methotrexate group who completed period

230 ng (or not) stable low disease activity with adalimumab plus methotrexate or methotrexate monotherapy

231 e and 386 [74%] of 523 patients who received adalimumab plus methotrexate reported treatment-emergent

232 ng the stable low disease activity target on adalimumab plus methotrexate who withdrew adalimumab mos

233 een certolizumab pegol plus methotrexate and adalimumab plus methotrexate, respectively.

234 tolizumab pegol plus methotrexate and 458 to adalimumab plus methotrexate.

235 eive certolizumab pegol plus methotrexate or adalimumab plus methotrexate.

236 b pegol plus methotrexate is not superior to adalimumab plus methotrexate.

237 Inadequate responders were offered adalimumab plus methotrexate.

238 drawn in patients who initially responded to adalimumab plus methotrexate.

239 and 1032 were randomised in period 1 (515 to adalimumab plus methotrexate; 517 to placebo plus methot

240 P < .0001) and in mothers at time of birth (adalimumab, r = -0.80; infliximab, r = -0.80; P < .0001

241 ntration of the drugs in the umbilical cord (adalimumab: r = -0.64, P = .0003; infliximab: r = -0.77,

242 gol and 40 (62%) of 65 patients switching to adalimumab responded 12 weeks later by achieving LDA or

243 (IL22) mRNA showing early downregulation for adalimumab responders (week 2, -3.17 [1.00], P < .001; w

244 Adalimumab responders demonstrated early downregulation

245 eous co-administration of nanoparticles with adalimumab resulted in the durable inhibition of ADAs, l

246 Overall, cluster analysis showed adalimumab, secukinumab, and ustekinumab were comparable

247 presence of antibodies to adalimumab or the adalimumab serum concentration when assessing patients'

248 Median trough adalimumab serum levels were higher in responders than i

249 Adalimumab significantly lowered the risk of uveitic fla

250 manifestation and was currently treated with Adalimumab since September 2008.

251 rom two patients, cultured, and screened for adalimumab specificity.

252 eks thereafter) through week 40, placebo, or adalimumab (standard dosage for psoriasis).

253 ents were randomized (2:1) to receive either adalimumab subcutaneously for 4 months or to control non

254 from the ascending aorta (primary endpoint) (adalimumab: TBR = 0.002, 95% confidence interval [CI] =

255 0.053 to 0.049; P = 0.916) and the carotids (adalimumab: TBR = 0.031, 95% CI = -0.005 to 0.066; place

256 ported more frequently in patients receiving adalimumab than in those receiving placebo (10.07 events

257 Before the start of adalimumab therapy and at time of serum sampling, Psoria

258 or dose intensification were frequent during adalimumab therapy and support the selective use of TDM

259 s) were observed within the first 8 weeks of adalimumab therapy compared with placebo.

260 talizations were observed during 52 weeks of adalimumab therapy compared with placebo.

261 Adalimumab therapy controlled inflammation and was assoc

262 s, included 80 sequential patients receiving adalimumab therapy for plaque-type psoriasis and had a f

263 disease and gastrointestinal remission under Adalimumab therapy presented with osteonecrosis of the j

264 ates in the event of red eye symptoms during adalimumab therapy since they respond to topical cortico

265 e to severe hidradenitis suppurativa failing adalimumab therapy, or those ineligible to receive it, r

266 72%) showed a favorable clinical response to adalimumab therapy.

267 anercept, but has also been described during adalimumab therapy.

268 1 year and 17.3% and 29.5% after 2 years of adalimumab therapy.

269 After 52 weeks of treatment with adalimumab there was no significant change from start of

270 ine use has been combined with etanercept or adalimumab to control psoriasis flares.

271 with moderate to severe UC, the addition of adalimumab to standard of care treatment reduced the num

272 Comparisons among adalimumab-treated patients were limited by the number o

273 tablished range, a therapeutic algorithm for adalimumab treatment for patients with psoriasis can be

274 One-third of patients had an adalimumab trough concentration exceeding 7 mg/L.

275 Adalimumab trough level and PASI score at the time of se

276 ent AAA+, which correlated with undetectable adalimumab trough levels (P = 0.014).

277 relation was observed between AAA titers and adalimumab trough levels (P = 0.2).Concomitant immunosup

278 A therapeutic range of adalimumab trough levels of 3.51 mg/L to 7.00 mg/L, whic

279 Overall, adalimumab trough levels were higher in responder patien

280 dictive factors of loss of response (LOR) to adalimumab using TDM in IBD patients.

281 articipants were included in the etanercept, adalimumab, ustekinumab cohorts, respectively, and 3,421

282 activation was higher for those treated with adalimumab vs infliximab (hazard ratio [HR] 13.4, P = .0

283 differ significantly between patients given adalimumab vs placebo.

284 When hypo-fucosylated adalimumab was added to PBMCs, a larger number of CD206(

285 dministration of immunomodulator therapy and adalimumab was associated with an increased risk of NMSC

286 Outcomes were much the same whether adalimumab was continued or withdrawn in patients who in

287 In our trial, adalimumab was found to be associated with a lower risk

288 inically relevant antidrug antibody (ADA) to adalimumab was frequently found.

289 t:background ratio in patients randomized to adalimumab was not different from controls.

290 Adalimumab was recently approved for the treatment of no

291 Adalimumab was superior to vedolizumab (OR, 2.4; 95% CrI

292 randomly assigned in a 1:1 ratio to 40 mg of adalimumab weekly or matching placebo for 12 weeks.

293 ignificantly higher for the groups receiving adalimumab weekly than for the placebo groups: 41.8% ver

294 tention-to-treat population, those receiving adalimumab were less likely than those in the placebo gr

295 Twenty patients not eligible for adalimumab were randomized to receive 12 weeks of blind

296 tched to adalimumab and 57 non-responders to adalimumab were switched to certolizumab pegol; 33 (58%)

297 begin therapy with biologics (infliximab or adalimumab) were included, with enrollment from June 1,

298 tients stepped-up to thiopurine, fortnightly adalimumab with thiopurine, or weekly adalimumab.

299 Combining biologics, such as etanercept or adalimumab, with phototherapy likely results in greater

300 ere randomised to adalimumab-continuation or adalimumab-withdrawal for an additional 52 weeks (period