ライフサイエンスコーパス: adalimumab

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

2 mmaRIIIa with a higher affinity than control adalimumab.

3 in carotids after 52 weeks of treatment with adalimumab.

4 reduced, compared with addition of a control adalimumab.

5 lammation in psoriasis patients treated with adalimumab.

6 esponse technology to receive secukinumab or adalimumab.

7 th hidradenitis suppurativa not eligible for adalimumab.

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

9 received her bimonthly dose of subcutaneous adalimumab.

10 ightly adalimumab with thiopurine, or weekly adalimumab.

11 ltrates following subcutaneous injections of adalimumab.

12 followed by remission, off medication, than adalimumab.

13 4 were 7 mg/L for infliximab and 12 mg/L for adalimumab.

14 .3) for infliximab and 28.5% (24.0-32.7) for adalimumab.

15 a pathway that involves BCL2 in response to adalimumab.

16 r; 202 with biosimilar) and 655 treated with adalimumab.

17 with a higher treatment retention rate than 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 ds ratio 0.35 [95% CI 0.20-0.62], p=0.00038; adalimumab: 0.13 [0.06-0.28], p<0.0001); the optimal wee

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

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

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

33 7 placebo) in VISUAL-1 and 226 patients (115 adalimumab, 111 placebo) in VISUAL-2 were studied using

34 2 (11.5-17.4); etanercept, 15.3 (11.6-20.1); adalimumab, 13.9 (11.4-16.6); and ustekinumab, 15.1 (10.

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

36 ly) with or without fortnightly administered adalimumab (20 or 40 mg, according to body weight) provi

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

38 st one dose of vedolizumab (383 patients) or adalimumab (386 patients).

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

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

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

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

43 835 serial samples were tested (414 adalimumab, 421 etanercept).

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

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

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

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

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

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

50 en risankizumab and 252 (60%) patients given adalimumab (adjusted absolute difference 23.3% [16.6-30.

51 nkizumab and 144 (47%) of 304 patients given adalimumab (adjusted absolute difference 24.9% [95% CI 1

52 zumab and 12 (21%) of 56 patients continuing adalimumab (adjusted absolute difference 45.0% [28.9-61.

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

54 e SYCAMORE study, 11 (92%) were restarted on adalimumab after withdrawal of the IMP for active JIA-U

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 commonly prescribed biologics for psoriasis: adalimumab (anti-TNF-alpha) and ustekinumab (anti-IL-12/

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

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

95 he efficacy and safety of secukinumab versus adalimumab as first-line biological monotherapy for 52 w

96 emonstrated significantly poorer response to adalimumab at 12 months (OR, 0.31; P = 3.42 x 10(-4)).

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

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

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

100 the time of first exposure to infliximab or adalimumab between March 7, 2013, and July 15, 2016.

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

102 Adalimumab bound to monocyte membrane TNF from RA patien

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

104 factor alpha (TNF-alpha) include etanercept, adalimumab, certolizumab, and infliximab.

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

106 year, were observed in patients treated with adalimumab combination therapy who did not carry HLA-DQA

107 % CI, 1.04 to 7.36; P = .01) associated with adalimumab compared with placebo.

108 1%) of 56 patients re-randomised to continue adalimumab completed part B.

109 Adalimumab concentration was the most significant indepe

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

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

112 red to determine how this pathway influences adalimumab effectiveness in patients with hidradenitis s

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

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

115 Adalimumab, etanercept, infliximab and tocilizumab all s

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

117 t infusion of or prescription for abatacept, adalimumab, etanercept, infliximab, rituximab, or tocili

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

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

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

121 All patients received 40 mg adalimumab every other week.

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

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

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

125 07 patients were randomized (1:1) to receive adalimumab for 52 weeks or placebo for 16 weeks followed

126 52 weeks or placebo for 16 weeks followed by adalimumab for 52 weeks.

127 ndpoint of superiority of secukinumab versus adalimumab for ACR20 response at week 52 was not met.

128 ), 25 of the 28 participants were started on adalimumab for active JIA-U.

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

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

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

132 Two participants stopped adalimumab for uncontrolled JIA-U.

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

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

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

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

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

138 atients in the vedolizumab group than in the adalimumab group (31.3% vs. 22.5%; difference, 8.8 perce

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

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

141 in the vedolizumab group and in 21.8% in the adalimumab group (difference, -9.3 percentage points; 95

142 nse at week 52 versus 62% of patients in the adalimumab group (OR 1.30, 95% CI 0.98-1.72; p=0.0719).

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

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

145 the risankizumab group and 291 (96%) in the adalimumab group completed part A, and 51 (96%) of 53 pa

146 ab group and six (1%) of 427 patients in the adalimumab group had serious infections.

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

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

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

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

151 % in the 10-mg tofacitinib group, 72% in the adalimumab group, 69% in the placebo group that switched

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

153 k 52 versus 101 (24%) of 427 patients in the adalimumab group.

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

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

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

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

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

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

160 Patients receiving adalimumab had significantly greater improvement than th

161 Adalimumab has proven to be effective in suppressing pso

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

163 ion was consistent for patients treated with adalimumab (HR, 1.89; 95% CI, 1.32-2.70) or infliximab (

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

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

166 The application to the mAbs rituximab and adalimumab illustrates the potential of our approach for

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

168 n 34 countries, we compared vedolizumab with adalimumab in adults with moderately to severely active

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

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

171 ectiveness, SafetY and Cost effectiveness of Adalimumab in combination with MethOtRExate for the trea

172 Adalimumab in combination with methotrexate resulted in

173 nkizumab and 179 (57%) of 304 patients given adalimumab in part A, and among adalimumab intermediate

174 ab and 37 (66%) of 56 patients who continued adalimumab in part B.

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

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

177 the efficacy and safety of risankizumab with adalimumab in patients with moderate-to-severe plaque ps

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

179 b showed significantly greater efficacy than adalimumab in providing skin clearance in patients with

180 tistical significance for superiority versus adalimumab in the primary endpoint of ACR20 response at

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

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

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

184 t with a biologic agent but had responded to adalimumab induction therapy, under scheduled monitoring

185 Adalimumab, infliximab, and infliximab + azathioprine we

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

187 the proactive monitoring group had received adalimumab intensification (87%) compared with 24 patien

188 For weeks 16-44 (part B), adalimumab intermediate responders were re-randomised 1:

189 tients given adalimumab in part A, and among adalimumab intermediate responders, adverse events were

190 In part B, among adalimumab intermediate responders, PASI 90 was achieved

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

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

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

194 Adalimumab is clinically effective in uveitis associated

195 Adalimumab is effective in a significant proportion of p

196 Adalimumab is indicated for the treatment of moderate to

197 Adalimumab is the only treatment approved by either the

198 Adalimumab is the only treatment approved by either the

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

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

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

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

203 ence to support the proactive measurement of adalimumab levels in psoriasis to direct treatment strat

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

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

206 is patients were included who were receiving adalimumab monotherapy and had at least one serum sample

207 uestions in a real-world psoriasis cohort on adalimumab monotherapy, defining a therapeutic range and

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

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

210 receive either risankizumab (n=301, 50%) or adalimumab (n=304, 50%).

211 3 patients to receive secukinumab (n=426) or adalimumab (n=427).

212 ls (etanercept, n = 84; infliximab, n = 101; adalimumab, n = 153; interferon [IFN]-beta-1a intramuscu

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

214 atment failure was lower when treatment used adalimumab (odds ratio, 0.4; 95% CI, 0.2-0.9; P = 0.03)

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

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

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

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

219 ers were re-randomised 1:1 to continue 40 mg adalimumab or switch to 150 mg risankizumab.

220 teraction between HLA-C*06:02 and drug type (adalimumab or ustekinumab) while accounting for potentia

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

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

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

224 6-0.52] for infliximab; 0.03 [0.01-0.12] for adalimumab; p<0.0001 for both).

225 2-0.46] for infliximab; 0.44 [0.31-0.64] for adalimumab; p<0.0001 for both).

226 Compared to adalimumab, patients receiving etanercept were more like

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

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

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

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

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

232 eive certolizumab pegol plus methotrexate or adalimumab plus methotrexate.

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

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

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

236 s per 100 patient-years with vedolizumab and adalimumab, respectively, and the corresponding rates fo

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

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

239 Adalimumab responders demonstrated early downregulation

240 To identify genetic variants associated with adalimumab response, we performed a genome-wide associat

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

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

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

244 Adalimumab significantly lowered the risk of uveitic fla

245 mab subcutaneously at weeks 0 and 4 or 80 mg adalimumab subcutaneously at randomisation, then 40 mg a

246 aortic valve regurgitation, controlled with adalimumab, tacrolimus, and prednisone.

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

248 0.053 to 0.049; P = 0.916) and the carotids (adalimumab: TBR = 0.031, 95% CI = -0.005 to 0.066; place

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

250 were significantly more likely to respond to adalimumab than ustekinumab at all time points (most str

251 erved similar internal initiation in the mAb adalimumab (the amino acid sequence of the drug Humira)

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

253 Adalimumab therapy controlled inflammation and was assoc

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

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

256 1 year and 17.3% and 29.5% after 2 years of adalimumab therapy.

257 with Crohn's disease starting infliximab or adalimumab therapy.

258 72%) showed a favorable clinical response to adalimumab therapy.

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

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

261 ged from 6.87% (95% CI, 5.30% to 8.90%) with adalimumab to 8.90% (CI, 5.70% to 13.52%) with rituximab

262 rice reduction of 84% would be necessary for adalimumab to be cost effective.

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

264 re identified for patients who switched from adalimumab to risankizumab.

265 ion of known antibody drugs (alemtuzumab and adalimumab) to generate recombinant single chain GloBodi

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

267 55 was increased in M2-macrophages except in adalimumab-treated patients.

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

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

270 th CD, we found that proactive monitoring of adalimumab trough concentrations and adjustment of doses

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

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

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

274 Overall, adalimumab trough levels were higher in responder patien

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

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

277 ariate adjustment, older age, treatment with adalimumab (versus infliximab), and inactive concomitant

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

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

280 Adalimumab was administered every 2 weeks from baseline

281 a tumor necrosis factor inhibitor other than adalimumab was allowed in up to 25% of patients.

282 Adalimumab was discontinued in 151 patients.

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

284 Adalimumab was prescribed as a second or greater biother

285 Adalimumab was recently approved for the treatment of no

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

287 Adalimumab was well tolerated and visual acuity outcomes

288 uced remission of JIA-U did not persist when adalimumab was withdrawn after 1-2 years of treatment.

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

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

291 In both groups, doses and intervals of adalimumab were adjusted to achieve trough concentration

292 The safety profiles of secukinumab and adalimumab were consistent with previous reports.

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

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

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

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

297 erative colitis, vedolizumab was superior to adalimumab with respect to achievement of clinical remis

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

299 cebo) or subcutaneous injections of 40 mg of adalimumab, with a total dose of 160 mg at week 1, 80 mg

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