ライフサイエンスコーパス: infliximab

1 Twenty-nine patients were treated with infliximab.

2 riatic arthritis, receiving methotrexate and infliximab.

3 raining lymph nodes following treatment with infliximab.

4 when previously treated with the originator infliximab.

5 were identified following the initiation of infliximab.

6 llocated to have resection and 70 to receive infliximab.

7 receive laparoscopic ileocaecal resection or infliximab.

8 reatment with both originator and biosimilar infliximab.

9 ctors were receipt of corticosteroids and/or infliximab.

10 raded 9-fold more slowly than the unmodified infliximab.

11 plete mucosal healing) or did not respond to infliximab.

12 pathic arthritis, and most were treated with infliximab.

13 -tumor necrosis factor (TNF) agents, such as infliximab.

14 de etanercept, adalimumab, certolizumab, and infliximab.

15 on between fecal and serum concentrations of infliximab.

16 ed with the separation of charge variants of Infliximab.

17 ons continued while receiving treatment with infliximab.

18 were switched from originator to biosimilar infliximab.

19 ion following treatment with prednisolone or infliximab.

20 stinct metabolic effects of prednisolone and infliximab.

21 (n = 2499), and had no other indications for infliximab.

22 nfliximab-abda (.92), than on the originator infliximab (0.19; P = .028).

23 n-remission at week 54 (0.29 [0.16-0.52] for infliximab; 0.03 [0.01-0.12] for adalimumab; p<0.0001 fo

24 es (hazard ratio 0.39 [95% CI 0.32-0.46] for infliximab; 0.44 [0.31-0.64] for adalimumab; p<0.0001 fo

25 tor and the duration while on the biosimilar infliximab (12.0 vs. 10.1 months, respectively; P = .307

26 eerts scores >/=i2 (22.4% vs 51.3%; ARR with infliximab, 28.9%; 95% confidence interval: 18.4% to 39.

27 the placebo group (30.6% vs 60.0%; ARR with infliximab, 29.4%; 95% confidence interval: 18.6% to 40.

28 2014: 36 received adalimumab and 44 received infliximab; 39 received concomitant thiopurines during p

29 clinical remission while being treated with infliximab, 42 (58.3%) required additional immunomodulat

30 ocated in 1:1 ratio to two treatment groups: infliximab 5 mg/kg at 1 mg/mL intravenously over 2 h or

31 spitals in the USA to assess the addition of infliximab (5 mg per kg) to standard therapy.

32 e randomly allocated (1:1) to receive either infliximab (5 mg/kg intravenous infusion given over 2 h

33 were randomly assigned (1:1) to groups given infliximab (5 mg/kg) or placebo every 8 weeks for 200 we

34 CT-P13-infliximab group) and 109 to initiate infliximab (54 to the infliximab-infliximab group and 55

35 The most commonly used biologic agent was infliximab (67.3%).

36 vs 20.0%; absolute risk reduction [ARR] with infliximab, 7.1%; 95% confidence interval: -1.3% to 15.5

37 We enrolled 955 patients treated with infliximab (753 with originator; 202 with biosimilar) an

38 (77 [69.4%, 95% CI 59.9 to 77.8] of 111) and infliximab (81 [74.3%, 95% CI 65.1 to 82.2] of 109; diff

39 dence interval [CI], 0.94-1.49) and 1.97 for infliximab (95% CI, 1.50-2.43).

40 limumab (95% CI, 2.9-5.0) and 7.3 months for infliximab (95% CI, 6.2-8.3; P < .0001).

41 mes more slowly than human IgG antibodies or infliximab (a monoclonal mouse-human chimeric IgG).

42 ibodies (ADAs), which reduce the efficacy of infliximab, a monoclonal antibody against tumor necrosis

43 differences) on maltose binding protein and infliximab, a monoclonal antibody, to evaluate the relia

44 Infliximab, a tumor necrosis factor antagonist, is effec

45 e flares per person-years after switching to infliximab-abda (.92), than on the originator infliximab

46 sage for patients who flared and remained on infliximab-abda (1.301 mg/kg/week) was higher than that

47 7%) who experienced flare after switching to infliximab-abda did so within 90 days.

48 Patients who were switched to biosimilar infliximab-abda experience more flares than when previou

49 from the originator infliximab to biosimilar infliximab-abda for nonmedical reasons were reviewed.

50 liximab went on to develop a single flare on infliximab-abda.

51 total serum level of 3 anti-TNFalpha drugs (infliximab, adalimumab, and certolizumab) was measured,

52 Infliximab, adalimumab, and etanercept were incubated wi

53 MMP3 and MMP12 cleaved infliximab, adalimumab, and etanercept, releasing a 32-k

54 th IBD reduced the integrity and function of infliximab, adalimumab, and etanercept.

55 methotrexate, azathioprine/6-mercaptopurine, infliximab, adalimumab, certolizumab, vedolizumab, or co

56 ss treatment cohorts, including ustekinumab, infliximab, adalimumab, etanercept, and nonbiologics (wi

57 Infliximab administration was associated with clinical i

58 transgenic (hTNF-Tg) mice were treated with infliximab after development of arthritis.

59 significantly higher fecal concentrations of infliximab after the first day of treatment than patient

60 lowing treatment with either prednisolone or infliximab (all p < 0.05).

61 e, although safe, was no more effective than infliximab alone in patients with CD receiving treatment

62 ine,compared with 22.1% (17 of 77) receiving infliximab alone(P =.017) and 23.7% (18 of 76) receiving

63 ethotrexate results in greater efficacy than infliximab alone.

64 tial superiority of combination therapy over infliximab alone.

65 gher levels of infliximab-TNF complexes than infliximab alone.

66 -inflammatory treatment with prednisolone or infliximab ameliorates symptoms and increases circulatin

67 e treated 5XFAD/Tg197 mice systemically with infliximab, an anti-huTNF-alpha antibody that does not p

68 did not differ significantly (11 [11.2%] for infliximab and 11 [11.3%] for placebo; p=0.81).

69 at both week 14 and week 54 were 7 mg/L for infliximab and 12 mg/L for adalimumab.

70 nogenicity) was 62.8% (95% CI 59.0-66.3) for infliximab and 28.5% (24.0-32.7) for adalimumab.

71 Infliximab and adalimumab can be considered as first-lin

72 Infliximab and adalimumab can be considered as second-li

73 Infliximab and adalimumab can be considered in these pat

74 After MMP degradation, infliximab and adalimumab functioned as F(ab')2 fragment

75 The immunogenicity of infliximab and adalimumab is a major concern because pat

76 nti-TNF-alpha biologic agents (in particular infliximab and adalimumab) are effective in the treatmen

77 i-tumor necrosis factor (TNF) agents such as infliximab and adalimumab, and etanercept is not effecti

78 Infliximab, the combination of infliximab and azathioprine (infliximab + azathioprine),

79 Infliximab and canakinumab were used to neutralize TNF a

80 Infliximab and ciclosporin are of similar efficacy in tr

81 ce plasmon resonance analysis indicated that infliximab and FpFinfliximab maintained binding affinity

82 Both Infliximab and FpFinfliximab suppressed ocular inflammat

83 two cohorts from phase 3 clinical trials of infliximab and golimumab, high pretreatment expression o

84 Uptake of infliximab and infliximab-TNF complexes by THP-1 cells w

85 The combination of infliximab and methotrexate, although safe, was no more

86 ing remission, except for the combination of infliximab and methotrexate.

87 elationships between serum concentrations of infliximab and outcomes of adults with moderate-to-sever

88 C57BL/6 mice were given injections of infliximab and recombinant human TNF or infliximab F(ab'

89 equiring immunosuppressive treatment such as infliximab and rituximab, were invited to participate in

90 G1m17,1 mAbs, such as infliximab and rituximab, were shown to bind more effici

91 Adalimumab, etanercept, infliximab and tocilizumab all showed statistically sign

92 older age, treatment with adalimumab (versus infliximab), and inactive concomitant systemic disease w

93 ly recommended, and methotrexate, acitretin, infliximab, and apremilast are recommended.

94 Adalimumab, infliximab, and infliximab + azathioprine were superior

95 ll biological agents (adalimumab, golimumab, infliximab, and vedolizumab) resulted in more clinical r

96 occurred in 2 patients (1 patient receiving infliximab,and 1 patient receiving azathioprine).

97 the progression of the disease, for example infliximab (anti-TNF-[Formula: see text]) and tocilizuma

98 estigated features of the immune system, the infliximab antibody, and its complex with TNF that might

99 Serum concentrations of infliximab are associated with efficacy in patients with

100 tis wherein the positive clinical effects of infliximab are demonstrated.

101 Methotrexate and infliximab are effective therapies for Crohn's disease (

102 Patients received 5 mg/kg CT-P13 or infliximab at weeks 0, 2, 6, and then every 8 weeks up t

103 : adalimumab (OR, 2.5; 95% CrI, 1.4-4.6) and infliximab + azathioprine (OR, 2.6; 95% CrI, 1.3-6.0).

104 .1), infliximab (OR, 1.6; 95% CrI, 1.0-2.5), infliximab + azathioprine (OR, 3.0; 95% CrI, 1.7-5.5) fo

105 risons of anti-tumor necrosis factor agents, infliximab + azathioprine (OR, 3.1; 95% CrI, 1.4-7.7) an

106 d on a network meta-analysis, adalimumab and infliximab + azathioprine are the most effective therapi

107 Adalimumab, infliximab, and infliximab + azathioprine were superior to azathioprine/

108 Adalimumab and infliximab + azathioprine were superior to certolizumab:

109 combination of infliximab and azathioprine (infliximab + azathioprine), adalimumab, and vedolizumab

110 ed in 62.8% (49 of 78) of patients receiving infliximab/azathioprine, compared with 54.6% (42 of 77)

111 ed by 39.7% (31 of 78) of patients receiving infliximab/azathioprine,compared with 22.1% (17 of 77) r

112 Infliximab-based therapy could, thus, still be of import

113 The infliximab biosimilar CT-P13 was approved for use in Cro

114 This infliximab-bovine IgG1 chimera (bovinized infliximab) re

115 We discovered that Dexamethasone and Infliximab can both modulate the adaptive remodeling of

116 her prevalence of psoriatic arthritis in the infliximab cohort).

117 the ustekinumab, etanercept, adalimumab, and infliximab cohorts, respectively, and 1.05 and 1.28 per

118 n infusion occurred in patients treated with infliximab compared with 13 (13.4%) patients given place

119 sk of serious infections with adalimumab and infliximab compared with nonmethotrexate and nonbiologic

120 Infliximab concentrations were measured in serum and sup

121 from mice given injections of human TNF and infliximab contained infliximab-TNF complexes; complex f

122 Treatment with Infliximab corrected these alterations.

123 iximab-infliximab group, and 40 [73%] in the infliximab-CT-P13 group).

124 he infliximab-infliximab group and 55 to the infliximab-CT-P13 group).

125 hTNF-Tg mice treated with infliximab demonstrated significant clinical and histolo

126 However, infliximab does reduce endoscopic recurrence.

127 Data included patient demographics, infliximab dosage information, additional immunosuppress

128 It is therefore important to optimize the infliximab dose to a level that is effective but does no

129 domly assigned (1:1) to groups that received infliximab dosing based on their clinical features (n =

130 ly observe patients who switch to biosimilar infliximab, especially within the first 90 days.

131 been occasionally associated with the use of infliximab, etanercept, and in a lesser extent adalimuma

132 We hypothesized that prednisolone and infliximab exert different effects on levels of STC2, PA

133 tus, smoking, significant infection history, infliximab exposure, and adalimumab exposure were each a

134 o analyze two high-purity mAbs (NIST mAb and Infliximab) expressed in a murine cell line.

135 s of infliximab and recombinant human TNF or infliximab F(ab')(2) fragments.

136 ng is superior to clinically based dosing of infliximab for maintaining remission in patients with CD

137 eated with vehicle (RA/WT) or Infliximab (RA Infliximab) for 4 weeks, before undergoing I/R brain inj

138 ave different half-lives, their influence on infliximab (G1m17,1 allotype) pharmacokinetics was inves

139 found ADA formation to increase with dose of infliximab given and concentration of infliximab-TNF com

140 tion group versus 172.0 (164.3-179.6) in the infliximab group (mean difference 6.1 points, 95% CI -4.

141 resection group versus 1.4 days (4.7) in the infliximab group (p<0.0001), days not able to take part

142 135 patients were allocated to the infliximab group and 135 to the ciclosporin group.

143 ents were enrolled and randomised: 98 to the infliximab group and 98 to placebo.

144 A smaller proportion of patients in the infliximab group had a clinical recurrence before or at

145 Participants in the infliximab group had a greater mean reduction in C-react

146 cantly smaller proportion of patients in the infliximab group had endoscopic recurrence based only on

147 cantly smaller proportion of patients in the infliximab group had endoscopic recurrence compared with

148 rs (IQR 2-6), 26 (37%) of 70 patients in the infliximab group had resection, and 19 (26%) of 73 patie

149 d survival (mean AUC 564.0 [SD 241.9] in the infliximab group vs 587.0 [226.2] in the ciclosporin gro

150 f colectomy (55 [41%] of 135 patients in the infliximab group vs 65 [48%] of 135 patients in the cicl

151 colectomy (811 [95% CI 707-912] days in the infliximab group vs 744 [638-850] days in the ciclospori

152 25 in 17 patients); or deaths (three in the infliximab group vs none in the ciclosporin group).

153 the CT-P13-CT-P13 group and 55 to the CT-P13-infliximab group) and 109 to initiate infliximab (54 to

154 CT-P13-CT-P13 group, 34 [62%] in the CT-P13-infliximab group, 37 [69%] in the infliximab-infliximab

155 verse events occurred in two patients in the infliximab group.

156 es of TNF antagonists such as etanercept and infliximab have been used successfully.

157 higher for those treated with adalimumab vs infliximab (hazard ratio [HR] 13.4, P = .01, 95% CI: 2.2

158 necrosis factor-alpha (TNF-alpha) inhibitor Infliximab herein.

159 n etanercept (HR 1.63; 95% CI: 1.45-1.84) or infliximab (HR 1.56; 95% CI: 1.16-2.09) were more likely

160 adalimumab (HR, 1.89; 95% CI, 1.32-2.70) or infliximab (HR, 1.92; 95% CI, 1.57-2.33), and for patien

161 of -20% was set (CT-P13 was non-inferior to infliximab if the lower limit of the two-sided 95% CI fo

162 Infliximab (IFX) is a chimeric mAb that can lead to the

163 Infliximab (IFX) is a therapeutic monoclonal antibody us

164 LH in pediatric patients with IBD exposed to infliximab (IFX) with patients not exposed to biologics

165 We generated aggregates by submitting infliximab (IFX), an immunogenic anti-TNF-alpha chimeric

166 oncentration of a therapeutic drug antibody, infliximab (IFX), is recommended for enhancing its effic

167 ligated (BDL) rats with PH were treated with Infliximab (IFX, a monoclonal antibody against TNF) and

168 se after clinical comparison with originator infliximab in ankylosing spondylitis and rheumatoid arth

169 gnificant difference between ciclosporin and infliximab in clinical effectiveness.

170 is study showed non-inferiority of CT-P13 to infliximab in patients with active Crohn's disease.

171 found in comparing biosimilar to originator infliximab in patients with chronic non-infectious uveit

172 vestigated whether CT-P13 is non-inferior to infliximab in patients with Crohn's disease who were nai

173 We evaluated the efficacy of infliximab in preventing postoperative recurrence of CD

174 High fecal concentrations of infliximab in the first days after therapy begins are as

175 regimens for intravenous corticosteroids and infliximab in these patients, and (7) role of adjunctive

176 irst case report documenting the benefits of infliximab in UC-related tracheobronchitis.

177 on in kidney transplantation and response to Infliximab in ulcerative colitis.

178 on in kidney transplantation and response to Infliximab in ulcerative colitis.

179 tigated the concentrations of adalimumab and infliximab in umbilical cord blood of newborns and rates

180 ravenous cyclophosphamide, methotrexate, and infliximab) in these patients may be associated with low

181 Infliximab induces a high rate of complete clinical remi

182 ) to receive CT-P13 then CT-P13, CT-P13 then infliximab, infliximab then infliximab, or infliximab th

183 p) and 109 to initiate infliximab (54 to the infliximab-infliximab group and 55 to the infliximab-CT-

184 the CT-P13-infliximab group, 37 [69%] in the infliximab-infliximab group, and 40 [73%] in the inflixi

185 agents (paclitaxel, oxaliplatin, rituximab, infliximab, irinotecan, and other drugs).

186 he G1m3,-1 mAb cetuximab, which explains why infliximab is a better competitor for endogenous IgG1 in

187 Infliximab is an antibody that neutralizes TNF-alpha and

188 Moderate-quality evidence suggests that infliximab is beneficial; RCT evidence for other interve

189 Infliximab is lost into stools of patients with UC.

190 Infliximab is not superior to placebo in preventing clin

191 b cross-reacts with murine TNF-alpha whereas infliximab is species specific.

192 n), based off the original product Remicade (infliximab, Janssen).

193 but prednisolone induces catabolism, whereas infliximab may promote protein synthesis.

194 isease, adalimumab, etanercept, ustekinumab, infliximab, methotrexate, apremilast, and golimumab are

195 iasis treatments: self-injectable biologics, infliximab, methotrexate, apremilast, and phototherapy.

196 ion therapy group compared with 29.8% in the infliximab monotherapy group (P = .63; hazard ratio, 1.1

197 year, were observed in patients treated with infliximab monotherapy who carried HLA-DQA1*05; converse

198 acy and safety of 16 weeks of treatment with infliximab monotherapy, azathioprine monotherapy, or the

199 These results suggest that infliximab more often is followed by remission, off medi

200 ds or other immunosuppressant agents such as infliximab; most irAEs will resolve with appropriate man

201 For infliximab, multivariable analysis of immunododulator us

202 treated with either prednisolone (n = 17) or infliximab (n = 21) were examined before and after 7 day

203 Most patients received infliximab (n = 40 [87%]), with systemic steroids in 28

204 adalimumab (n=1,879), etanercept (n=1,098), infliximab (n=96), and ustekinumab (n=450) were availabl

205 rent biopharmaceuticals (etanercept, n = 84; infliximab, n = 101; adalimumab, n = 153; interferon [IF

206 5050 infliximab-naive patients with CD who were older than 15

207 ss of CT-P13 is equivalent to that of RP for infliximab-naive patients with CD.

208 ponse was low drug concentration at week 14 (infliximab: odds ratio 0.35 [95% CI 0.20-0.62], p=0.0003

209 t screening, 115 of 263 patients had a TC of infliximab of 3-7 mug/mL (43.7%).

210 n's disease at the time of first exposure to infliximab or adalimumab between March 7, 2013, and July

211 naive patients with Crohn's disease starting infliximab or adalimumab therapy.

212 e scheduled to begin therapy with biologics (infliximab or adalimumab) were included, with enrollment

213 knockout mice were injected once with either infliximab or adalimumab, alone or preincubated with TNF

214 duals with IBD, exposure to corticosteroids, infliximab or adalimumab, metronidazole, hospitalization

215 ulcerative colitis following treatment with infliximab or ciclosporin, surgery, or other medication.

216 ulcerative colitis were randomised to either infliximab or ciclosporin.

217 s (PBMCs) from healthy donors incubated with infliximab or infliximab-TNF complexes; toll-like recept

218 oking status, previous thiopurines, previous infliximab or methotrexate, previous surgery, duration o

219 oup analyses (previous thiopurines, previous infliximab or methotrexate, previous surgery, duration o

220 ine: adalimumab (OR, 2.9; 95% CrI, 1.6-5.1), infliximab (OR, 1.6; 95% CrI, 1.0-2.5), infliximab + aza

221 tatic injury with anti-TNF-alpha antibodies (Infliximab) or glucocorticoids (Dexamethasone).

222 P13, CT-P13 then infliximab, infliximab then infliximab, or infliximab then CT-P13, with switching oc

223 osporine, acitretin, adalimumab, etanercept, infliximab, or ustekinumab or phototherapy for psoriasis

224 ne, compared with 54.6% (42 of 77) receiving infliximab (P = .295) and 36.8% (28 of 76) receiving aza

225 PAPP-A levels were only increased by infliximab (p = 0.005), whereas the inhibitor STC2 did n

226 ents with moderate to severe UC treated with infliximab plus azathioprine were more likely to achieve

227 Mice given increasing doses of infliximab produced increasing levels of ADAs.

228 ers at time of birth (adalimumab, r = -0.80; infliximab, r = -0.80; P < .0001 for both).

229 ical cord (adalimumab: r = -0.64, P = .0003; infliximab: r = -0.77, P < .0001) and in mothers at time

230 animals were treated with vehicle (RA/WT) or Infliximab (RA Infliximab) for 4 weeks, before undergoin

231 Infliximab reduced only IL1B and TNF expression.

232 h chronic, recalcitrant uveitis treated with infliximab (Remicade; Janssen Biotech, Inc., Titusville,

233 ing immune complexes with TNF-alpha, an anti-infliximab response was elicited.

234 is infliximab-bovine IgG1 chimera (bovinized infliximab) retained the antigen binding and neutralizat

235 ption for abatacept, adalimumab, etanercept, infliximab, rituximab, or tocilizumab before surgery.

236 e value of measuring serum concentrations of infliximab should be performed before these data can be

237 Infliximab significantly improved 7-day survival and red

238 Infliximab-specific plasma cells were detected in patien

239 ples, contained infliximab-TNF complexes and infliximab-specific plasma cells.

240 therapy with prednisone (strategy 3) or with infliximab (strategy 4), all followed by targeted treatm

241 Targeting patients' infliximab TCs to 3-7 mug/mL results in a more efficient

242 ents were more positive about treatment with infliximab than ciclosporin, mainly due to the cumbersom

243 umin and a higher incidence of antibodies to infliximab than patients in other quartiles.

244 Infliximab, the combination of infliximab and azathiopri

245 n infliximab, infliximab then infliximab, or infliximab then CT-P13, with switching occurring at week

246 CT-P13 then CT-P13, CT-P13 then infliximab, infliximab then infliximab, or infliximab then CT-P13, w

247 interquartile range [IQR]: 20.0-52.2) before infliximab therapy and 83.0 (IQR: 62.0-92.0) at follow-u

248 verely active UC during the first 2 weeks of infliximab therapy at the University of Amsterdam hospit

249 m patients having endoscopy who had received infliximab therapy for inflammatory bowel diseases; infl

250 were switched from originator to biosimilar infliximab therapy from 2014 to 2017.

251 were reversible with corticosteroids or with infliximab therapy in 2 cases.

252 nt of HRQOL changes over time in response to infliximab therapy in children with small bowel Crohn di

253 Infliximab therapy was commenced and was demonstrated to

254 Infliximab therapy was effective for a smaller proportio

255 iagnosed small bowel Crohn disease receiving infliximab therapy were prospectively enrolled.

256 owel Crohn disease (a) change in response to infliximab therapy, (b) correlate with proxy parent or g

257 experienced at least 1 side effect while on infliximab therapy, and 17 patients (19.3%) discontinued

258 ld be considered a reasonable alternative to infliximab therapy.

259 ith UC) with stable responses to maintenance infliximab therapy.

260 eks and weekly thereafter for up to 6 weeks; infliximab-TNF complexes and ADAs were measured by enzym

261 m patients, but not blood samples, contained infliximab-TNF complexes and infliximab-specific plasma

262 Uptake of infliximab and infliximab-TNF complexes by THP-1 cells was measured wit

263 ose of infliximab given and concentration of infliximab-TNF complexes detected in blood.

264 l tissues and blood samples, we propose that infliximab-TNF complexes formed in the intestine are end

265 Incubation of PBMCs with infliximab-TNF complexes resulted in a 4.74-fold increas

266 THP-1 cells endocytosed higher levels of infliximab-TNF complexes than infliximab alone.

267 mab therapy for inflammatory bowel diseases; infliximab-TNF complexes were measured with ELISA.

268 ctions of human TNF and infliximab contained infliximab-TNF complexes; complex formation was associat

269 healthy donors incubated with infliximab or infliximab-TNF complexes; toll-like receptors (TLRs) wer

270 pared laparoscopic ileocaecal resection with infliximab to assess how they affect health-related qual

271 veitis who were switched from the originator infliximab to biosimilar infliximab-abda for nonmedical

272 The addition of infliximab to primary treatment in acute Kawasaki diseas

273 that would predict a higher success rate of infliximab to treat various types of noninfectious uveit

274 res were found significantly decreased after infliximab treatment (all P < 0.001).

275 e initial reduction of macrophages following infliximab treatment in hTNF-Tg mice.

276 aire (MCIBDQ), and to evaluate the impact of infliximab treatment on HRQOL in patients with IBD for t

277 Infliximab treatment was found to significantly improve

278 Infliximab treatment was suggested to significantly redu

279 Infliximab treatment, at least in these steatotic and ch

280 ior immunomodulatory treatments, duration of infliximab treatment, dose received, secondary side effe

281 Upon infliximab treatment, total IGF-I levels were augmented

282 ative colitis who were candidates to receive infliximab treatment.

283 Infliximab-treatment restored the phenotype of RA-mice t

284 the combination of maintenance methotrexate-infliximab trial, we evaluated the potential superiority

285 roved for psoriasis (adalimumab, etanercept, infliximab, ustekinumab) with the possibility to switch

286 a randomized trial to compare the ability of infliximab vs placebo to prevent CD recurrence.

287 s (16 reactions in 14 participants receiving infliximab vs ten in nine patients receiving ciclosporin

288 Infliximab was cleared more slowly than adalimumab from

289 Infliximab was detected in 129 of 195 fecal samples (66%

290 Infliximab was found to have a shorter half-life in pati

291 Infliximab was modified to incorporate the sequences fro

292 The safety profile of infliximab was similar to that from previous reports.

293 nly 1 patient had flares while on originator infliximab went on to develop a single flare on inflixim

294 Ixekizumab and infliximab were differentiated by very high efficacy but

295 .0 microg/mL [IQR, 1.6 to 5.9 microg/mL]) of infliximab were similar in patients with and without les

296 ed in 45 episodes, the most common one being infliximab, which achieved success in 80% of patients.

297 IgG2 proved to have similar modifications to Infliximab with lower relative abundances of the lysine

298 A combination of infliximab with methotrexate results in greater efficacy

299 We compared serum concentrations of infliximab with outcomes of 728 patients with moderately

300 s a biosimilar of the reference product (RP) infliximab, with demonstrated efficacy and safety for so