ライフサイエンスコーパス: eculizumab

1 nsplant recipients treated with prophylactic eculizumab.

2 to therapy including the prophylactic use of eculizumab.

3 be more likely to benefit from therapy with eculizumab.

4 m the basis of the sole renal indication for eculizumab.

5 ent dense deposit disease being managed with eculizumab.

6 f a therapeutic regimen with the C5 antibody eculizumab.

7 cal response following the administration of eculizumab.

8 a presented with aHUS but did not respond to eculizumab.

9 Participants received repeated intravenous eculizumab.

10 to determine which patients may benefit from eculizumab.

11 s abrogation by heat inactivation, EDTA, and eculizumab.

12 physicians to manage PNH patients receiving eculizumab.

13 ed recently in individuals not responsive to eculizumab.

14 episodes benefit from treatment with PLEX + Eculizumab.

15 related to the time to initiate therapy with eculizumab.

16 odies, which paved the way to treatment with eculizumab.

17 ved for patients with suboptimal response to eculizumab.

18 patient-years) compared with 2 thromboses on eculizumab (0.8 events per 100 patient-years; P < .001).

19 HUS-related end-stage renal disease received eculizumab: 10 from day 0 and 2 at the time of recurrenc

20 ients (27%) had a thrombosis before starting eculizumab (5.6 events per 100 patient-years) compared w

21 dent patients with PNH received infusions of eculizumab (600 mg) every week for four weeks, followed

22 Eculizumab, a first-in-class monoclonal antibody that in

23 Eculizumab, a humanized anti-complement C5 monoclonal an

24 We tested the clinical efficacy of eculizumab, a humanized antibody that inhibits the activ

25 Eculizumab, a humanized monoclonal antibody against comp

26 olysis, which is effectively controlled with eculizumab, a humanized monoclonal antibody that binds c

27 Eculizumab, a monoclonal antibody against the complement

28 n be inhibited in patients by treatment with eculizumab, a monoclonal antibody that binds complement

29 Eculizumab, a monoclonal antibody that blocks terminal c

30 Results from a phase 2 study suggested that eculizumab, a terminal complement inhibitor, produced cl

31 of this study was to investigate the use of eculizumab--a therapeutic monoclonal IgG that neutralise

32 Patients were treated with Eculizumab according to the aHUS therapeutic scheme.

33 tient developed AMR while being treated with eculizumab after a relapse of atypical hemolytic uremic

34 We present two cases of AMR resistant to eculizumab after renal transplantation.

35 Three patients on eculizumab, all over 50 years old, died of causes unrela

36 phenotype by using splenectomy alone (n=14), eculizumab alone (n=5), or splenectomy plus eculizumab (

37 glomerulopathy in the splenectomy-alone and eculizumab-alone groups at 1 year, whereas splenectomy p

38 (median=320 days), compared to four of five eculizumab-alone patients with graft failure (median=95

39 We treated him with eculizumab, an anti-C5 monoclonal antibody that blocks a

40 peutic agents have recently emerged, such as eculizumab, an anticomplement protein-C5 monoclonal anti

41 t report of the use and clinical efficacy of eculizumab, an inhibitor of complement activation, in th

42 y assigned and treated 125 patients, 62 with eculizumab and 63 with placebo.

43 t, as shown by >99% inhibition by anti-C5 Ab eculizumab and a lack of NK cell activation in whole blo

44 Eculizumab and combined liver-kidney transplantation off

45 sis showed no significant difference between eculizumab and placebo (least-squares mean rank 56.6 [SE

46 re 2.55 +/- 0.94 and 2.02 +/- 0.74 mm in the eculizumab and placebo groups, respectively (P = 0.13).

47 of 0.19 +/- 0.12 and 0.18 +/- 0.15 mm in the eculizumab and placebo groups, respectively (P = 0.96).

48 re was not statistically significant between eculizumab and placebo, as measured by the worst-rank an

49 Three patients were treated with eculizumab and plasmapheresis for recurrent aHUS after k

50 ase in immunized patients being treated with eculizumab and suggest that vaccination may provide bett

51 By using eculizumab and the tick-derived C5 inhibitor coversin, w

52 rm outcome of patients with PNH treated with eculizumab and to define the relationship between PNH an

53 Ten patients received plasmapheresis, 6 eculizumab, and 7 a combination of both.

54 C5 cleavage was inhibited using eculizumab, and C5aR1 was blocked by an antagonist.

55 sion or exchange, rituximab, sulodexide, and eculizumab are additional options.

56 atients with bone marrow transplantation and eculizumab are explored.

57 tions suggest that PNH patients treated with eculizumab are left with clinically significant immune-m

58 of the efficacy of the complement inhibitor eculizumab are promising, the outcome of a recent clinic

59 The recent approval of eculizumab as a first-in-class complement inhibitor for

60 and a Fab fragment with the same sequence as eculizumab at a resolution of 4.2 A.

61 Administration of eculizumab, at doses that blocked complement activity, a

62 Eculizumab binds complement component C5 and prevents it

63 ezomib depletes plasma cell populations, and eculizumab blocks the terminal effects of antibody actio

64 biomarkers, complement assessment, and free eculizumab circulating levels were systematically measur

65 elestat (neutrophil elastase inhibitor), and eculizumab (complement inhibitor).

66 Eculizumab completely prevented electrophysiological and

67 The apparent effects of eculizumab deserve further investigation in larger, rand

68 Eculizumab dramatically alters the natural course of PNH

69 Intravenous injection of eculizumab effectively prevented respiratory paralysis a

70 5b-9 endothelial deposits might help monitor eculizumab effectiveness, avoid drug overexposure, and s

71 ntion of posttransplant aHUS recurrence with eculizumab emerged a few years ago.

72 No patients treated with splenectomy plus eculizumab experienced graft loss.

73 The treatment group received 6 mo of eculizumab followed by 6 mo of observation, whereas cont

74 e who were 12 years of age or older received eculizumab for 26 weeks and during long-term extension p

75 s (17 in trial 1 and 20 in trial 2) received eculizumab for a median of 64 and 62 weeks, respectively

76 ses and explain the exquisite selectivity of eculizumab for human C5 and how polymorphisms in C5 caus

77 Forty of 61 (66%) patients on eculizumab for more than 12 months achieved transfusion

78 , a brief discussion of the effectiveness of eculizumab for the prevention of antibody-mediated rejec

79 Our results suggest that eculizumab functions by sterically preventing C5 from bi

80 Six (10%) patients in the eculizumab group and 12 (19%) in the placebo group requi

81 infection (ten [16%] for both events in the eculizumab group and 12 [19%] for both in the placebo gr

82 s were reported by six (10%) patients in the eculizumab group and 15 (24%) in the placebo group.

83 imester, the dose or the frequency of use of eculizumab had to be increased.

84 Complement inhibition with eculizumab has a dramatic effect in PNH and has a major

85 Eculizumab has been associated with impressive results i

86 In the last year the complement inhibitor eculizumab has been used successfully to treat patients

87 The anti-C5 antibody eculizumab has proven clinically effective, but uncontro

88 In the setting of renal transplantation, eculizumab has so far proved effective both for preventi

89 ients with clinical PNH who are treated with eculizumab have a benign clinical course.

90 The PLEX + Eculizumab improved graft survival for TMA patients (P =

91 linical safety and efficacy study evaluating eculizumab in a broader PNH patient population.

92 ublished data establish the effectiveness of eculizumab in a select group of renal diseases that have

93 ng number of case reports support the use of eculizumab in C3 glomerulopathy (C3G).

94 The use of eculizumab in C4d-negative or C1q-negative AMR does not

95 ary to clarify the effectiveness and role of eculizumab in dense deposit disease but the response in

96 spectively analyzed 12 patients who received Eculizumab in France between 2010 and 2013 for severe po

97 aluated 79 consecutive patients treated with eculizumab in Leeds between May 2002 and July 2010.

98 Response rate and overall survival after Eculizumab in our cohort compare favorably with previous

99 rst systematic pharmacodynamic (PD) study of eculizumab in PNH patients which shows that CH50 is a pr

100 We assessed the safety and efficacy of eculizumab in pregnant patients with PNH by examining th

101 ontrolled trials exist to support the use of eculizumab in renal disease.

102 y, there are conflicting data for the use of eculizumab in STEC HUS.

103 This review considers the use of eculizumab in the treatment of atypical haemolytic uraem

104 The results of clinical trials of eculizumab in this condition are eagerly awaited.

105 further assessed the efficacy and safety of eculizumab in this patient population in a phase 3 trial

106 and overall survival, but data on the use of eculizumab in women during pregnancy are scarce.

107 Although chronic treatment with eculizumab increases the risk of infections with Neisser

108 le meningitis about 2 months after the first eculizumab infusion, but resumed treatment after full re

109 Eculizumab inhibited complement-mediated thrombotic micr

110 Eculizumab inhibits the intravascular haemolysis of PNH,

111 Eculizumab inhibits the terminal, lytic pathway of compl

112 entified 28 residues as important for the C5-eculizumab interaction, and the structure of the complex

113 e successful introduction of the C inhibitor eculizumab into clinical practice.

114 Eculizumab is a humanised monoclonal antibody that binds

115 Eculizumab is a humanized mAb approved for treatment of

116 oped for treatment of ultra-orphan diseases, eculizumab is expensive, and treatment must continue ind

117 These data confirm that eculizumab is highly effective in preventing posttranspl

118 eneous nature of the disease, treatment with eculizumab is not appropriate for all patients with PNH.

119 Eculizumab is safe and well tolerated in patients with P

120 that both CH50 activity and circulating free eculizumab levels may help physicians to manage PNH pati

121 Low levels of circulating free eculizumab (<50 microg/mL) correlated with detectable CH

122 Marked clinical improvement suggests that eculizumab may be a life-saving treatment for patients w

123 Early initiation of Eculizumab may have a favorable effect on long-term rena

124 This case provides the first evidence that eculizumab may have a place in the management of crescen

125 nifesting early severe AMR, splenectomy plus eculizumab may provide an effective intervention for res

126 al features, complement assessment, and free eculizumab measurements were analyzed.

127 Eculizumab might benefit C3 glomerulopathies mediated by

128 ma exchange and 50 patients (47.2%) received eculizumab (monoclonal anti-C5 antibody).

129 Patients treated with eculizumab (n = 11) and/or plasmapheresis (n = 13) durin

130 eculizumab alone (n=5), or splenectomy plus eculizumab (n=5), in addition to plasmapheresis.

131 e C3 convertase regulation; however, neither eculizumab nor tagged compstatin had any effect.

132 lockade with the anti-C5 monoclonal antibody eculizumab on biomarkers of cellular processes involved

133 d after 3-hour incubation in the presence of eculizumab or control complement factor D inhibitor ACH-

134 ned participants (1:1) to either intravenous eculizumab or intravenous matched placebo for 26 weeks.

135 s were randomized 2:1 to receive intravenous eculizumab or placebo over 6 months.

136 all randomly assigned patients who received eculizumab or placebo.

137 nsplant receiving rejection prophylaxis with eculizumab or standard of care (plasma exchange and intr

138 suppressed in patients even under excess of eculizumab over C5, indicating that residual C5 activity

139 to 5.0 units in the most recent 12 months on eculizumab (P < .001).

140 tter than 30 similar patients managed before eculizumab (P = .030).

141 e groups at 1 year, whereas splenectomy plus eculizumab patients had almost no transplant glomerulopa

142 er, in essentially all patients treated with eculizumab, persistent anemia, reticulocytosis, and bioc

143 We show that eculizumab protects against complement-mediated damage i

144 Eculizumab provided benefit for women with PNH during pr

145 Eculizumab reduced terminal complement activation (C5a a

146 ase IIa study, we aimed to determine whether eculizumab reduces chronic hemolysis, and cumulative dos

147 r human C5 and how polymorphisms in C5 cause eculizumab-resistance in a small number of patients with

148 Patients treated with eculizumab responded with an 87% reduction in hemolysis,

149 of meningococci killing by blood containing eculizumab resulted from inhibition of release of C5a, a

150 Eculizumab resulted in increases in the platelet count;

151 Eculizumab seems to be well tolerated, significantly red

152 rapies, i.e., hydroxychloroquine, rituximab, eculizumab, sirolimus, and defibrotide, that can be cons

153 dy directed against complement component C5, eculizumab (Soliris; Alexion Pharmaceuticals Inc., Chesh

154 an antibody against complement component C5 (eculizumab; Soliris), in March 2007, was a long-awaited

155 Compared with standard of care, eculizumab specifically abrogated this histomolecular re

156 ell as by the terminal complement pathway Ab eculizumab, the purinergic P2 receptor antagonist surami

157 od samples were examined for the presence of eculizumab; the drug was detected in 7 of the samples.

158 breast milk was examined for the presence of eculizumab; the drug was not detected in any of the 10 b

159 eport renal biopsy findings before and after eculizumab therapy in three patients with dense deposit

160 patients with hemolytic PNH while receiving eculizumab therapy.

161 In the presence of eculizumab, there was a >22-fold increase in geometric m

162 Four patients received prophylactic eculizumab; three of them received 6 months and one has

163 tion carriers, and (3) search for a tool for eculizumab titration.

164 n requirement reduced from 19.3 units before eculizumab to 5.0 units in the most recent 12 months on

165 lasses, suggesting the binding of monoclonal eculizumab to C5 in renal tissues.

166 In 8 eculizumab-treated aHUS patients, C3/SC5b-9 circulating

167 nlarged by a mean of 0.37 +/- 0.22 mm in the eculizumab-treated eyes and by a mean of 0.37 +/- 0.21 m

168 In the eculizumab treatment arm, the first 10 patients received

169 Unsuccessful eculizumab treatment has only been reported once in the

170 demonstrates that the beneficial effects of eculizumab treatment in patients with PNH are applicable

171 of this work was to report on the outcome of eculizumab treatment in pediatric patients with recurren

172 Eculizumab treatment led to an improvement in anemia.

173 Our data suggest that eculizumab treatment may stabilize kidney function in pa

174 of residual terminal pathway activity under eculizumab treatment with important implications for ant

175 After 12 months of eculizumab treatment, 12 patients were relapse free; two

176 al nocturnal hemoglobinuria (PNH) undergoing eculizumab treatment, which are opsonized with the compl

177 at a screening visit and 2 weeks later began eculizumab treatment.

178 ife measures were also broadly improved with eculizumab treatment.

179 l nocturnal hemoglobinuria (PNH) patients on eculizumab treatment.

180 Approval of eculizumab validates the complement system as therapeuti

181 Dosing for eculizumab was 900 mg on day 1 and at weeks 1, 2, and 3;

182 Eculizumab was administered by intravenous infusion at 6

183 Eculizumab was also associated with improvement in healt

184 Eculizumab was associated with significant improvement i

185 Earlier intervention with eculizumab was associated with significantly greater imp

186 Eculizumab was considered after the failure of corticost

187 lusters for C5 activation in the presence of eculizumab was corroborated by the finding that residual

188 monstrate that treatment or prophylaxis with eculizumab was effective in reversing or preventing aHUS

189 The survival of patients treated with eculizumab was not different from age- and sex-matched n

190 Long-term safety and efficacy of eculizumab was observed in a large group of patients.

191 The terminal complement inhibitor eculizumab was recently shown to be effective and well t

192 Eculizumab was safely administered to these patients.

193 Systemic complement inhibition with eculizumab was well tolerated through 6 months but did n

194 Eculizumab was well tolerated.

195 They received 600 mg intravenous eculizumab weekly for 4 weeks, 900 mg in the fifth week,

196 ily PP/IVIg, a second dose of anti-CD20, and eculizumab were administered.

197 , fatigue, and transfusion requirements with eculizumab were independent of baseline levels of hemoly

198 fficacy of the humanized monoclonal antibody eculizumab, which blocks the formation of human C5a and

199 egies for LETM in the context of NMO include eculizumab, which could be considered in patients with a

200 individuals with TMAs who may not respond to eculizumab will avoid prolonged exposure of such individ

201 Nine patients were treated with eculizumab with 7/9 (78%) responding to therapy.

202 previous thrombosis discontinued warfarin on eculizumab with no thrombotic sequelae.

203 e patients were reported within 12 months of eculizumab withdrawal.