ライフサイエンスコーパス: eculizumab

1 n injury treated with the complement blocker eculizumab.

2 physicians to manage PNH patients receiving eculizumab.

3 episodes benefit from treatment with PLEX + Eculizumab.

4 related to the time to initiate therapy with eculizumab.

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

6 ved for patients with suboptimal response to eculizumab.

7 to therapy including the prophylactic use of eculizumab.

8 be more likely to benefit from therapy with eculizumab.

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

10 ent dense deposit disease being managed with eculizumab.

11 f a therapeutic regimen with the C5 antibody eculizumab.

12 cal response following the administration of eculizumab.

13 anicopan as add-on therapy to ravulizumab or eculizumab.

14 ings, and (in 1 case) a clinical response to eculizumab.

15 eived standard of care (SOC) and 51 received eculizumab.

16 norrhoeae infection among patients receiving eculizumab.

17 to determine which patients may benefit from eculizumab.

18 ed recently in individuals not responsive to eculizumab.

19 nsplant recipients treated with prophylactic eculizumab.

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

21 S patients and alternative to C5 blockade by eculizumab.

22 Participants received repeated intravenous eculizumab.

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

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

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

26 reatment with pegcetacoplan (41 patients) or eculizumab (39 patients).

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

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

29 treatment failure rate was observed between eculizumab (9.8%) and SOC (13.7%; P = .760).

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

31 Eculizumab, a humanized anti-complement C5 monoclonal an

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

33 Eculizumab, a humanized monoclonal antibody against comp

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

35 as evaluated through the characterization of eculizumab, a hybrid therapeutic IgG2/4 mAb.

36 In particular, eculizumab, a monoclonal antibody against complement C5,

37 Eculizumab, a monoclonal antibody against the complement

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

39 Eculizumab, a monoclonal antibody that blocks terminal c

40 Eculizumab, a monoclonal antibody, inhibits terminal com

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

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

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

44 tive response technology to pegcetacoplan or eculizumab (according to their regimen at enrolment) for

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

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

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

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

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

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

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

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

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

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

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

56 Eculizumab and combined liver-kidney transplantation off

57 3 inhibitor Compstatin and the C5 inhibitors eculizumab and Coversin reported here demonstrate that C

58 C1-INH contrasts with eculizumab and other distal inhibitors, which do not aff

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

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

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

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

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

64 Eculizumab and ravulizumab are safe and effective therap

65 Drug Administration-approved C5 inhibitors (eculizumab and ravulizumab) to treat PNH.

66 Furthermore, C5 inhibition with eculizumab and ravulizumab, as well as inhibition of the

67 t failure rates were 11.8% and 21.6% for the eculizumab and SOC groups, respectively (nominal P = .28

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

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

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

71 s PREVENT and the OLE, 137 patients received eculizumab and were monitored for a median (range) of 13

72 AMR, the treatment failure rates were 11.8% (eculizumab) and 29.4% (SOC; nominal P = .048).

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

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

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

76 atients with bone marrow transplantation and eculizumab are explored.

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

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

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

80 Participants received eculizumab as follows: 1200 mg immediately before reperf

81 We investigated the role of eculizumab as primary therapy for active AMR early postt

82 e, within a single run, the hybrid nature of eculizumab as well as specific subclass domain assignmen

83 l haemoglobinuria and suboptimal response to eculizumab at 16 weeks.

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

85 nce rates may be overestimated, and starting eculizumab at relapse ("rescue therapy") may prevent gra

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

87 Single inhibition of C5 by eculizumab attenuated the release of IL-6, IL-8, TNF, MC

88 Eculizumab binds complement component C5 and prevents it

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

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

91 nts with intestinal bleeding had the fastest eculizumab clearance, required the highest number of ecu

92 his finding suggests a potential benefit for eculizumab compared with SOC in preventing acute AMR in

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

94 Eculizumab completely prevented electrophysiological and

95 a frequency of 10% to 15% over 6 months with eculizumab, crovalimab, and pegcetacoplan, and <5% with

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

97 A strategy of eculizumab discontinuation in aHUS patients based on com

98 n addition, increased sC5b-9 plasma level at eculizumab discontinuation was associated with a higher

99 At eculizumab discontinuation, 17 (30%) and 4 patients (7%)

100 Included patients had at least 1 eculizumab dose within the 3 months prior to N. gonorrho

101 ab clearance, required the highest number of eculizumab doses (20 vs 9; P = .0015), and had lower 1-y

102 Eculizumab dosing included intensive loading, induction,

103 Eculizumab dramatically alters the natural course of PNH

104 of care, patients received nine infusions of eculizumab during the first 2 months posttransplant.

105 Intravenous injection of eculizumab effectively prevented respiratory paralysis a

106 5b-9 endothelial deposits might help monitor eculizumab effectiveness, avoid drug overexposure, and s

107 therapy for STEC-HUS, a controlled study of eculizumab efficacy in treating this condition is a prio

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

109 w atypical HUS epidemiology in France in the eculizumab era evolved, we undertook a population-based

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

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

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

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

114 yte count >=120 x 10(9)/L) on ravulizumab or eculizumab for at least 6 months.

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

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

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

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

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

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

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

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

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

124 Eculizumab has been associated with impressive results i

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

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

127 nal complement pathway with the C5 inhibitor eculizumab has revolutionized the clinical management of

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

129 Eculizumab has the potential to provide prophylaxis agai

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

131 f biopsy-proven AMR in patients treated with eculizumab (HR = 0.36, 95% CI = 0.14-0.95, p = .032).

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

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

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

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

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

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

138 he success of the humanised anti-C5 antibody eculizumab in effectively treating paroxysmal nocturnal

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

140 ibitor, pegcetacoplan, showed superiority to eculizumab in improving haematological outcomes in adult

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

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

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

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

145 trial to evaluate the safety and efficacy of eculizumab in preventing acute AMR in recipients of dece

146 study evaluating the safety and efficacy of eculizumab in preventing acute antibody-mediated rejecti

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

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

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

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

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

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

153 At week 12, danicopan plus ravulizumab or eculizumab increased haemoglobin versus placebo plus rav

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

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

156 Eculizumab inhibited complement-mediated thrombotic micr

157 Eculizumab inhibits the intravascular haemolysis of PNH,

158 Eculizumab inhibits the terminal, lytic pathway of compl

159 o be transfusion-dependent at 6 months after eculizumab initiation (P = .015).

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

161 ed dosing, requiring a median of 11 doses of eculizumab (interquartile range [IQR] 7-20).

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

163 Eculizumab is a humanised monoclonal antibody that binds

164 Eculizumab is a humanized mAb approved for treatment of

165 In summary, complement blockade with eculizumab is an effective therapeutic strategy for hrTA

166 C5 inhibition with eculizumab is an important therapeutic resource to manag

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

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

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

170 Eculizumab is safe and well tolerated in patients with P

171 emoglobin versus placebo plus ravulizumab or eculizumab (least squares mean [LSM] change from baselin

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

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

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

175 Patients receiving eculizumab may be at higher risk for DGI than the genera

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

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

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

179 atients (including 19 children) discontinued eculizumab (mean treatment duration, 16.5 months).

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

181 Eculizumab might benefit C3 glomerulopathies mediated by

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

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

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

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

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

187 are encouraged to educate patients receiving eculizumab on their risk for serious gonococcal infectio

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

189 Anticoagulation alone or in combination with eculizumab or intravenous immunoglobulin (IVIG) resolved

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

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

192 all randomly assigned patients who received eculizumab or placebo.

193 er than 10 g/dL on anti-C5 treatment (stable eculizumab or ravulizumab regimen for >=6 months) were r

194 or to continue their individual intravenous eculizumab or ravulizumab regimen for 24 weeks (anti-C5

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

196 of complement C3 by CP40 (compstatin), C5 by eculizumab, or C5aR1 by PMX53 blocked CC-induced PTF1.2

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

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

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

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

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

202 irst 30 days posttransplant and treated with eculizumab +/- plasmapheresis.

203 1) days posttransplant and were treated with eculizumab +/- plasmapheresis.

204 After a 4-week run-in with eculizumab plus pegcetacoplan, patients were randomly as

205 function, no immunosuppression and continues eculizumab prevention of aHUS (1 infusion every 21 days)

206 plants; in four cases, patients had received eculizumab prophylaxis and in 39 cases they did not.

207 ional study are consistent with benefit from eculizumab prophylaxis based on pretransplant risk strat

208 Guidelines advise eculizumab prophylaxis for most kidney transplant recipi

209 Eculizumab prophylaxis was used in 52 kidney transplants

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

211 Eculizumab provided benefit for women with PNH during pr

212 0.15; P = .0014) and required more doses of eculizumab (r = 0.43; P = .0004).

213 Eculizumab reduced terminal complement activation (C5a a

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

215 e regime, death-censored graft survival with eculizumab rescue therapy was not inferior to prophylaxi

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

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

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

219 Eculizumab resulted in increases in the platelet count;

220 tested the efficacy of three new therapies (eculizumab, satralizumab, and inebilizumab) for patients

221 Eculizumab seems to be well tolerated, significantly red

222 An acidic mAb (eculizumab) showed improved recovery, more stable retent

223 During PREVENT (NCT01892345), eculizumab significantly reduced relapse risk versus pla

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

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

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

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

228 nistic differences between pegcetacoplan and eculizumab that determine their efficacy in patients wit

229 Eculizumab, the first-in-class complement inhibitor, was

230 lonal antibodies: the complement C5 antibody eculizumab, the IL-6 receptor antibody satralizumab, the

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

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

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

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

235 If antimicrobial prophylaxis is used during eculizumab therapy, prescribers should consider trends i

236 patients with hemolytic PNH while receiving eculizumab therapy.

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

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

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

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

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

242 cept a short (2 days) course of steroids and eculizumab to prevent aHUS relapse.

243 d complement blockade-based prophylaxis with eculizumab to prevent post-transplant atypical HUS recur

244 10.14 points (9.06), and for patients in the eculizumab-to-pegcetacoplan group mean 9.62 points (10.3

245 s (eight pegcetacoplan-to-pegcetacoplan, ten eculizumab-to-pegcetacoplan) had at least one serious tr

246 n] or 28 weeks of pegcetacoplan monotherapy [eculizumab-to-pegcetacoplan]).

247 -thymocyte globulin, basiliximab, rituximab, eculizumab, tofacitinib, tacrolimus, mycophenolate mofet

248 blocking antibodies, including pozelimab and eculizumab, transformed CHAPLE management.

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

250 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

251 s indicated a reduction of renal sequelae in eculizumab-treated patients at 1-year follow-up.

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

253 Prompt eculizumab treatment as primary therapy is safe and effe

254 t-associated thrombotic microangiopathy, and eculizumab treatment correlated with poor response, whil

255 In pediatric patients with STEC-HUS, eculizumab treatment does not appear to be associated wi

256 Prior reports of eculizumab treatment for AMR have been in heterogeneous

257 Unsuccessful eculizumab treatment has only been reported once in the

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

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

260 Graft survival without eculizumab treatment is described by complement defect s

261 Eculizumab treatment led to an improvement in anemia.

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

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

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

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

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

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

268 ife measures were also broadly improved with eculizumab treatment.

269 0.50 g/dL after 3 months or longer of stable eculizumab treatment.

270 d showed a close correlation with increasing eculizumab use among the transplant recipients.

271 nefited from a brief but intensive course of eculizumab using pharmacokinetic/pharmacodynamic-guided

272 Approval of eculizumab validates the complement system as therapeuti

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

274 Eculizumab was administered by intravenous infusion at 6

275 Eculizumab was also associated with improvement in healt

276 Eculizumab was associated with significant improvement i

277 Earlier intervention with eculizumab was associated with significantly greater imp

278 Eculizumab was considered after the failure of corticost

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

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

281 Use of prophylactic eculizumab was independently associated with a significa

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

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

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

285 Eculizumab was restarted in 6 individuals with functioni

286 Eculizumab was safely administered to these patients.

287 Eculizumab was well tolerated and no new safety concerns

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

289 Eculizumab was well tolerated with no new safety concern

290 Eculizumab was well tolerated.

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

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

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

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

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

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

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

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

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

300 gonorrhoeae infection in patients receiving eculizumab worldwide were obtained from US Food and Drug