ライフサイエンスコーパス: alemtuzumab

1 ultiple sclerosis considering treatment with alemtuzumab.

2 % of these sero (+) patients at 1 month post-alemtuzumab.

3 ation alemtuzumab, and FR with consolidation alemtuzumab.

4 g regimen consisting of cyclophosphamide and alemtuzumab.

5 ), corresponding to a 49.4% improvement with alemtuzumab.

6 ), corresponding to a 54.9% improvement with alemtuzumab.

7 n CD52 transgenic (CD52Tg) mice treated with alemtuzumab.

8 consistently responded better than others to alemtuzumab.

9 acteristics affect the beneficial effects of alemtuzumab.

10 ab to be equally as effective as intravenous alemtuzumab.

11 translpant NK cell levels were detected post-alemtuzumab.

12 by 2 months and 95% did so by 3 months post-alemtuzumab.

13 implications for the safety and efficacy of alemtuzumab.

14 and are rendered resistant to destruction by alemtuzumab.

15 t patients (52%) required just two cycles of alemtuzumab.

16 mong patients treated with thymoglobulin and alemtuzumab.

17 yeloablative transplant study, consisting of alemtuzumab (1 mg/kg in divided doses), total-body irrad

18 tained accumulation of disability, comparing alemtuzumab 12 mg and interferon beta 1a in all patients

19 , stratified by site, to receive intravenous alemtuzumab 12 mg per day or subcutaneous interferon bet

20 neous interferon beta 1a 44 mug, intravenous alemtuzumab 12 mg per day, or intravenous alemtuzumab 24

21 426 (98%) of 436 patients randomly allocated alemtuzumab 12 mg were included in the primary analyses.

22 For 435 patients allocated alemtuzumab 12 mg, 393 (90%) had infusion-associated rea

23 irst patients with progressive MS to receive alemtuzumab (1991-1997).

24 The cohorts consisted of 189 patients given alemtuzumab, 2155 patients given interferon beta, 828 pa

25 Treatment with cyclophosphamide and alemtuzumab (22 patients) or cyclophosphamide and thymog

26 us alemtuzumab 12 mg per day, or intravenous alemtuzumab 24 mg per day.

27 2) per day: n = 139) or FC plus subcutaneous alemtuzumab 30 mg day 1 (FCA, n = 133).

28 reatment (fludarabine 30 mg/m(2) per day and alemtuzumab 30 mg per day on days 1-3) or monotherapy (f

29 All patients had been treated with alemtuzumab; 61/141 had developed secondary autoimmunity

30 -4.43; p=0.0004) among patients treated with alemtuzumab (66 of 133 patients, Kaplan-Meier estimate 5

31 Alemtuzumab, a CD52-depleting monoclonal antibody, effec

32 ceptor (TCR) and CD52, a protein targeted by alemtuzumab, a chemotherapeutic agent.

33 Studies show that alemtuzumab, a potent lymphocyte-depleting agent, is wel

34 lemtuzumab were monitored for Treg and serum alemtuzumab activity.

35 CART (RNA-CART123); (2) T-cell ablation with alemtuzumab after treatment with lentivirally transduced

36 .09); after induction immunosuppression with alemtuzumab (aIRR = 3.12), monoclonal antibodies (aIRR =

37 ective of our study was to determine whether alemtuzumab (AL) induction abolishes this discrepancy an

38 Purine analogues and alemtuzumab alter cell-mediated immunity, resulting in o

39 Alemtuzumab, an anti-CD52 antibody, is proven to be more

40 aimed to explore the activity and safety of alemtuzumab, an anti-CD52 monoclonal antibody, in patien

41 -year survival was 83% (95% CI, 68%-99%) for alemtuzumab and 60% (95% CI, 43%-85%) for rabbit ATG (P

42 However, relapse was more frequent with alemtuzumab and ATG compared with T cell-replete regimen

43 ional evidence indicates that, compared with alemtuzumab and basiliximab, rATG associates with lower

44 CD52 expression, binding of alemtuzumab and both complement-mediated killing and Ab-

45 When compared with alemtuzumab and IL-2 receptor blocker, r-ATG induction s

46 Patients were treated with alemtuzumab and methylprednisolone for induction, follow

47 ter phase II study was developed to evaluate alemtuzumab and methylprednisolone in combination.

48 INTERPRETATION: Alemtuzumab and natalizumab seem to have similar effects

49 Treatment decisions between alemtuzumab and natalizumab should be primarily governed

50 nsplant rejection; among high-risk patients, alemtuzumab and rabbit antithymocyte globulin had simila

51 ory submissions of the pivotal Comparison of Alemtuzumab and Rebif Efficacy in Multiple Sclerosis I a

52 years for the ATG group and 5 years for the alemtuzumab and T cell-replete groups.

53 Depleting antibody induction therapy with alemtuzumab and Thymoglobulin appear equally effective i

54 Study cohort included 1149 patients each in alemtuzumab and Thymoglobulin groups.

55 After rescue therapy with intravenous alemtuzumab and/or pentostatin, median progression-free

56 n phase II/III trials of multiple sclerosis (alemtuzumab) and type I diabetes mellitus (teplizumab, o

57 40%, P < .0001) and chronic GVHD, lower with alemtuzumab, and ATG regimens compared with T-replete ap

58 MS patients: they are reduced by fingolimod, alemtuzumab, and dimethyl fumarate, whereas natalizumab

59 tuximab (FR), fludarabine with consolidation alemtuzumab, and FR with consolidation alemtuzumab.

60 ed for surveillance of patients treated with alemtuzumab, and the possible role for increased melanom

61 All patients received alemtuzumab (anti-CD52 antibody).

62 Alemtuzumab (anti-CD52 mAb) provides long-lasting diseas

63 We also examined the CDC activity of alemtuzumab (anti-CD52) and mAb W6/32 (anti-HLA), which

64 ma exchange (PE), rituximab (anti-CD20), and alemtuzumab (anti-CD52), before receiving tocilizumab.

65 ction therapy by lymphocyte depletion, using alemtuzumab (anti-human CD52), is associated with an inc

66 the primary outcome measure of 97.6% in the alemtuzumab arm and 95.1% in the daclizumab arm at 1 yea

67 =0.049); however, a single extra case in the alemtuzumab arm included when considering clinically tre

68 sponse rate was 19% (95% CI 0%-40%), and the alemtuzumab arm was discontinued early.

69 Rejection was less frequent in the alemtuzumab arm with 1- and 2-year rejection-free surviv

70 ustine, anti-CD20 antibody, chlorambucil, or alemtuzumab as first-line or second-line treatment; and

71 The use of alemtuzumab as induction immunosuppression for renal tra

72 Patients received alemtuzumab at 30 mg IV 3 times weekly for up to 12 week

73 We hypothesized that higher levels of alemtuzumab at day 0 would result in a low risk of acute

74 We evaluated a novel alemtuzumab-based conditioning regimen in HSCT for acqui

75 In recent studies when comparing alemtuzumab-based conditioning with standard antithymocy

76 f adenoviral infection in patients receiving alemtuzumab-based HSCT appears to be less than that prev

77 Our data suggest that the use of an alemtuzumab-based HSCT regimen for SAA results in durabl

78 We evaluated 105 recipients of alemtuzumab-based reduced-intensity HSCT and collated de

79 se chain reaction on all adult recipients of alemtuzumab-based reduced-intensity HSCT at our institut

80 a, these patients should be managed using an alemtuzumab-based therapy.

81 a) and 9 treatment agents (interferon-alpha, alemtuzumab, bendamustine, bortezomib, dasatinib, imatin

82 Agents in development include alemtuzumab, BG-12, daclizumab, teriflunomide, laquinimo

83 ownregulation of CD52 expression, absence of alemtuzumab binding, minimal change in complement inhibi

84 cs were associated with rapid development of alemtuzumab-binding and -neutralizing antibodies and sub

85 aft loss rates among recipients treated with alemtuzumab but similar patient survival between all reg

86 Alemtuzumab, but not Bas/rATG, profoundly depleted perip

87 ed kidney transplant recipients treated with alemtuzumab (C1H) induction and tacrolimus and mycopheno

88 ts received either conventional treatment or alemtuzumab (Campath-1H) induction.

89 Alemtuzumab (Campath-1H) is a humanized monoclonal antib

90 sistant to the anti-CD52 monoclonal antibody alemtuzumab (Campath-1H).

91 Infusion of alemtuzumab caused potent depletion of all lymphocytes,

92 We found that alemtuzumab caused protracted CD4 more than CD8 T-lympho

93 disability status scale (EDSS) score of the alemtuzumab cohort improved compared with baseline.

94 Grade 2 to 4 acute GVHD was lower with alemtuzumab compared with ATG or T cell- replete regimen

95 to assess efficacy and safety of first-line alemtuzumab compared with interferon beta 1a in a phase

96 We aimed to assess efficacy and safety of alemtuzumab compared with interferon beta 1a in patients

97 mes showed evidence of beneficial effects of alemtuzumab compared with interferon beta-1a across all

98 characteristics enable the administration of alemtuzumab concurrently or prior to engineered T cells,

99 ne, thiotepa, and anti-thymocyte globulin or alemtuzumab conditioning were used in 77% of cases, and

100 Alemtuzumab consolidation did not provide benefit over s

101 r probabilities of LFS after ATG-containing, alemtuzumab-containing, and T cell-replete transplantati

102 tory relapsing-remitting multiple sclerosis, alemtuzumab could be used to reduce relapse rates and su

103 Alemtuzumab delivered intravenously, but not subcutaneou

104 Moreover, the combination of YM155 with alemtuzumab demonstrated markedly additive antitumor act

105 Both YM155 alone and its combination with alemtuzumab demonstrated therapeutic efficacy by lowerin

106 Alemtuzumab depleted CD4+ T cells by more than 95%, incl

107 Induction with alemtuzumab did not significantly affect incidence of BK

108 is model to show that the anti-CD52 antibody alemtuzumab effectively eliminates lymphoma cells from t

109 Median times from initial and last alemtuzumab exposure to ITP diagnosis were 24.5 and 10.5

110 cytic leukemia refractory to fludarabine and alemtuzumab (FA-ref) and patients refractory to fludarab

111 ne, 500 mg/m(2) in all subsequent cycles) or alemtuzumab (FCCam; 30 mg subcutaneously injected on cyc

112 ematopoietic cell transplantation (HCT) with alemtuzumab, fludarabine, and melphalan is an effective

113 g (RIC) regimens predominantly consisting of alemtuzumab, fludarabine, and melphalan.

114 The conditioning regimen included alemtuzumab, fludarabine, and melphalan.

115 d lymphocyte recovery following RIC HCT with alemtuzumab, fludarabine, and melphalan.

116 emotherapy plus the CD52 monoclonal antibody alemtuzumab for high-risk chronic lymphocytic leukemia,

117 ently completed and led to the submission of alemtuzumab for U.S. Food and Drug Administration approv

118 Alemtuzumab given intravenously as first-line treatment

119 ents) compared with 82 (22%) patients in the alemtuzumab group (119 events; rate ratio 0.45 [95% CI 0

120 nts) compared with 147 (35%) patients in the alemtuzumab group (236 events; rate ratio 0.51 [95% CI 0

121 length of stay was significantly shorter in alemtuzumab group (4 days vs 5 days, P < 0.001).

122 of disability compared with 54 (13%) in the alemtuzumab group (hazard ratio 0.58 [95% CI 0.38-0.87];

123 n of disability compared with 30 (8%) in the alemtuzumab group (hazard ratio 0.70 [95% CI 0.40-1.23];

124 cute rejection by 12 months was lower in the alemtuzumab group (n=6 vs. n=14 in basiliximab arm) just

125 ears compared with 278 (65%) patients in the alemtuzumab group (p<0.0001).

126 2 years compared with 78% of patients in the alemtuzumab group (p<0.0001).

127 een the groups at 1 year (57+/-26 mL/min for alemtuzumab group and 53+/-21 mL/min for basiliximab gro

128 lymphocyte count were significantly lower in alemtuzumab group at 30 days (P < 0.0001) and at 1 year

129 Two patients in the alemtuzumab group developed thyroid papillary carcinoma.

130 338 (90%) of patients in the alemtuzumab group had infusion-associated reactions; 12

131 By 24 months, 68 (18%) patients in the alemtuzumab group had thyroid-associated adverse events

132 Forty-seven (81.0%) of the patients in the alemtuzumab group remained on tacrolimus monotherapy at

133 ute rejection was significantly lower in the alemtuzumab group than in the conventional-therapy group

134 biopsy score was significantly lower in the alemtuzumab group than the basiliximab group (0.12 +/- 0

135 ), corresponding to a 42% improvement in the alemtuzumab group.

136 bulin (Thymoglobulin) (group A, N=43) versus alemtuzumab (group B, N=43) versus daclizumab (group C,

137 62 (16%) patients treated with alemtuzumab had herpes infections (predominantly cutaneo

138 Patients who received alemtuzumab had significantly higher numbers of B cells

139 Recipients with alemtuzumab had the highest relative risk for graft loss

140 tions and patient survival was inferior with alemtuzumab (HR 1.29, 95% CI 1.08-1.55, P=0.006).

141 The use of alemtuzumab (humanized anti-CD52 monoclonal antibody) ha

142 We investigated the influence of alemtuzumab (i) on ex vivo-expanded cynomolgus monkey re

143 We examined the activity of alemtuzumab in 28 symptomatic LPL (27 IgM and 1 IgA) pat

144 pressant YM155 alone and in combination with alemtuzumab in a murine model of human ATL (MET-1).

145 erm experience of the efficacy and safety of alemtuzumab in active RRMS.

146 ts recovered to LLN after a single course of alemtuzumab in approximately 8 months (B cells) and 3 ye

147 nical trial of the combination of YM155 with alemtuzumab in ATL.

148 Natalizumab seems superior to alemtuzumab in enabling recovery from disability.

149 outcomes of induction with Thymoglobulin and alemtuzumab in KTRs through paired-kidney analysis.

150 is the largest and only prospective study of alemtuzumab in patients with T-LGL.

151 hocytic leukemia (CLL) patients treated with alemtuzumab in the CLL2H trial.

152 Thus, alemtuzumab-induced B cell depletion/reconstitution may

153 Lymphocytes from 20 recipients undergoing alemtuzumab-induced depletion and belatacept/sirolimus i

154 to the prolonged RRMS suppression following alemtuzumab-induced lymphocyte depletion.

155 delayed CD4(+) T cell repopulation following alemtuzumab-induced lymphopenia may contribute to its lo

156 ximab (375 mg/m x1) for desensitization with alemtuzumab induction (15-30 mg, 1 dose, subcutaneous),

157 Alemtuzumab induction and belatacept/sirolimus immunothe

158 Most received alemtuzumab induction and standard immunosuppression.

159 ng kidney transplant recipients who received alemtuzumab induction compared to patients receiving les

160 Renal transplantation with alemtuzumab induction followed by tacrolimus monotherapy

161 owed by tacrolimus and MMF maintenance or to alemtuzumab induction followed by tacrolimus monotherapy

162 tization with IVIG + rituximab combined with alemtuzumab induction gives HLA-sensitized patients an o

163 Alemtuzumab induction has a lower risk of BPAR compared

164 Over last several years, alemtuzumab induction has been increasingly used in kidn

165 Alemtuzumab induction immunosuppression was associated w

166 We report on the use of alemtuzumab induction in highly HLA sensitized (HS) pedi

167 renal transplantation, and the experience of alemtuzumab induction in pancreas transplantation is sti

168 Alemtuzumab induction is beneficial in reducing hospital

169 The effect of alemtuzumab induction on renal function and the incidenc

170 Following either basiliximab or alemtuzumab induction patients with lower numbers of B c

171 Alemtuzumab induction produced profound lymphopenia foll

172 Alemtuzumab induction reduces the risk of BPAR compared

173 ants from four centers and treated them with alemtuzumab induction therapy and a steroid-free, calcin

174 tric renal transplant recipients who receive alemtuzumab induction therapy are unknown.

175 Alemtuzumab induction therapy effectively depletes B cel

176 udy was to evaluate the current evidence for alemtuzumab induction therapy in kidney transplantation.

177 ents, before and at 6, 9 and 12 months after alemtuzumab induction therapy.

178 Alemtuzumab induction was associated with higher adjuste

179 erence was observed in the risk of BPAR when alemtuzumab induction was compared with rabbit antithymo

180 The reduction rate in patients treated with alemtuzumab induction was slightly higher than that in d

181 Alemtuzumab induction with desensitization led to nearly

182 th standard maintenance immunosuppression to alemtuzumab induction with reduced dose maintenance immu

183 A single dose of 30 mg alemtuzumab induction with steroid-free maintenance immu

184 Alemtuzumab induction with tacrolimus maintenance monoth

185 randomized controlled trial (RCT) comparing alemtuzumab induction with tacrolimus monotherapy agains

186 sing a steroid-sparing regimen consisting of alemtuzumab induction, 1 week of corticosteroids and tac

187 The immunosuppressive regimen included alemtuzumab induction, donor hematopoietic stem cells, t

188 idemiology of BK virus (BKV) infection after alemtuzumab induction.

189 tive and 45 quiescent) 2.8+/-1.4 years after alemtuzumab induction.

190 n and that this pattern is more common after alemtuzumab induction.

191 s from 33 desensitized patients who received alemtuzumab induction.

192 n and recipient of the mate kidney underwent alemtuzumab induction.

193 otype of repopulated T-lymphocytes following alemtuzumab induction; however there has been less scrut

194 d (ii) on naturally occurring Treg following alemtuzumab infusion.

195 sis, exposure to one of the study therapies (alemtuzumab, interferon beta, fingolimod, or natalizumab

196 Alemtuzumab is a chimeric CD52 monoclonal antibody with

197 Alemtuzumab is a humanised monoclonal antibody that depl

198 Alemtuzumab is a lymphocyte depleting monoclonal antibod

199 Alemtuzumab is a monoclonal antibody that has shown effi

200 Alemtuzumab is a newly licensed treatment of active rela

201 Intravenous alemtuzumab is an effective and well-tolerated treatment

202 Alemtuzumab is associated with disease stabilisation in

203 Here, we show that T-cell recovery after alemtuzumab is driven by homeostatic proliferation, lead

204 We conclude that alemtuzumab is effective in SAA, but best results are ob

205 dence of mixed chimerism in patients with an alemtuzumab level </=0.15 mug/mL was 21%, vs 42% with le

206 d delayed early lymphocyte recovery and that alemtuzumab level thresholds for increased risks of thes

207 Patients with alemtuzumab levels </=0.15 or 0.16 to 0.56 mug/mL had hi

208 I-IV, and III-IV acute GVHD in patients with alemtuzumab levels </=0.15 vs >/=0.16 mug/mL were 68% vs

209 We conclude that peritransplant alemtuzumab levels impact acute GVHD, mixed chimerism, a

210 s to examine the influence of peritransplant alemtuzumab levels on acute GVHD, mixed chimerism, and l

211 dose per day on days -5 to -3]; or low-dose alemtuzumab [<1 mg/kg on days -8 to -6]), and low-dose (

212 Alemtuzumab (MabCampath or Campath; Genzyme, Cambridge,

213 cyclophosphamide 300 mg/m(2) for 4 days, and alemtuzumab median total dose of 60 mg (range:40-100 mg)

214 OFA-mediated CDC but retained sensitivity to alemtuzumab-mediated CDC in vitro.

215 nded cynomolgus monkey Treg are resistant to alemtuzumab-mediated, complement-dependent cytotoxicity.

216 ypothesized that the humanized anti-CD52 mAb alemtuzumab might be active in SAA because of its lympho

217 After infusion of alemtuzumab, monkey serum killed fresh PBMC, but not exp

218 We investigated alemtuzumab monotherapy from 2003-2010 in treatment-naiv

219 ded antithymocyte globulin (ATG; n = 191) or alemtuzumab (n = 132) and no in vivo T-cell depletion (n

220 g (RIC) included fludarabine (Flu)/melphalan/alemtuzumab (n = 20), Flu/busulfan (Bu)/alemtuzumab (n =

221 ceived high-dose cyclophosphamide (n = 7) or alemtuzumab (n = 21) treatment alone, suggesting an addi

222 tween rabbit ATG + cyclosporine (n = 27) and alemtuzumab (n = 27); the response rate for alemtuzumab

223 alan/alemtuzumab (n = 20), Flu/busulfan (Bu)/alemtuzumab (n = 8), and Flu/Bu/antithymocyte globulin (

224 ), adjusted graft survival was inferior with alemtuzumab (n=2428, hazards ratio [HR] 1.26, 95% confid

225 Alemtuzumab, natalizumab, and fingolimod were associated

226 the lymphocyte-depleting monoclonal antibody alemtuzumab offer a unique opportunity to study this phe

227 sessments, from all 87 patients treated with alemtuzumab on investigator-led studies in Cambridge, UK

228 te whether the data describing the effect of alemtuzumab on lymphocyte subsets collected during the p

229 The 335 low-risk patients received alemtuzumab (one dose of 30 mg, in 164 patients) or basi

230 ge- and gender-matched controls induced with alemtuzumab or basiliximab (Bas)/low-dose rabbit anti-th

231 dy, we randomly assigned patients to receive alemtuzumab or conventional induction therapy (basilixim

232 II clinical trials (methylprednisolone plus alemtuzumab or ibrutinib) seem better than chemoimmunoth

233 istance to the anti-CD52 monoclonal antibody alemtuzumab or methylprednisolone.

234 Response may also occur with alemtuzumab or the thrombopoietin mimetic eltrombopag in

235 with rabbit-antithymocyte globulin (r-ATG), alemtuzumab, or an interleukin-2 (IL-2) receptor blocker

236 rovide benefit over similar regimens without alemtuzumab (P > .20), irrespective of age.

237 monotherapy with either YM155 (P < .001) or alemtuzumab (P < .05).

238 rejection was seen in HS patients receiving alemtuzumab (P = 0.001), there was a nonsignificant diff

239 Alemtuzumab plus methypredisolone is the most effective

240 Alemtuzumab provided superior outcomes in regard to aver

241 ER among induction categories: no-induction, alemtuzumab, rabbit antithymocyte globulin (r-ATG), and

242 c characteristics, we generated 1:1 pairs of alemtuzumab-rabbit antithymocyte globulin (rATG) (5330 p

243 Compared with rATG recipients, alemtuzumab recipients had higher risk of death (hazard

244 esource utilization was slightly lower among alemtuzumab recipients than among rATG recipients, but d

245 Alemtuzumab reduced disease activity compared with inter

246 The anti-CD52 monoclonal antibody alemtuzumab reduced disease activity in a phase 2 trial

247 lapsing-remitting multiple sclerosis (RRMS), alemtuzumab reduced relapse rate and the risk of sustain

248 The anti-CD52 monoclonal antibody alemtuzumab reduces disease activity in previously untre

249 Alemtuzumab relatively spared CD4(+)CD25(+)FoxP3(+) regu

250 In conclusion, induction therapy with alemtuzumab results in a long-term shift toward naive B

251 bendamustine, and the monoclonal antibodies alemtuzumab, rituximab, and ofatumumab) and many more dr

252 5 and RR = 0.55; P < .0001, respectively) or alemtuzumab (RR = 0.09; P < .003 and RR = 0.21; P < .000

253 INTERPRETATION: Alemtuzumab's consistent safety profile and benefit in t

254 strategies allow for early identification of alemtuzumab's main adverse effect of secondary autoimmun

255 Both natalizumab and alemtuzumab seem highly effective and viable immunothera

256 Alemtuzumab seems superior to fingolimod and interferon

257 e inhibitors, and antibody therapies such as alemtuzumab, systemic chemotherapy, and allogeneic trans

258 nt recipients were randomized 2:1 to receive alemtuzumab/tacrolimus or daclizumab/tacrolimus/mycophen

259 provement in disability after treatment with alemtuzumab than interferon beta-1a.

260 irmed acute rejection was less frequent with alemtuzumab than with conventional therapy.

261 For alemtuzumab there was also a correlation between these s

262 association of common induction treatments (alemtuzumab, thymoglobulin, interleukin-2 receptor block

263 lymphocytic leukemia have shown subcutaneous alemtuzumab to be equally as effective as intravenous al

264 ed cardiac allografts were transplanted into alemtuzumab treated CD52Tg mice and showed no acute reje

265 term dominance in naive B cells was found in alemtuzumab-treated kidney transplant recipients, which

266 Alemtuzumab-treated patients exhibited a nearly complete

267 be a distinctive form of ITP associated with alemtuzumab treatment characterized by delayed presentat

268 previously shown that autoimmunity following alemtuzumab treatment of multiple sclerosis can be predi

269 use of intense lymphodepletion expected with alemtuzumab use (and hoped-for achievement of a truer im

270 There was evidence for clustering of alemtuzumab use within transplant centers which did not

271 occurred in 253 (67%) patients treated with alemtuzumab versus 85 (45%) patients treated with interf

272 on (5.7% vs 4.5%, P = 0.97) were similar for alemtuzumab versus Thymoglobulin groups.

273 , 0.69-1.05) survivals were also similar for alemtuzumab versus Thymoglobulin groups.

274 erleukin-2 receptor antagonists [IL-2RA], or alemtuzumab; vs. no induction) on rejection (initial hos

275 alemtuzumab (n = 27); the response rate for alemtuzumab was 37% (95% confidence interval [CI], 18%-5

276 For relapsed disease (n = 25), alemtuzumab was administered in a single-arm study; the

277 Alemtuzumab was associated with a higher incidence of de

278 Alemtuzumab was associated with increased NHL (aIRR, 1.7

279 For the disability outcomes, alemtuzumab was associated with similar probabilities of

280 Alemtuzumab was associated with similar probabilities of

281 In treatment-naive patients (n = 16), alemtuzumab was compared with horse and rabbit ATG in a

282 diabetes mellitus after transplantation when alemtuzumab was compared with IL-2RAs or rATG induction.

283 Alemtuzumab was given intravenously at 10 mg per day for

284 n beta 1a was given three-times per week and alemtuzumab was given once per day for 5 days at baselin

285 n beta 1a was given three-times per week and alemtuzumab was given once per day for 5 days at baselin

286 ansplant recipients receiving induction with alemtuzumab were compared with those receiving another i

287 161 of 215 patients treated with alemtuzumab were free of CDA at 36 months (Kaplan-Meier

288 376 (97%) of 386 patients randomly allocated alemtuzumab were included in the primary analyses.

289 going allogeneic heart transplantation given alemtuzumab were monitored for Treg and serum alemtuzuma

290 the 2 groups; however, patients who received alemtuzumab were older and at lower risk of viral infect

291 Two doses of alemtuzumab were used for induction (30 mg, 6 and 24 h a

292 Depletional antibodies (r-ATG and alemtuzumab) were more cost-effective across all willing

293 the best treatment for T-PLL is intravenous alemtuzumab, which has resulted in very high response ra

294 safety of the combination of fludarabine and alemtuzumab with fludarabine monotherapy in previously t

295 We compared the effectiveness of alemtuzumab with natalizumab, fingolimod, and interferon

296 There were two trials comparing alemtuzumab with no induction, but neither trial reporte

297 The apparent superiority of alemtuzumab with respect to early biopsy-confirmed acute

298 y was to compare induction therapy involving alemtuzumab with the most commonly used induction regime

299 limod, teriflunomide, dimethyl fumarate, and alemtuzumab-with regard to their mechanism of action, cl

300 g can be infused into graft recipients given alemtuzumab without risk of complement-mediated killing.