ライフサイエンスコーパス: alemtuzumab

1 and are rendered resistant to destruction by alemtuzumab.

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

3 mong patients treated with thymoglobulin and alemtuzumab.

4 ultiple sclerosis considering treatment with alemtuzumab.

5 ation alemtuzumab, and FR with consolidation alemtuzumab.

6 g regimen consisting of cyclophosphamide and alemtuzumab.

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

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

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

10 tiramer acetate, fingolimod, natalizumab, or alemtuzumab.

11 % of these sero (+) patients at 1 month post-alemtuzumab.

12 of graft versus host disease and the use of alemtuzumab.

13 translpant NK cell levels were detected post-alemtuzumab.

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

15 implications for the safety and efficacy of alemtuzumab.

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

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

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

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

20 426 (98%) of 436 patients randomly allocated alemtuzumab 12 mg were included in the primary analyses.

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

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

23 5)/rituximab (150 mg/m x 1; begun in 2013), alemtuzumab (2001-2011), and less intensive forms.

24 kg x5)/rituximab(150mg/m x1)(begun in 2013), alemtuzumab(2001-2011), and less intensive forms.

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

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

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

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

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

30 Alemtuzumab, a CD52-depleting monoclonal antibody, effec

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

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

33 lemtuzumab were monitored for Treg and serum alemtuzumab activity.

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

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

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

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

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

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

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

41 ain encoding region of known antibody drugs (alemtuzumab and adalimumab) to generate recombinant sing

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

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

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

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

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

47 INTERPRETATION: Alemtuzumab and natalizumab seem to have similar effects

48 Treatment decisions between alemtuzumab and natalizumab should be primarily governed

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 ate analysis, pre-HCT AIC, mismatched donor, alemtuzumab, anti-thymocyte antiglobulin, and acute and

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

65 =0.049); however, a single extra case in the alemtuzumab arm included when considering clinically tre

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

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

68 The use of alemtuzumab as induction immunosuppression for renal tra

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

70 within an islet transplant program favoring alemtuzumab (ATZ) lymphodepleting induction and examined

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 ) Rabbit anti-thymocyte globulin (rATG); (2) Alemtuzumab (C1H); (3) IL2-receptor antagonists (IL2-RA;

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

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

88 Infusion of alemtuzumab caused potent depletion of all lymphocytes,

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

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

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

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

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

94 Alemtuzumab consolidation did not provide benefit over s

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

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

97 Alemtuzumab delivered intravenously, but not subcutaneou

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

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

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

101 Induction with alemtuzumab did not significantly affect incidence of BK

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

103 rotective effects of both rATG/rituximab and alemtuzumab existed during the first 6 months posttransp

104 rotective effects of both rATG/rituximab and alemtuzumab existed during the first 6mo posttransplant

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 2 years compared with 78% of patients in the alemtuzumab group (p<0.0001).

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

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

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

124 338 (90%) of patients in the alemtuzumab group had infusion-associated reactions; 12

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

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

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

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

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

130 62 (16%) patients treated with alemtuzumab had herpes infections (predominantly cutaneo

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

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

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

134 an follow-up, 4.9 years [IQR, 4.4-5.8]); and alemtuzumab (HR, 0.52; 95% CI, 0.32-0.85; P = .009; 5-ye

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

150 b induction (P < 0.000001 and P < 0.01), and alemtuzumab induction (P = 0.004 and P = 0.07).

151 Alemtuzumab induction and belatacept/sirolimus immunothe

152 Most received alemtuzumab induction and standard immunosuppression.

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

154 Forty patients underwent alemtuzumab induction followed by belatacept and sirolim

155 Renal transplantation with alemtuzumab induction followed by tacrolimus monotherapy

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

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

158 Alemtuzumab induction has a lower risk of BPAR compared

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

160 Alemtuzumab induction immunosuppression was associated w

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

162 Alemtuzumab induction is beneficial in reducing hospital

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

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

165 Alemtuzumab induction produced profound lymphopenia foll

166 Alemtuzumab induction reduces the risk of BPAR compared

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

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

169 Alemtuzumab induction therapy effectively depletes B cel

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

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

172 Alemtuzumab induction was associated with higher adjuste

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

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

175 Alemtuzumab induction with desensitization led to nearly

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

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

178 ituximab induction(P<0.000001 and 0.01), and alemtuzumab induction(P=0.004 and 0.07).

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

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

181 32) for those receiving versus not receiving alemtuzumab induction, respectively.

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

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

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

185 s from 33 desensitized patients who received alemtuzumab induction.

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

187 ter accounting for the propensity to receive alemtuzumab induction.

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

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

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

191 Alemtuzumab is a humanised monoclonal antibody that depl

192 Alemtuzumab is a lymphocyte depleting monoclonal antibod

193 Alemtuzumab is a monoclonal antibody that has shown effi

194 Alemtuzumab is a newly licensed treatment of active rela

195 Alemtuzumab is associated with disease stabilisation in

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

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

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

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

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

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

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

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

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

205 Alemtuzumab (MabCampath or Campath; Genzyme, Cambridge,

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

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

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

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

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

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

212 sulfanbased in 84% of patients; 84% received alemtuzumab (n = 14) or anti-thymocyte globulin (n = 8)

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

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

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

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

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

218 Patients not receiving alemtuzumab (n=4) showed no UCART19 expansion or antileu

219 Alemtuzumab, natalizumab, and fingolimod were associated

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

221 The prognostic effects of rATG/rituximab and alemtuzumab on ACR/severe ACR disappeared beyond 24 days

222 The prognostic effects of rATG/rituximab and alemtuzumab on ACR/severe ACR disappeared beyond 24 days

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

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

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

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

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

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

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

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

231 Initial treatment with fingolimod, alemtuzumab, or natalizumab was associated with a lower

232 tting MS, initial treatment with fingolimod, alemtuzumab, or natalizumab was associated with a lower

233 nterferon beta were escalated to fingolimod, alemtuzumab, or natalizumab within 5 years vs later, the

234 erapy (rituximab, ocrelizumab, mitoxantrone, alemtuzumab, or natalizumab) either 0-2 years (early) or

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

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

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

238 Alemtuzumab plus methypredisolone is the most effective

239 Alemtuzumab produced profound lymphopenia followed by gr

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

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

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

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

249 ion cladribine and the monoclonal antibodies alemtuzumab, rituximab and ocrelizumab are frequently ca

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

251 5 and RR = 0.55; P < .0001, respectively) or alemtuzumab (RR = 0.09; P < .003 and RR = 0.21; P < .000

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

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

254 Both natalizumab and alemtuzumab seem highly effective and viable immunothera

255 Alemtuzumab seems superior to fingolimod and interferon

256 After multivariate analysis, alemtuzumab (subdistribution hazard ratio, 9.0; 95% CI,

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 arabine and cyclophosphamide with or without alemtuzumab, then children received UCART19 at 1.1-2.3 x

261 For alemtuzumab there was also a correlation between these s

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

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

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

265 Alemtuzumab-treated patients exhibited a nearly complete

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

267 , 4 during natalizumab therapy and one after alemtuzumab treatment, and in treated patients who did n

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

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

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

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

272 , 0.69-1.05) survivals were also similar for alemtuzumab versus Thymoglobulin groups.

273 isceral [MV] or MV) allograft (P = 0.00003), alemtuzumab (versus no induction, anti-CD25, rabbit anti

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 the protective effects of rATG/rituximab and alemtuzumab were highly significant (P <= 0.000005 for A

289 the protective effects of rATG/rituximab and alemtuzumab were highly significant(P<=0.000005 for ACR;

290 376 (97%) of 386 patients randomly allocated alemtuzumab were included in the primary analyses.

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

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

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

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

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

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

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

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

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.