ライフサイエンスコーパス: daclizumab

1 re than nondepleting agents (basiliximab and daclizumab).

2 bition in vivo, although it was required for daclizumab.

3 B received Alemtuzumab, and group C received Daclizumab.

4 of the radiolabeled anti-CD25 antibody (90)Y-daclizumab.

5 IT-T15 cells or rat islets after exposure to daclizumab.

6 ither a prick nor an intradermal response to daclizumab.

7 sion consisted of sirolimus, tacrolimus, and daclizumab.

8 was no correlative decrease associated with daclizumab.

9 adverse effects in the patients treated with daclizumab.

10 tions and no serious side effects related to daclizumab.

11 ith advanced or steroid-refractory GVHD with daclizumab.

12 n older people and participants treated with daclizumab.

13 rferon beta and high-dose daclizumab group), daclizumab 1 mg/kg every 4 weeks (interferon beta and lo

14 Daclizumab 1 mg/kg given immediately after pediatric liv

15 The treatment arm (n=61) received daclizumab 1 mg/kg immediately after liver transplantati

16 econd cohort of 19 patients was treated with daclizumab 1 mg/kg on days 1, 4, 8, 15, and 22.

17 first cohort of 24 patients was treated with daclizumab 1 mg/kg on days 1, 8, 15, 22, and 29.

18 ily equivalent was given in conjunction with daclizumab 1 mg/kg or placebo on study days 1, 4, 8, and

19 patients were randomized into three groups: daclizumab 1 mg/kg per dose every 14 days for five doses

20 02/00 (n=29) received induction with either daclizumab (1 mg/kg on day 0, 7, 14), OKT 3 (5 mg/day x0

21 We administered daclizumab (1.0 mg per kilogram of body weight) or place

22 ion to receive either induction therapy with daclizumab (1.0 mg per kilogram of body weight), given i

23 Daclizumab, 1 mg/kg of body weight, every 2 weeks for a

24 ded into two groups according to the dose of daclizumab: 1 mg/kg on day 0 and every 14 days for five

25 era, 1994 to 2002, when basiliximab (1998), daclizumab (1998), and rabbit antithymocyte globulin (rA

26 omly assigned to receive add-on subcutaneous daclizumab 2 mg/kg every 2 weeks (interferon beta and hi

27 ery 14 days for five doses (group I, n=107), daclizumab 2 mg/kg per dose every 14 days for two doses

28 Moreover, the two-dose regimen of daclizumab (2 mg/kg on days 0 and 14) compares favorably

29 steroids, and 15 patients (group B) received daclizumab, 2 mg/kg on POD 0 and 14, with tacrolimus, my

30 Of the 126 patients given daclizumab, 28 (22 percent) had biopsy-confirmed episode

31 ng hospitalization appeared to be lower with daclizumab (7.3 vs. 16%, P<0.0036) with a similar trend

32 he first 6 months when compared with OKT3 or daclizumab (7.7 vs. 60 vs. 50%).

33 in the group receiving corticosteroids plus daclizumab (77% vs 94%; P =.02).

34 val was excellent in both placebo- (91%) and daclizumab- (93%) treated patients.

35 ell subset, which is selectively expanded by daclizumab, a CD25-blocking Ab that suppresses multiple

36 Daclizumab, a highly humanized, specific interleukin-2 r

37 Daclizumab, a humanised monoclonal antibody, reduced mul

38 Administration of daclizumab, a humanized mAb directed against the IL-2Ral

39 In search of the mechanisms by which daclizumab, a humanized monoclonal antibody against CD25

40 Daclizumab, a humanized monoclonal antibody against the

41 Therefore, we investigated the effects of daclizumab, a humanized monoclonal antibody directed aga

42 We examined whether treatment with daclizumab, a humanized monoclonal antibody specific for

43 The immunosuppression regimen consisted of daclizumab, a humanized monoclonal antibody that binds t

44 Daclizumab, a humanized monoclonal IgG1 directed against

45 T-cell-directed therapies (thymoglobulin and daclizumab, all patients), alone or with the addition of

46 After cessation of daclizumab, allograft rejection increased to levels seen

47 i (0.444 MBq) of (211)At-7G7/B6 (P < .05) or daclizumab alone (P < .05).

48 , compared with those in the depsipeptide or daclizumab alone groups (P < .001).

49 ement was not statistically significant with daclizumab (alone or with steroids), basiliximab alone,

50 Prophylaxis with daclizumab also delayed the onset of the first biopsy-pr

51 study, 28 were randomly assigned to receive daclizumab and 27 served as the control group.

52 Daclizumab and 7G7/B6 are directed toward different epit

53 er of reports of anti-interleukin therapies, daclizumab and anakinra, have supported a role for these

54 A combination of daclizumab and anti-IL-2 efficiently blocked IL-2-induce

55 Daclizumab and antithymocyte globulin (ATG) have been sh

56 Both daclizumab and ATG therapy resulted in a significant red

57 mmunosuppression consisted of induction with daclizumab and maintenance therapy with tacrolimus and s

58 tocol transplant biopsies (n=246), and serum daclizumab and mycophenolic acid (MPA) trough levels wer

59 There were no adverse reactions to daclizumab and no significant differences between the gr

60 Daclizumab and ocrelizumab are monoclonal antibodies tha

61 Forty subjects received daclizumab and their clinical outcomes were compared aga

62 receptor antagonists (IL2-RA; basiliximab or daclizumab), and (4) No antibody induction.

63 CW (tacrolimus, mycophenolate mofetil (MMF), daclizumab, and corticosteroids until day 4) with tacrol

64 ual induction therapy with thymoglobulin and daclizumab, and low-dose maintenance tacrolimus and cort

65 adjunct use of the interleukin-2 antagonist daclizumab, and most recently allograft irradiation may

66 New monoclonal antibodies such as daclizumab, and tumor necrosis factor alpha inhibitors s

67 tem facilitated the development of effective daclizumab antibody therapy for select patients with leu

68 Daclizumab appears safe; its efficacy in this pilot prot

69 Basiliximab and daclizumab are potent and relatively safe immunosuppress

70 7.6% in the alemtuzumab arm and 95.1% in the daclizumab arm at 1 year (95% confidence interval of dif

71 d 89.9% compared with 82.3% and 82.3% in the daclizumab arm.

72 pectively evaluated 27 patients who received daclizumab as induction immunosuppression and compared t

73 Thirty-two patients were given daclizumab as induction therapy in the setting of hepati

74 -T-cell depleting antibody to the CD25 cell, daclizumab, as a single-dose induction agent immediately

75 munosuppressive regimen with the addition of daclizumab at 1 mg/kg for five doses over 10 weeks in th

76 activity to their respective marketed drugs daclizumab, bevacizumab, and infliximab.

77 However, daclizumab can be used safely in patients with preexisti

78 Daclizumab can decrease the incidence of acute rejection

79 afety and efficacy of two dosing regimens of daclizumab compared with no antibody induction in SKPT r

80 rolimus, and the anti-IL-2 receptor antibody daclizumab consistently resulted in formation of inhibit

81 Collectively, our results indicate that daclizumab could inhibit CD25(+) effector T-cell functio

82 on therapy with antithymocyte globulin (ATG)/daclizumab (Dac) (each with fewer doses than if used alo

83 Daclizumab (Dac), an Ab against the IL-2R alpha-chain, i

84 Given the recent withdrawal of daclizumab (DAC), the safety and efficacy of thymoglobul

85 ICG was conjugated to the antibodies daclizumab (Dac), trastuzumab (Tra), or panitumumab (Pan

86 The patients given daclizumab did not have any adverse reactions to the dru

87 he proliferation of karpas299 cells, whereas daclizumab did not inhibit cell proliferation.

88 s then stratified according to the number of daclizumab doses: 4-5 doses (n=45) or 1-3 doses (n=26).

89 d, double-blind, placebo-controlled study of daclizumab (DZB) and mycophenolate mofetil (MMF) includi

90 addition of humanized IL-2 receptor antibody daclizumab (DZB) to CsA-based immunosuppression decrease

91 Daclizumab effectively reduced the incidence and delayed

92 Combination of depsipeptide with daclizumab enhanced the antitumor effect, as shown by bo

93 ion; in this group 0 of 13 (0%) treated with daclizumab experienced at least one high-grade rejection

94 Daclizumab first-dose doubling and extended use for 6 mo

95 volved the use of sirolimus, tacrolimus, and daclizumab for immunosuppression.

96 d; and era 4, 1998 to 2000 (n = 275), use of daclizumab for induction immunosuppression, primarily en

97 zed study of corticosteroids with or without daclizumab for initial treatment of acute GVHD was condu

98 ntravenously or receptor-saturating doses of daclizumab given at 100 microg weekly for 4 weeks intrav

99 at 0.5 mg/kg every other day for 2 weeks, or daclizumab, given at 100 microg weekly for 4 weeks, inhi

100 t), as compared with 5 of 28 patients in the daclizumab group (18 percent; relative risk, 2.8; 95 per

101 and 3.58 in the interferon beta and low-dose daclizumab group (25%, -76% to 68%; p=0.51).

102 compared with 77 of the 216 patients in the daclizumab group (47.7 percent vs. 35.6 percent, P=0.007

103 th 1.32 in the interferon beta and high-dose daclizumab group (difference 72%, 95% CI 34% to 88%; p=0

104 te rejection compared with four (18%) in the daclizumab group (P<0.04).

105 e control group, as compared with two in the daclizumab group (P= 0.03), and the time to a first epis

106 he control group and 0.19 per patient in the daclizumab group (P=0.02).

107 of rejection was significantly longer in the daclizumab group (P=0.04).

108 ejection rates (<6 months) were lower in the daclizumab group as compared with the OKT3 group, i.e.,

109 point was almost three times as long in the daclizumab group as in the placebo group during the firs

110 group p=0.002; interferon beta and high-dose daclizumab group p<0.0001).

111 placebo group (interferon beta and low-dose daclizumab group p=0.002; interferon beta and high-dose

112 The daclizumab group received 2 mg/kg intravenously before o

113 The rate of rejection was lower in the daclizumab group than in the placebo group (41.3 percent

114 More patients in the daclizumab group than in the placebo group died of infec

115 in the control group and 22 patients in the daclizumab group were available for analysis at 6 months

116 every 2 weeks (interferon beta and high-dose daclizumab group), daclizumab 1 mg/kg every 4 weeks (int

117 every 4 weeks (interferon beta and low-dose daclizumab group), or interferon beta and placebo for 24

118 from 44% in the placebo group to 28% in the daclizumab group.

119 in the placebo group to 73+/-70 days in the daclizumab group.

120 3) versus alemtuzumab (group B, N=43) versus daclizumab (group C, N=42), using exactly the same three

121 ells was seven to eight times higher in both daclizumab groups than in the interferon beta and placeb

122 al rate in those with DGF in the placebo and daclizumab groups were 93% and 98%, respectively.

123 tients who received mycophenolate mofetil or daclizumab had a less likelihood of achieving a BR.

124 Daclizumab had little toxicity.

125 Daclizumab had no effect on the radiographic or immediat

126 Induction therapy with daclizumab has been shown to be efficacious in the preve

127 Daclizumab has substantial activity for the treatment of

128 Humanized anti-CD25 antibodies (eg, daclizumab) have been successfully used to treat several

129 e the alpha chain of the IL-2 receptor (e.g. daclizumab) have been used to prevent allograft rejectio

130 atients with multiple sclerosis who received daclizumab high-yield process (HYP) for 52 weeks.

131 Daclizumab high-yield process (HYP) is a humanized monoc

132 f depsipeptide alone and in combination with daclizumab (humanized anti-Tac) in a murine model of hum

133 ogression confirmed at 12 weeks was 16% with daclizumab HYP and 20% with interferon beta-1a (P=0.16).

134 autoimmune hepatitis; a contributory role of daclizumab HYP could not be excluded.

135 :1) to receive 150 mg or 300 mg subcutaneous daclizumab HYP every 4 weeks for 52 weeks (treatment ini

136 These results support further assessment of daclizumab HYP for relapsing-remitting multiple sclerosi

137 were reported in 15% of the patients in the daclizumab HYP group and in 10% of those in the interfer

138 Infections were more common in the daclizumab HYP group than in the interferon beta-1a grou

139 the second year of continuous treatment with daclizumab HYP or during treatment washout and re-initia

140 with relapsing-remitting multiple sclerosis, daclizumab HYP showed efficacy superior to that of inter

141 The annualized relapse rate was lower with daclizumab HYP than with interferon beta-1a (0.22 vs. 0.

142 RI) over a period of 96 weeks was lower with daclizumab HYP than with interferon beta-1a (4.3 vs. 9.4

143 s on liver-function testing were higher with daclizumab HYP than with interferon beta-1a.

144 nt initiation group); those who had received daclizumab HYP were randomly assigned (1:1) to continue

145 the washout and re-initiation group (300 mg daclizumab HYP) died because of autoimmune hepatitis; a

146 sing-remitting multiple sclerosis to compare daclizumab HYP, administered subcutaneously at a dose of

147 points were the safety and immunogenicity of daclizumab HYP.

148 nd immunogenicity of extended treatment with daclizumab HYP.

149 beta-1a (0.22 vs. 0.39; 45% lower rate with daclizumab HYP; P<0.001).

150 .3 vs. 9.4; 54% lower number of lesions with daclizumab HYP; P<0.001).

151 In the presence of daclizumab, IL-2 serum concentrations increased and IL-2

152 This nonrandomized study examined the use of daclizumab in 39 of the last 97 liver transplants perfor

153 Since March 1998, we studied the effect of daclizumab in a nonrandomized, prospective study of 233

154 transplants were included; 43 (50%) received daclizumab in addition to conventional immunosuppression

155 n a pilot study to determine the efficacy of daclizumab in conjunction with corticosteroids and mycop

156 We review our experience with the use of daclizumab in liver transplant recipients.

157 GA4 respectively mirror the known effects of daclizumab in multiple sclerosis and vedolizumab in infl

158 y in induction patients, but the efficacy of daclizumab in preventing rejection was independent of th

159 Treatment with daclizumab in the pooled analysis demonstrated a signifi

160 ith a humanized antibody preparation such as daclizumab in the presence of a negative skin test to th

161 humanized monoclonal antibody against CD25 (daclizumab) in 10 multiple sclerosis patients with incom

162 d on naive and memory cells and inhibited by daclizumab independently of cell division.

163 recipients receiving combined thymoglobulin/daclizumab induction along with reduced tacrolimus dosin

164 tocol modifications were introduced in 1998: daclizumab induction and frequent rejection surveillance

165 All patients received daclizumab induction and maintenance corticosteroids.

166 Each group received daclizumab induction and methylprednisolone maintenance.

167 es, under immunosuppression therapy based on daclizumab induction and tacrolimus/sirolimus maintenanc

168 ulticenter survey of initial experience with daclizumab induction in combination with TAC, MMF, and s

169 creas transplant (SKPT) recipients receiving daclizumab induction in combination with tacrolimus (TAC

170 al pretransplant (P=0.007) and not receiving daclizumab induction therapy (P=0.02) (24 such deaths).

171 s the largest published series to date using daclizumab induction therapy in a renal-sparing regimen.

172 Daclizumab induction therapy is as efficacious as OKT3 i

173 l dysfunction have less acute rejection with daclizumab induction therapy.

174 y comparing 209 adult liver transplants with daclizumab induction to 115 transplants with no inductio

175 -month results in 10 patients using extended daclizumab induction to safely eliminate steroid use in

176 In 1995, cyclophosphamide or daclizumab induction was added to the tacrolimus-steroid

177 I under Edmonton-like immunosuppression with daclizumab induction, either without interventions (SI-c

178 r EC-MPS along with a combined thymoglobulin/daclizumab induction, low tacrolimus dosing and steroid

179 , and combined rabbit antithymocyte globulin/daclizumab induction, previously showed at 1 year posttr

180 Extended daclizumab induction, tacrolimus, and mycophenolate mofe

181 ransplant renal dysfunction is possible with daclizumab induction.

182 In conclusion, repeated (90)Y-daclizumab infusions directed predominantly toward nonma

183 ardized schedule, while ultimately receiving Daclizumab infusions every 4 weeks.

184 Consistent with this are reports that daclizumab inhibits human CD25(+) effector cell cytokine

185 Daclizumab is a genetically engineered human IgG1 monocl

186 Daclizumab is a humanized mAb that binds the IL-2 recept

187 Daclizumab is a humanized monoclonal antibody against th

188 Daclizumab is a monoclonal antibody directed against the

189 hese data suggest that the truncated dose of daclizumab is as effective as the standard regimen for A

190 Daclizumab is safe and effective in reducing the inciden

191 egative skin test and safe administration of daclizumab is surprising because the similarity of these

192 d dosing schedule resulted in subtherapeutic daclizumab levels in liver transplant recipients.

193 Early daclizumab levels of more than 5 microg/mL were observed

194 Combination therapy with daclizumab may be an important adjunct in immunosuppress

195 ptor with the human IgG1 monoclonal antibody daclizumab may prevent rejection of allografts after car

196 In this study, we investigated the effect of daclizumab-mediated CD25 blockade on Treg homeostasis in

197 The remaining 25 patients received daclizumab, mycophenolate mofetil, and steroids, with th

198 Either OKT3 (n=26) or daclizumab (n=21) were used for induction therapy, with

199 ned to receive interferon beta and high-dose daclizumab (n=75), interferon beta and low-dose daclizum

200 lizumab (n=75), interferon beta and low-dose daclizumab (n=78), or interferon beta and placebo (n=77)

201 1, n = 29), group 3a (April 2001 to present, daclizumab, n = 51), and group 3b (April 2001 to present

202 these differences, as does a humanized form (daclizumab) now approved for the prevention of renal all

203 tly in late-phase clinical trials, including daclizumab, ocrelizumab, and ofatumumab.

204 ditional follow-up is needed to determine if daclizumab offers any long-term benefit in terms of redu

205 There was no beneficial effect of daclizumab on graft survival at 3 years, but the trial w

206 Effects of daclizumab on prespecified subsets of lymphocytes and qu

207 Daclizumab or ATG combined with a maintenance immunosupp

208 We assessed the safety and efficacy of daclizumab or ATG prophylaxis in combination with triple

209 to receive prophylactic therapy with either daclizumab or ATG.

210 Patients were randomized to receive either daclizumab or basiliximab versus RATG for induction in c

211 nduction therapy with alemtuzumab or IL-2RA (daclizumab or basiliximab) was used.

212 Protocols with daclizumab or etanercept during induction had higher rat

213 oids, and antibody induction therapy (either daclizumab or OKT3).

214 nd corticosteroids) to receive five doses of daclizumab or placebo.

215 h most patients receiving rATG, basiliximab, daclizumab, or alemtuzumab (2003).

216 iver) transplant (P = 0.002), induction with daclizumab (P = 0.005), patient at home prior to transpl

217 The recent approval of daclizumab prompted us to initiate this pilot study usin

218 The beneficial effect of daclizumab prophylaxis upon the incidence of acute rejec

219 We aimed to assess whether daclizumab reduces disease activity in patients with act

220 Daclizumab reduces the frequency of acute rejection in k

221 Treg declines were not associated with daclizumab-related clinical benefit or cutaneous adverse

222 Therapy with daclizumab resulted in a significant decrease in the inc

223 mphocytes, whereas other medications such as Daclizumab (Roche Laboratories, Nutley, NJ) block the in

224 Because of daclizumab's favorable toxicity profile and response rat

225 tokine production is also dependent on IL-2, daclizumab's inhibition of CD40L expression could be due

226 Induction therapy with daclizumab safely reduces the frequency and severity of

227 tacrolimus, mycophenolate and standard dose daclizumab (SB group) or extended dose daclizumab (SF gr

228 dose daclizumab (SB group) or extended dose daclizumab (SF group).

229 or anticipated use of cytolytic therapy with daclizumab should be avoided.

230 The combination of corticosteroids and daclizumab should not be used as initial therapy of acut

231 Treatment with daclizumab significantly prevented development of high-g

232 tandard cyclosporin-based immunosuppression, daclizumab significantly reduced the frequency of acute

233 th HCV were randomized to receive tacrolimus+daclizumab (steroid-free) vs. tacrolimus+corticosteroids

234 then tacrolimus+mycophenolate mofetil (MMF)+daclizumab (steroid-free) vs. tacrolimus+MMF+corticoster

235 ic efficacy by combining (211)At-7G7/B6 with daclizumab support a clinical trial of this regimen in p

236 utic efficacy by combining depsipeptide with daclizumab supports a clinical trial of this combination

237 To prevent rejection, primates were given daclizumab, tacrolimus, and rapamycin.

238 The combination of daclizumab, tacrolimus, mycophenolate mofetil, and stero

239 zed 2:1 to receive alemtuzumab/tacrolimus or daclizumab/tacrolimus/mycophenolate.

240 s in development include alemtuzumab, BG-12, daclizumab, teriflunomide, laquinimod, and B-cell-target

241 We report that daclizumab therapy caused an ~50% decrease in Tregs over

242 Instead, daclizumab therapy was associated with a gradual decline

243 immunoregulation of activated T cells during daclizumab therapy.

244 ctivity of humanized anti-IL-2 receptor mAb (Daclizumab) therapy in the treatment of patients with se

245 Anti-IL-2Ralpha (daclizumab) therapy targeting cell surface-expressed rec

246 46 evaluable HL patients treated with (90)Y-daclizumab there were 14 complete responses and nine par

247 The addition of daclizumab to a tacrolimus-mycophenolate mofetil-based i

248 were 78% in the placebo group and 82% in the daclizumab treated group.

249 ograft; daclizumab treated, right allograft; daclizumab treated, left allograft.

250 l, right allograft; control, left allograft; daclizumab treated, right allograft; daclizumab treated,

251 ntation did not significantly differ between daclizumab-treated and control groups.

252 A trend toward improved survival in the daclizumab-treated group was noted.

253 acute rejection, whereas no patients in the daclizumab-treated group with DGF had graft loss due to

254 al function was similar between placebo- and daclizumab-treated groups in both the TT and DT trials.

255 iferative disorder (PTLD) in placebo- versus daclizumab-treated groups was comparable in both clinica

256 aily edema scores and curves for control and daclizumab-treated groups were compared.

257 b induction was slightly higher than that in daclizumab-treated patients (28.8+/-24.6% vs 21.3+/-21.3

258 In addition, 1 of 12 (9%) daclizumab-treated patients experienced one or more epis

259 significantly different between placebo and daclizumab-treated patients in the TT trial (83% vs. 84%

260 ival rates were similar between placebo- and daclizumab-treated patients with DGF.

261 survival at 12 months was 95 percent in the daclizumab-treated patients, as compared with 90 percent

262 pretransplantation GAD autoantibody-positive daclizumab-treated recipients compared with GAD autoanti

263 having at least one event compared to 33% of daclizumab-treated subjects (P=0.04).

264 Here we show that daclizumab treatment leads to only a mild functional blo

265 Daclizumab treatment produced significant reduction in m

266 Add-on daclizumab treatment reduced the number of new or enlarg

267 Finally, we demonstrated that daclizumab treatment significantly enhanced this newly d

268 Steroids were substituted with extended daclizumab use, in combination with tacrolimus and mycop

269 No major adverse events were attributed to daclizumab use.

270 In contrast, daclizumab used at the same dose and schedule was not as

271 Daclizumab used in liver transplant recipients without a

272 tified interleukin-2-receptor induction with daclizumab versus antithymocyte globulin was independent

273 The serum half-life of daclizumab was 20 days, and its administration resulted

274 2 months, patient and graft survival for the daclizumab was 98 and 96 vs. 96 and 94% for the OKT3 gro

275 Administration of daclizumab was accompanied by a dramatic drop in the pop

276 In 1997, daclizumab was approved by the FDA for use in the preven

277 Daclizumab was compared to placebo on a background of cy

278 Daclizumab was efficacious as prophylaxis against acute

279 ntibody 7G7/B6 alone and in combination with daclizumab was evaluated in nonobese diabetic/severe com

280 Daclizumab was generally well tolerated.

281 In the pharmacodynamic substudy, daclizumab was not associated with significant changes i

282 In the pilot study, induction therapy with daclizumab was safe, facilitated improvement in renal fu

283 Daclizumab was very well tolerated and led to a 78% redu

284 ody against the high-affinity IL-2 receptor (daclizumab) was performed in 70 adult, cardiac-transplan

285 junct immunosuppressant (cyclophosphamide or daclizumab) was used for 74 transplantations, adjunct do

286 antibody recognizing interleukin-2 receptor (daclizumab), which has proven to be a successful immunos

287 te on CD30, and humanized anti-Tac antibody (daclizumab), which recognizes CD25, in a murine model of

288 The patient was administered daclizumab without any adverse effects.

289 Daclizumab (Zenapax) identifies the alpha subunit of the

290 Daclizumab (Zenapax, Roche Pharmaceuticals), a humanized

291 (Simulect; Novartis, Basel, Switzerland) and daclizumab (Zenapax; Roche, Basel, Switzerland) combined

292 ctive study was to determine the benefits of daclizumab, (Zenapax, Roche Pharmaceuticals) a humanized