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1 mpared with three (2%) patients treated with interferon beta 1a.
2 uzumab versus 85 (45%) patients treated with interferon beta 1a.
3 crelizumab and in 2.9% of those treated with interferon beta-1a.
4 o-controlled, multicenter phase III trial of interferon beta-1a.
5 ng were higher with daclizumab HYP than with interferon beta-1a.
6 crelizumab and in 0.2% of those treated with interferon beta-1a.
7 rophy in high risk CIS patients treated with interferon beta-1a.
8 bility after treatment with alemtuzumab than interferon beta-1a.
9 relapse rates and MRI outcomes compared with interferon beta-1a.
10 le sclerosis, as compared with intramuscular interferon beta-1a.
11 improved after alemtuzumab but not following interferon beta-1a.
12 part of a clinical trial of natalizumab and interferon beta-1a.
13 ltiple sclerosis patients being treated with interferon-beta-1a.
14 rate was lower with daclizumab HYP than with interferon beta-1a (0.22 vs. 0.39; 45% lower rate with d
15 5% CI 43.2-60.7%) than patients treated with interferon beta-1a (15 of 66 patients, 27.2%, 17.2-41.4%
16 eeks was lower with daclizumab HYP than with interferon beta-1a (4.3 vs. 9.4; 54% lower number of les
17 ompared with 52 of 107 patients treated with interferon beta-1a (42.6%, 32.4-52.4%; hazard ratio [HR]
18 stratified by site, to receive subcutaneous interferon beta 1a 44 mug, intravenous alemtuzumab 12 mg
20 andomly assigned in a 1:1:1 ratio to receive interferon beta-1a (44 mug subcutaneously three times pe
22 gnificantly lower with ocrelizumab than with interferon beta-1a (9.1% vs. 13.6%; hazard ratio, 0.60;
23 eficial effects of alemtuzumab compared with interferon beta-1a across all analysed patient subsets,
24 usly at a dose of 150 mg every 4 weeks, with interferon beta-1a, administered intramuscularly at a do
25 e of relapse over a two-year period than was interferon beta-1a alone (0.34 vs. 0.75, P<0.001) and wi
26 eta-1a was significantly more effective than interferon beta-1a alone in patients with relapsing mult
29 se of either 1.25 or 0.5 mg or intramuscular interferon beta-1a (an established therapy for multiple
30 187 (96%) of 195 patients randomly allocated interferon beta 1a and 376 (97%) of 386 patients randoml
31 202 (87%) of 231 patients randomly allocated interferon beta 1a and 426 (98%) of 436 patients randoml
32 kly intramuscular injections of 30 microg of interferon beta-1a and 190 were assigned to receive week
34 vous system, developed during treatment with interferon beta-1a and a selective adhesion-molecule blo
36 There was no significant difference between interferon beta-1a and glatiramer acetate in the primary
37 ion of disability compared with subcutaneous interferon beta-1a, and the mean expanded disability sta
38 however, in patients who initially received interferon beta-1a, ARR was lower after switching to fin
39 ose of 600 mg every 24 weeks or subcutaneous interferon beta-1a at a dose of 44 mug three times weekl
41 ive of this work was to assess the effect of interferon beta-1a (Avonex) on the rate of development o
42 rpose of this study was to determine whether interferon beta-1a could slow the progressive, irreversi
43 ecific for interleukin-10, as treatment with interferon-beta-1a did not result in accumulation of tra
44 that has demonstrated superior efficacy over interferon beta-1a for relapsing-remitting multiple scle
50 plan-Meier estimates, 59% of patients in the interferon beta 1a group were relapse-free at 2 years co
51 mpared with 134 [66%] of 202 patients in the interferon beta 1a group) that were mostly mild-moderate
52 adverse events compared with 12 (6%) in the interferon beta 1a group, and three (1%) had immune thro
54 mmon in the daclizumab HYP group than in the interferon beta-1a group (in 65% vs. 57% of the patients
55 ower than expected: 258 patients (126 in the interferon beta-1a group and 132 in the glatiramer aceta
56 tients in the placebo group, patients in the interferon beta-1a group had a relative reduction in the
57 ple sclerosis was significantly lower in the interferon beta-1a group than in the placebo group (rate
60 cing lesions, although patients treated with interferon beta-1a had significantly fewer gadolinium-en
62 ertaken to determine whether combined use of interferon beta-1a (IFN) 30 mug intramuscularly weekly a
63 clerosis (SENTINEL) study, patients received interferon beta-1a (IFN-beta-1a) plus natalizumab 300 mg
65 A systematic mutational analysis of human interferon-beta-1a (IFN-beta) was performed to identify
68 t benefits of fingolimod 0.5 or 1.25 mg over interferon beta-1a (IFNbeta-1a) in patients with relapsi
70 nter, phase III, placebo-controlled study of interferon beta-1a (IFNbeta-1a; AVONEX) in relapsing for
71 arison, SPMS subjects from the intramuscular interferon beta-1a (IM IFNbeta-1a) IMPACT study were als
73 disability, comparing alemtuzumab 12 mg and interferon beta 1a in all patients who received at least
74 cacy and safety of alemtuzumab compared with interferon beta 1a in patients who have relapsed despite
77 od before randomization to receive continued interferon beta-1a in combination with 300 mg of nataliz
78 zumab reduced disease activity compared with interferon beta-1a in most of the analysed subgroups.
79 Efficacy of Natalizumab in Combination with Interferon Beta-1a in Patients with Relapsing Remitting
80 Efficacy of Natalizumab in Combination With Interferon Beta-1a in Patients With Relapsing-Remitting
82 ibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitti
83 se rate was lower with ocrelizumab than with interferon beta-1a in trial 1 (0.16 vs. 0.29; 46% lower
84 n was 0.02 with ocrelizumab versus 0.29 with interferon beta-1a in trial 1 (94% lower number of lesio
85 ment) significantly favored ocrelizumab over interferon beta-1a in trial 2 (0.28 vs. 0.17, P=0.004) b
86 me the fourth study of the beta interferons (interferon-beta-1a, in this case) to demonstrate a parti
90 on natalizumab monotherapy >18 months, 6 on interferon beta-1a monotherapy >36 months, and 5 untreat
91 of the study was to determine the effect of interferon-beta-1a on the expression of interleukin-10,
92 within the brain were randomized to receive interferon beta-1a or placebo after initial treatment wi
99 uced compared with the previous 12 months of interferon beta-1a therapy (p<0.0001 for T2 lesions at b
100 randomly assigned 1171 patients who, despite interferon beta-1a therapy, had had at least one relapse
101 re randomised to receive 44 mug subcutaneous interferon beta-1a three times per week or 20 mg subcuta
102 olimod compared with the previous 12 months (interferon beta-1a to 0.5 mg fingolimod [n=167], 0.31 [9
103 s 0.22 [0.15-0.31], in months 13-24 p=0.049; interferon beta-1a to 1.25 mg fingolimod [n=174], 0.29 [
105 tients to assess the effect of a change from interferon beta-1a to fingolimod, and to compare over 24
107 s compared with the group that switched from interferon beta-1a to fingolimod, we recorded lower ARRs
110 tively evaluated the effect of intramuscular interferon beta-1a treatment following the first demyeli
111 enrolled in the Observational Study of Early Interferon beta-1a Treatment in High Risk Subjects after
117 ginally received 30 mug weekly intramuscular interferon beta-1a were randomly reassigned (1:1) to rec
118 n Relapsing MS Disease) study was to compare interferon beta-1a with glatiramer acetate in patients w
119 umab HYP showed efficacy superior to that of interferon beta-1a with regard to the annualized relapse
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