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1 reated with parenteral agents (interferon or glatiramer acetate).
2 th BG-12) and injection-related events (with glatiramer acetate).
3  (primarily with type-1 beta interferons and glatiramer acetate).
4 first reported case of exacerbation of SS by glatiramer acetate.
5 a; their recruitment was further enhanced by glatiramer acetate.
6  B cells obtained from patients who received glatiramer acetate.
7  contribute to the therapeutic mechanisms of glatiramer acetate.
8 ned using a well-established MS therapeutic, glatiramer acetate.
9 uperiority or noninferiority of BG-12 versus glatiramer acetate.
10 ells compared to amino-acid polymers such as glatiramer acetate.
11 signed: 386 to interferon beta-1a and 378 to glatiramer acetate.
12 ulating therapy, such as interferon beta and glatiramer acetate.
13 re stimulated with mitogens, recall Ags, and glatiramer acetate.
14 BG-12 (0.22), thrice-daily BG-12 (0.20), and glatiramer acetate (0.29) than with placebo (0.40) (rela
15 placebo, each in combination with injectable glatiramer acetate 20 mg daily.
16 were randomized 4.3:4.3:1 to receive generic glatiramer acetate (20 mg), brand glatiramer acetate (20
17 ve generic glatiramer acetate (20 mg), brand glatiramer acetate (20 mg), or placebo by daily subcutan
18 , P<0.001; thrice-daily BG-12, 51%, P<0.001; glatiramer acetate, 29%, P=0.01).
19                    We examined the effect of glatiramer acetate, a random copolymer of alanine, lysin
20 ever, for most patients, daily injections of glatiramer acetate abolished this T-cell response and pr
21 zation of glatiramer acetate, as compared to glatiramer acetate alone.
22 juvant that is well tolerated in humans plus glatiramer acetate, an FDA-approved synthetic copolymer
23 uperior to dimethyl fumarate, teriflunomide, glatiramer acetate and interferon beta.
24                    Two approved medications, glatiramer acetate and Natalizumab, were developed direc
25 yl fumarate, teriflunomide, interferon beta, glatiramer acetate and no treatment.
26  sought to determine whether combinations of glatiramer acetate and parenteral or ingested type I int
27 ned to test a possible synergistic effect of glatiramer acetate and type I interferon in humans shoul
28                       Interferon beta-1a and glatiramer acetate are commonly prescribed for relapsing
29 atory therapies, such as interferon beta and glatiramer acetate, are ineffective.
30 herapies for MS, such as interferon-beta and glatiramer acetate, are limited by incomplete responses
31 els, with and without weekly immunization of glatiramer acetate, as compared to glatiramer acetate al
32 ty despite treatment with interferon beta or glatiramer acetate, clinicians often switch therapy to e
33                                              Glatiramer acetate (Copaxone) functioned as a universal
34 e batch release of complex products, namely, glatiramer acetate (Copaxone), collagen hydrolysate (Col
35                           Copolymer 1 [Cop1, glatiramer acetate, Copaxone, poly(Y,E,A,K)n] is widely
36      In post hoc comparisons of BG-12 versus glatiramer acetate, differences were not significant exc
37 ocrelizumab) or injectable (interferon-beta, glatiramer acetate) DMTs.
38  pathology, whereas weekly administration of glatiramer acetate enhanced cerebral recruitment of inna
39 ocyte-derived macrophages, demonstrated that glatiramer acetate enhanced the ability of macrophages t
40 ming of the following DMTs: interferon beta, glatiramer acetate, fingolimod, natalizumab, or alemtuzu
41 had received fingolimod, interferon beta, or glatiramer acetate for a minimum of 3 months following a
42                                              Glatiramer acetate (GA) (Copaxone), a well-established d
43 a-1a (IFN) 30 mug intramuscularly weekly and glatiramer acetate (GA) 20 mg daily is more efficacious
44                            Immunization with glatiramer acetate (GA) alleviates the neuropathology as
45                Interferon beta (INFbeta) and glatiramer acetate (GA) are widely used in patients with
46                                          Two glatiramer acetate (GA) drugs, commercially available Co
47                                              Glatiramer acetate (GA) has been used as an immunomodula
48                                              Glatiramer Acetate (GA) has provided safe and effective
49                                              Glatiramer acetate (GA) is a synthetic polypeptide that
50                                              Glatiramer acetate (GA) is a treatment option for multip
51                                              Glatiramer acetate (GA) is a widely used and safe formul
52                                              Glatiramer acetate (GA) is widely prescribed for the tre
53 and has a different mechanism of action than glatiramer acetate (GA), a parenterally administered imm
54                              The capacity of glatiramer acetate (GA), a random copolymer of alanine,
55 and glutamate toxicity, the immune modulator glatiramer acetate (GA, Cop-1; Copaxone; Teva Pharmaceut
56                               Treatment with glatiramer acetate (GA, copolymer-1, Copaxone), a drug a
57 inal cord axons is promoted by antibodies to glatiramer acetate (GA, Copolymer-1, Copaxone), a therap
58 at treatment of multiple sclerosis (MS) with glatiramer acetate (GA; Copaxone) induces differential u
59                                              Glatiramer acetate (GA; Copaxone) is a random copolymer
60                                              Glatiramer acetate (GA; copolymer-1, Copaxone) suppresse
61 apeutic efficiency of the MS drug, Copaxone (Glatiramer acetate-GA).
62  for relapsing-remitting multiple sclerosis, glatiramer acetate generic drug and brand drug had equiv
63  the interferon beta-1a group and 132 in the glatiramer acetate group) had one or more relapses (the
64 n combination to wild-type mice, IFN-tau and glatiramer acetate had a synergistic beneficial effect i
65 umab, a high-efficacy DMT, versus interferon/glatiramer acetate (IFN/GA) in pwMS over the age of 60.
66                                       Weekly glatiramer acetate immunization of transgenic mice model
67                                           In glatiramer acetate-immunized mice and, moreover, in the
68                                 In contrast, glatiramer acetate in conjunction with either subcutaneo
69 l IFN-tau alone and in combination with oral glatiramer acetate in experimental allergic encephalomye
70 study was to compare interferon beta-1a with glatiramer acetate in patients with RRMS.
71 latiramer acetate in relapsing/remitting MS, glatiramer acetate in primary progressive MS, and intrav
72              Our aim in the REGARD (REbif vs Glatiramer Acetate in Relapsing MS Disease) study was to
73 sults have not yet been published (e.g. oral glatiramer acetate in relapsing/remitting MS, glatiramer
74 nt difference between interferon beta-1a and glatiramer acetate in the primary outcome.
75 he activity of copolymer 1 (Cop 1, Copaxone, glatiramer acetate) in suppressing experimental autoimmu
76 ar adjuvant therapy of AD animal models with glatiramer acetate induces anti-inflammatory responses a
77  some individuals, in vivo administration of glatiramer acetate induces highly cross-reactive T cells
78                                              Glatiramer acetate is a mixture of randomly synthesized
79                            To our knowledge, glatiramer acetate is the first agent that suppresses hu
80         Moreover, our case report shows that glatiramer acetate may also exacerbate the course of SS.
81 is case report indicates that treatment with glatiramer acetate may modulate or even exacerbate the c
82                                 Estriol plus glatiramer acetate met our criteria for reducing relapse
83 approved for use in multiple sclerosis (MS): glatiramer acetate, mitoxantrone, and natalizumab.
84          Prophylactic treatment of mice with glatiramer acetate normalized gene marker expression, an
85 a three times per week or 20 mg subcutaneous glatiramer acetate once per day for 96 weeks to assess t
86                               Treatment with glatiramer acetate or IFN-beta reversed this functional
87 sk of conversion than initial treatment with glatiramer acetate or interferon beta (HR, 0.66; 95% CI,
88              Patients initially treated with glatiramer acetate or interferon beta had a lower hazard
89 The probability of conversion was lower when glatiramer acetate or interferon beta was started within
90                                         When glatiramer acetate or interferon beta were escalated to
91 ary progressive MS vs initial treatment with glatiramer acetate or interferon beta.
92  Natalizumab, no treatment, interferon beta, glatiramer acetate, or fingolimod.
93 ted with platform compounds (interferons and glatiramer acetate; p<0.0001 for the interaction term be
94 ecreting regulatory T cell lines specific to glatiramer acetate [poly(Y,E,A,K)n] or poly(Y,F,A,K)n ha
95 l study of treatment with interferon beta or glatiramer acetate provide evidence that their effects o
96                                The surviving glatiramer acetate-reactive T cells exhibited a greater
97                                Compared with glatiramer acetate (reference), several therapies showed
98 e circulation or by weekly immunization with glatiramer acetate, resulted in substantial attenuation
99 ultiple sclerosis, BG-12 (at both doses) and glatiramer acetate significantly reduced relapse rates a
100 , twice-daily BG-12, thrice-daily BG-12, and glatiramer acetate significantly reduced the numbers of
101                                              Glatiramer acetate, subcutaneous murine interferon-alpha
102  first with interferon beta-1a and then with glatiramer acetate, suggests that these drugs may influe
103             These drugs include interferons, glatiramer acetate, teriflunomide, sphingosine 1-phospha
104          In contrast to beta-interferons and glatiramer acetate, the first-generation DMTs, several n
105                      These data suggest that glatiramer acetate therapy affects several aspects of dy
106 enty-two patients with MS who were receiving glatiramer acetate therapy and 22 treatment-naive patien
107  B cells was observed in patients undergoing glatiramer acetate therapy as well as a significant redu
108                                              Glatiramer acetate therapy for at least 3 months at the
109  knowledge, the previously unknown effect of glatiramer acetate therapy on B cells in patients with r
110                                              Glatiramer acetate therapy remodels the composition of t
111        The diagnosis of MS was excluded, and glatiramer acetate therapy was discontinued.
112                                        These glatiramer acetate-treated macrophages exhibited increas
113 ients with multiple sclerosis, as well as 16 glatiramer acetate-treated patients as a non-metabolite
114                                Additionally, glatiramer acetate treatment also significantly reduced
115                           Upon initiation of glatiramer acetate treatment, the patient developed the
116 g the obtained results to those reported for glatiramer acetate using MALLS, the technique commonly e
117 h twice-daily BG-12, thrice-daily BG-12, and glatiramer acetate versus placebo (21%, 24%, and 7%, res
118                             An active agent, glatiramer acetate, was also included as a reference com
119 s include the combination of interferons and glatiramer acetate with each other or with approved seco
120 ce (NICE) concluded that interferon beta and glatiramer acetate would be cost effective as disease-mo

 
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