ライフサイエンスコーパス: glatiramer acetate

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 a; their recruitment was further enhanced by glatiramer acetate.

5 B cells obtained from patients who received glatiramer acetate.

6 contribute to the therapeutic mechanisms of glatiramer acetate.

7 ned using a well-established MS therapeutic, glatiramer acetate.

8 uperiority or noninferiority of BG-12 versus glatiramer acetate.

9 signed: 386 to interferon beta-1a and 378 to glatiramer acetate.

10 ulating therapy, such as interferon beta and glatiramer acetate.

11 re stimulated with mitogens, recall Ags, and glatiramer acetate.

12 BG-12 (0.22), thrice-daily BG-12 (0.20), and glatiramer acetate (0.29) than with placebo (0.40) (rela

13 placebo, each in combination with injectable glatiramer acetate 20 mg daily.

14 were randomized 4.3:4.3:1 to receive generic glatiramer acetate (20 mg), brand glatiramer acetate (20

15 ve generic glatiramer acetate (20 mg), brand glatiramer acetate (20 mg), or placebo by daily subcutan

16 , P<0.001; thrice-daily BG-12, 51%, P<0.001; glatiramer acetate, 29%, P=0.01).

17 We examined the effect of glatiramer acetate, a random copolymer of alanine, lysin

18 ever, for most patients, daily injections of glatiramer acetate abolished this T-cell response and pr

19 zation of glatiramer acetate, as compared to glatiramer acetate alone.

20 juvant that is well tolerated in humans plus glatiramer acetate, an FDA-approved synthetic copolymer

21 Two approved medications, glatiramer acetate and Natalizumab, were developed direc

22 sought to determine whether combinations of glatiramer acetate and parenteral or ingested type I int

23 ned to test a possible synergistic effect of glatiramer acetate and type I interferon in humans shoul

24 Interferon beta-1a and glatiramer acetate are commonly prescribed for relapsing

25 atory therapies, such as interferon beta and glatiramer acetate, are ineffective.

26 els, with and without weekly immunization of glatiramer acetate, as compared to glatiramer acetate al

27 ty despite treatment with interferon beta or glatiramer acetate, clinicians often switch therapy to e

28 Glatiramer acetate (Copaxone) functioned as a universal

29 Copolymer 1 [Cop1, glatiramer acetate, Copaxone, poly(Y,E,A,K)n] is widely

30 In post hoc comparisons of BG-12 versus glatiramer acetate, differences were not significant exc

31 pathology, whereas weekly administration of glatiramer acetate enhanced cerebral recruitment of inna

32 ocyte-derived macrophages, demonstrated that glatiramer acetate enhanced the ability of macrophages t

33 had received fingolimod, interferon beta, or glatiramer acetate for a minimum of 3 months following a

34 Glatiramer acetate (GA) (Copaxone), a well-established d

35 a-1a (IFN) 30 mug intramuscularly weekly and glatiramer acetate (GA) 20 mg daily is more efficacious

36 Immunization with glatiramer acetate (GA) alleviates the neuropathology as

37 Interferon beta (INFbeta) and glatiramer acetate (GA) are widely used in patients with

38 Glatiramer acetate (GA) has been used as an immunomodula

39 Glatiramer Acetate (GA) has provided safe and effective

40 Glatiramer acetate (GA) is a treatment option for multip

41 Glatiramer acetate (GA) is a widely used and safe formul

42 and has a different mechanism of action than glatiramer acetate (GA), a parenterally administered imm

43 The capacity of glatiramer acetate (GA), a random copolymer of alanine,

44 and glutamate toxicity, the immune modulator glatiramer acetate (GA, Cop-1; Copaxone; Teva Pharmaceut

45 Treatment with glatiramer acetate (GA, copolymer-1, Copaxone), a drug a

46 inal cord axons is promoted by antibodies to glatiramer acetate (GA, Copolymer-1, Copaxone), a therap

47 at treatment of multiple sclerosis (MS) with glatiramer acetate (GA; Copaxone) induces differential u

48 Glatiramer acetate (GA; Copaxone) is a random copolymer

49 Glatiramer acetate (GA; copolymer-1, Copaxone) suppresse

50 for relapsing-remitting multiple sclerosis, glatiramer acetate generic drug and brand drug had equiv

51 the interferon beta-1a group and 132 in the glatiramer acetate group) had one or more relapses (the

52 n combination to wild-type mice, IFN-tau and glatiramer acetate had a synergistic beneficial effect i

53 Weekly glatiramer acetate immunization of transgenic mice model

54 In glatiramer acetate-immunized mice and, moreover, in the

55 In contrast, glatiramer acetate in conjunction with either subcutaneo

56 l IFN-tau alone and in combination with oral glatiramer acetate in experimental allergic encephalomye

57 study was to compare interferon beta-1a with glatiramer acetate in patients with RRMS.

58 latiramer acetate in relapsing/remitting MS, glatiramer acetate in primary progressive MS, and intrav

59 Our aim in the REGARD (REbif vs Glatiramer Acetate in Relapsing MS Disease) study was to

60 sults have not yet been published (e.g. oral glatiramer acetate in relapsing/remitting MS, glatiramer

61 nt difference between interferon beta-1a and glatiramer acetate in the primary outcome.

62 he activity of copolymer 1 (Cop 1, Copaxone, glatiramer acetate) in suppressing experimental autoimmu

63 ar adjuvant therapy of AD animal models with glatiramer acetate induces anti-inflammatory responses a

64 some individuals, in vivo administration of glatiramer acetate induces highly cross-reactive T cells

65 Glatiramer acetate is a mixture of randomly synthesized

66 To our knowledge, glatiramer acetate is the first agent that suppresses hu

67 Estriol plus glatiramer acetate met our criteria for reducing relapse

68 approved for use in multiple sclerosis (MS): glatiramer acetate, mitoxantrone, and natalizumab.

69 Prophylactic treatment of mice with glatiramer acetate normalized gene marker expression, an

70 a three times per week or 20 mg subcutaneous glatiramer acetate once per day for 96 weeks to assess t

71 Treatment with glatiramer acetate or IFN-beta reversed this functional

72 Natalizumab, no treatment, interferon beta, glatiramer acetate, or fingolimod.

73 ecreting regulatory T cell lines specific to glatiramer acetate [poly(Y,E,A,K)n] or poly(Y,F,A,K)n ha

74 l study of treatment with interferon beta or glatiramer acetate provide evidence that their effects o

75 The surviving glatiramer acetate-reactive T cells exhibited a greater

76 e circulation or by weekly immunization with glatiramer acetate, resulted in substantial attenuation

77 ultiple sclerosis, BG-12 (at both doses) and glatiramer acetate significantly reduced relapse rates a

78 , twice-daily BG-12, thrice-daily BG-12, and glatiramer acetate significantly reduced the numbers of

79 Glatiramer acetate, subcutaneous murine interferon-alpha

80 In contrast to beta-interferons and glatiramer acetate, the first-generation DMTs, several n

81 These data suggest that glatiramer acetate therapy affects several aspects of dy

82 enty-two patients with MS who were receiving glatiramer acetate therapy and 22 treatment-naive patien

83 B cells was observed in patients undergoing glatiramer acetate therapy as well as a significant redu

84 Glatiramer acetate therapy for at least 3 months at the

85 knowledge, the previously unknown effect of glatiramer acetate therapy on B cells in patients with r

86 Glatiramer acetate therapy remodels the composition of t

87 These glatiramer acetate-treated macrophages exhibited increas

88 Additionally, glatiramer acetate treatment also significantly reduced

89 h twice-daily BG-12, thrice-daily BG-12, and glatiramer acetate versus placebo (21%, 24%, and 7%, res

90 An active agent, glatiramer acetate, was also included as a reference com

91 s include the combination of interferons and glatiramer acetate with each other or with approved seco

92 ce (NICE) concluded that interferon beta and glatiramer acetate would be cost effective as disease-mo