ライフサイエンスコーパス: sulfasalazine

1 , and auxiliary gas using the model compound sulfasalazine.

2 ficantly greater with TwHF extract than with sulfasalazine.

3 ing unexpected similarity to the activity of sulfasalazine.

4 be prevented by the clinically relevant drug sulfasalazine.

5 oid in chronic arthritis, and broader use of sulfasalazine.

6 an be modified and down-regulated in vivo by sulfasalazine.

7 to penicillamine, 2 to allopurinol, and 1 to sulfasalazine.

8 Treatment of hepatic stellate cells with sulfasalazine (0.5-2.0 mmol/L) induced apoptosis of acti

9 (0.8 [95% confidence interval 0.6-110]) and sulfasalazine (0.7 [95% confidence interval 0.5-1.0]) di

10 TwHF extract, 60 mg 3 times daily, or sulfasalazine, 1 g twice daily.

11 flammation in vivo, we studied the effect of sulfasalazine (100 mg/kg/day by gastric gavage for 3 day

12 hloride followed by recovery with or without sulfasalazine (150 mg/kg) treatment.

13 Mesalamine or sulfasalazine (2 mM), but not sulfapyridine, significant

14 7.5 to 17.5 mg per week), the combination of sulfasalazine (500 mg twice daily) and hydroxychloroquin

15 the important advance was the development of sulfasalazine, a drug initially used for the treatment o

16 reparation, or the pretreatment of AECs with sulfasalazine, a potent and specific inhibitor of NF-kap

17 sted IRR 2.51, 95% CI 1.29-4.89, P = 0.004), sulfasalazine (adjusted IRR 1.74, 95% CI 1.04-2.91, P =

18 p with a clinically approved candidate drug, sulfasalazine, already in hand.

19 Low-dose sulfasalazine also prevented morphologically evident tig

20 Sulfasalazine (also as a representative of the salicylat

21 It also cooperated with sulfasalazine, an FDA-approved inhibitor of cystine xCT

22 In addition, 1 patient continued receiving sulfasalazine and 1 patient remained on a regimen of sul

23 ching a sensitivity of 0.03 and 1.3mug/L for sulfasalazine and atrazine, respectively.

24 Sulfasalazine and calpain inhibitor I, inhibitors of NF-

25 g group), and 14 of 35 patients treated with sulfasalazine and hydroxychloroquine (40 percent), P = 0

26 ct to clinical benefit, triple therapy, with sulfasalazine and hydroxychloroquine added to methotrexa

27 Other established DMARDs, such as sulfasalazine and hydroxychloroquine, have also demonstr

28 azine and 1 patient remained on a regimen of sulfasalazine and hydroxychloroquine.

29 Our studies provide evidence that sulfasalazine and methotrexate may be described as a new

30 ation due to toxicity did not differ between sulfasalazine and methotrexate.

31 Sulfasalazine and metronidazole may prove to be useful,

32 e is experimental data to support the use of sulfasalazine and metronidazole.

33 atment of ulcerative colitis (UC) began with sulfasalazine and was driven by sulfapyridine toxicity.

34 itis, combination therapy with methotrexate, sulfasalazine, and hydroxychloroquine is more effective

35 modifying antirheumatic drugs (methotrexate, sulfasalazine, and hydroxychloroquine) or etanercept plu

36 ither methotrexate alone or a combination of sulfasalazine, and hydroxychloroquine.

37 he triple combination of hydroxychloroquine, sulfasalazine, and methotrexate is very effective even i

38 MTX, 4) triple therapy (hydroxychloroquine, sulfasalazine, and MTX), 5) continuation of MTX monother

39 ase reports have suggested that minocycline, sulfasalazine, and penicillamine are associated with ant

40 We conclude that mesalamine, sulfasalazine, and rosiglitazone significantly reduced t

41 c for the herbicide atrazine, the antibiotic sulfasalazine, and the vitamin biotin in mice and rabbit

42 alathion, pentachlorophenol, pyraclostrobin, sulfasalazine, and triclosan, achieving detection limits

43 thelial cell line, A549 cells, the effect of sulfasalazine appeared to be mediated in part by inhibit

44 Hydroxychloroquine and sulfasalazine are compatible with nursing.

45 ent studies have shown that methotrexate and sulfasalazine are relatively safe and effective for JRA.

46 on, 45% of patients in the EI group received sulfasalazine as opposed to 14% in the CT group (chi(2)

47 ely reversed the anti-inflammatory effect of sulfasalazine (at concentrations <1 microM in this in vi

48 reatment with pyrrolidine dithiocarbamate or sulfasalazine attenuated the iNOS-dependent production o

49 ent with > or = 1 DMARD (hydroxychloroquine, sulfasalazine, auranofin, intramuscular gold, D-penicill

50 antiinflammatory effects of methotrexate and sulfasalazine both in vitro and in vivo, but the mechani

51 ed antiinflammatory agents, methotrexate and sulfasalazine, both in vitro and in vivo.

52 ease was inhibited using either S-(4)-CPG or sulfasalazine, both potent blockers of system xC.

53 By contrast, sulfasalazine clearly inhibited HRV-16 induction of mRNA

54 with RA were being treated with methotrexate-sulfasalazine combined therapy, and two of the patients

55 for rheumatoid arthritis, with 51 receiving sulfasalazine compared with 38 receiving placebo; and 3)

56 Sulfasalazine completely blocked the development of tact

57 th the clinically approved anti-inflammatory sulfasalazine decreases tumor growth, revealing a therap

58 came evident that many patients treated with sulfasalazine developed intolerance to the drug and, in

59 68 receiving placebo; 2) a 37-week trial of sulfasalazine for rheumatoid arthritis, with 51 receivin

60 ts, 3 subjects with sickle cell disease took sulfasalazine (given orally at 1 g every 8 hours), and t

61 group and 32.8% (CI, 21.3% to 46.0%) of the sulfasalazine group met the ACR 20 response criteria (P=

62 ure to methotrexate, thiopurines, anti-TNFs, sulfasalazine, hydroxychloroquine, abatacept, or rituxim

63 A review of therapeutic use of sulfasalazine in children with chronic arthritis, includ

64 Companion studies were also performed using sulfasalazine in sickle transgenic mice to verify its ef

65 antiinflammatory effects of methotrexate and sulfasalazine in the murine air pouch model of inflammat

66 Sulfasalazine increased the exudate adenosine concentrat

67 is a critical mediator of methotrexate- and sulfasalazine-induced antiinflammatory activity in vitro

68 It has recently been shown that sulfasalazine inhibits 5-aminoimidazole-4-carboxamidorib

69 onsistent with the in vitro observation that sulfasalazine inhibits AICAR transformylase.

70 Sulfasalazine is moderately effective for ankylosing spo

71 The anti-inflammatory mechanism of sulfasalazine is not well understood.

72 One of these drugs, sulfasalazine, is clinically used to treat inflammatory

73 exate plus cyclosporine, hydroxychloroquine, sulfasalazine, leflunomide, etanercept, and infliximab.

74 These results indicate that sulfasalazine, like methotrexate, enhances adenosine rel

75 ere developed consisting of either a similar sulfasalazine-like prodrug formulation requiring luminal

76 Treatment with sulfasalazine markedly decreased the number of leukocyte

77 actile allodynia in experimental diabetes by sulfasalazine may stem from its ability to regulate both

78 Sulfasalazine might be useful in the treatment of nocice

79 rences between methotrexate, leflunomide and sulfasalazine monotherapies; early disease-modifying ant

80 based drugs (aspirin, sodium salicylate, and sulfasalazine) on the development of early stages of dia

81 ination therapy with either methotrexate and sulfasalazine or methotrexate and cyclosporine is being

82 s (limited to methotrexate, leflunomide, and sulfasalazine) or among anti-tumor necrosis factor drugs

83 ocked by inhibitors to NF-kappaB activation (sulfasalazine) or PI 3-kinase (LY294002), and both inhib

84 ANCA seroconversion induced by minocycline, sulfasalazine, or penicillamine.

85 gitis; Child-Pugh classification; and use of sulfasalazine, other 5-aminosalicylic acid preparations,

86 use of MTX monotherapy with the addition of sulfasalazine plus hydroxychloroquine (or etanercept, if

87 n therapies (MTX plus etanercept or MTX plus sulfasalazine plus hydroxychloroquine) at week 24 if the

88 ept, immediate oral triple therapy (MTX plus sulfasalazine plus hydroxychloroquine), or step-up from

89 ion therapy (MTX plus etanercept or MTX plus sulfasalazine plus hydroxychloroquine).

90 A single in vivo administration of sulfasalazine promoted accelerated recovery from fibrosi

91 on and targets of the anti-inflammatory drug sulfasalazine prompted us to investigate its effect on n

92 atients continued receiving TwHF extract and sulfasalazine, respectively, during the 24 weeks of the

93 We examined the effects of sulfasalazine, salicylates, and the poly(ADP-ribose) pol

94 e tumor and the ensuing hyperexcitability by sulfasalazine (SAS), a US Food and Drug Administration-a

95 CT activity with the pharmacologic inhibitor sulfasalazine (SASP).

96 Mechanistic studies showed that sulfasalazine selectively blocks nuclear factor-kappaB-d

97 In these mice sulfasalazine significantly reduced CEC expression of va

98 In humans with sickle cell disease, sulfasalazine significantly reduced CEC expression of VC

99 flammation, so we tested the hypothesis that sulfasalazine similarly promotes intracellular AICAR acc

100 Sulfasalazine (SSZ) an FDA approved anti-inflammatory ag

101 We investigated the effects of sulfasalazine (SSZ) and its metabolites, sulfapyridine (

102 To compare the efficacy of sulfasalazine (SSZ) with its two moieties, 5-aminosalicy

103 were randomized to receive step-up therapy (sulfasalazine [SSZ] monotherapy, then after 3 months, me

104 er the inhibitor of kappaB kinase suppressor sulfasalazine stimulates hepatic myofibroblast apoptosis

105 a in diabetic mice lacking expression of the sulfasalazine target nuclear factor-kappaB (NF-kappaB) p

106 We also evaluated the levels of sulfasalazine targets in sciatic nerves and dorsal root

107 g intraarticular corticosteroids followed by sulfasalazine therapy if resistant demonstrated reduced

108 ion use was excellent, ranging from 0.71 for sulfasalazine to 0.96 for methotrexate.

109 vioral findings, sciatic nerves and DRG from sulfasalazine-treated diabetic rats displayed a decrease

110 Sulfasalazine treatment also increased inosine levels in

111 Moreover, sulfasalazine treatment promoted a marked increase in sp

112 ly reversed the anti-inflammatory effects of sulfasalazine treatment.

113 zepine, phenobarbital, phenytoin, primidone, sulfasalazine, triamterene, and trimethoprim) during the

114 cholangitis, severity of liver disease, and sulfasalazine use (adjusted odds ratio, 0.14 [CI, 0.03 t

115 icular corticosteroid injections followed by sulfasalazine versus conservative therapy in patients wi

116 Sulfasalazine was a combination designer drug consisting

117 needed for nuclear factor-kappaB inhibition, sulfasalazine was able to prevent TNF-alpha-induced barr

118 Sulfasalazine was able to reduce glutathione levels in t

119 Sulfasalazine was administered in both groups for persis

120 FMLP) to endothelial cells preincubated with sulfasalazine was inhibited in a dose-dependent manner.