ライフサイエンスコーパス: 5-ASA

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1 The 5-aminosalicylic acid (5-ASA) agents and oral steroids remain the first-line ap

2 ecently reported that 5-aminosalicylic acid (5-ASA) inhibits TNFalpha-regulated IkappaB degradation a

3 ne expression whereas 5-aminosalicylic acid (5-ASA) or indomethacin had no effect.

4 etic acid (4-APAA) or 5-aminosalicylic acid (5-ASA) with peptides, including an antibiotic peptide te

5 ulfapyridine (SP) and 5-aminosalicylic acid (5-ASA), on components of angiogenesis, namely, endotheli

6 d on 5 main drug classes: 5-aminosalicylate (5-ASA), corticosteroids, immunosuppressants, anti-tumor

7 SSZ, SP, and 5-ASA were assayed for their effects on basic fibroblast

8 cells or cellular extracts is not blocked by 5-ASA.

9 S-transferase-IkappaBalpha are inhibited by 5-ASA.

10 cells treated with TNFalpha is inhibited by 5-ASA.

11 o-bond releasing the 5-ASA or a pH-dependent 5-ASA packaging system that permitted release in the dis

12 st 6 months prior to and 12 months following 5-ASA initiation (index date).

13 These findings suggest a novel role for 5-ASA in the management of IBD by disrupting TNFalpha ac

14 fic non-pharmacy claims, at least 30 days of 5-ASA treatment and at least one corticosteroid prescrip

15 a number of alternative forms of delivery of 5-ASA were developed consisting of either a similar sulf

16 To determine the mechanism of 5-ASA inhibition of IkappaB degradation, we studied youn

17 In general, women on 5-ASA, thiopurine, or anti-tumor necrosis factor (TNF) m

18 to moderate disease flare while on optimized 5-ASA or thiopurine therapy should be managed with syste

19 duced by incubation with either SSZ (19%) or 5-ASA (23%) (P<0.05; [n = 6]).

20 w prescription for either corticosteroids or 5-ASA medications following an interval of at least 4 mo

21 adherent with their prescribed doses of oral 5-ASA.

22 005 for a UC diagnosis and at least one oral 5-ASA prescription on or after the first observed UC dia

23 Oral and rectal 5-ASA are recommended first-line therapy for mild to mod

24 As a result, 5-ASA-containing medications continue to provide a valua

25 antibacterial agent, and 5-amino-salicylate (5-ASA), an anti-inflammatory agent.

26 We show 5-ASA inhibits TNFalpha-stimulated phosphorylation of Ik

27 In summary, 5-ASA inhibits TNFalpha-stimulated IKKalpha kinase activ

28 to target a therapeutic concentration of the 5-ASA component of the medication primarily in the colon

29 nal destruction of an azo-bond releasing the 5-ASA or a pH-dependent 5-ASA packaging system that perm

30 inclusion criteria: 72% were nonadherent to 5-ASA treatment (n=1,217) and 28% were adherent (n=476)

31 l corticosteroid therapy, with transition to 5-ASA, thiopurine, anti-TNF (with or without thiopurine

32 P decreased basal HMVEC proliferation, while 5-ASA increased proliferation (P<0.05; [n = 5]).

33 treated cells (but not in cells treated with 5-ASA or indomethacin) for up to 24 h after treatment.

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