ライフサイエンスコーパス: piroxicam

1 menon which may be termed mechanochromism of piroxicam.

2 receptor antagonists, tetrodotoxin (TTX), or piroxicam.

3 time-dependent inhibition by nimesulide and piroxicam.

4 , and this increase was blocked by NS-389 or piroxicam.

5 or 1500 ppm celecoxib mixed in the diet) or piroxicam.

6 ly shown to be most effective in this model, piroxicam.

7 with the prostaglandin inhibitory effect of piroxicam.

8 mM alphaKG, 80%; 1 mM probenecid, 100%; 1 mM piroxicam, 100%; 1 mM octanoate, 100%.

9 s ratio [OR] of indomethacin, meclofenamate, piroxicam = 2.8), and for high dosages of other NSAIDs (

10 laddering, and caspase-3 activation, whereas piroxicam, a COX-1-specific inhibitor, displays no appre

11 ver, in the present study we found that both piroxicam, a general COX inhibitor, and NS-398, a COX-2

12 In addition, we evaluated the ability of piroxicam, a potent COX inhibitor, to prevent postinitia

13 In contrast, none of the doses of piroxicam alone decreased tumor multiplicity in the prox

14 inflammation was increased by treatment with piroxicam and decreased with anti-TL1A treatment, FDG up

15 modifier Mom1 and the pharmacological agents piroxicam and difluoromethylornithine each reduced intes

16 desmoid fibromas, whereas the combination of piroxicam and difluoromethylornithine exerted a moderate

17 a selectivity profile for COX-2 superior to piroxicam and other marketed NSAIDs.

18 Treatment with piroxicam and sulindac resulted in 95% and 52% fewer tum

19 mice bearing established tumors with NSAIDs (piroxicam and sulindac, 0.5 and 0.6 mg/mouse/day, respec

20 low doses of the nonselective COX inhibitor piroxicam and the ornithine decarboxylase (ODC) inhibito

21 crypt foci were counted, and serum levels of piroxicam and thromboxane B2 were quantitated.

22 min)/+ progeny of pregnant dams treated with piroxicam and/or DFMO were reduced in number and their r

23 xygenase (COX) inhibitors including aspirin, piroxicam, and NS398 markedly inhibited CXCR4 expression

24 was also inhibited by about 50% by NS-398 or piroxicam, and this inhibitory effect was accompanied by

25 Crystalline piroxicam anhydrate exists as colorless single crystals

26 seven groups, including groups treated with piroxicam at 0, 50, 100, and 200 ppm in the AIN93G diet.

27 Piroxicam at 12, 25, and 50 ppm in the diet caused dose-

28 Rats treated with sulindac at 400 ppm and piroxicam at 150 ppm were used as positive controls.

29 Piroxicam caused reduction in tumor volume in 12 of 18 d

30 roscopy indicates that most of the amorphous piroxicam consists of neutral piroxicam molecules; the c

31 Colons from rats treated with sulindac or piroxicam contained PGE2 levels that ranged from approxi

32 sly suppressing inflammatory infiltration in piroxicam-exposed IL-10(-/-) mice.

33 ontrol to 2.1 +/- 1.1 (12%) in the high-dose piroxicam group (P < 0.001).

34 sulfone at 1000 and 2000 ppm, sulindac, and piroxicam had significantly fewer colonic adenomas and c

35 that the nonsteroidal anti-inflammatory drug piroxicam has strong biological and therapeutic effects,

36 Structural and solid-state changes of piroxicam in its crystalline form under mechanical stres

37 ractions of charged and neutral molecules of piroxicam in the amorphous phase highlights the unique c

38 Administration of piroxicam in the diet produced no significant reductions

39 ny dosage of indomethacin, meclofenamate, or piroxicam increase the risk of dyspepsia by about 3-fold

40 spirin, but not salicylate, indomethacin, or piroxicam, increased plasma nitric oxide (NO), which cor

41 o il10(-/-) mice, dKO mice were resistant to piroxicam-induced colitis; they also developed less seve

42 wild-type Cox-2(+/+) cells, both NS-398 and piroxicam inhibited UVB-induced phosphorylation of c-Jun

43 The yellow color of amorphous piroxicam is attributed to charged piroxicam molecules.

44 AP-1 activity by COX-2 inhibitors NS-398 or piroxicam may occur by a mechanism that is independent o

45 amorphous piroxicam is attributed to charged piroxicam molecules.

46 of the polymorphic form and contains neutral piroxicam molecules.

47 re yellow, are known to contain zwitterionic piroxicam molecules.

48 the amorphous piroxicam consists of neutral piroxicam molecules; the charged species comprise only a

49 Between 2% (ibuprofen) and 23.5% (piroxicam) of courses were discontinued due to toxicity.

50 determined the effects of the cox inhibitor, piroxicam, on tumor response, apoptotic index, prolifera

51 Following exposure of il10(-/-) mice to piroxicam or infection with T muris, production of IL-13

52 ted by either the nonselective COX inhibitor piroxicam or the selective COX-2 inhibitor DFP, but by i

53 was induced with the gastrointestinal toxin piroxicam or Trichuris muris infection.

54 Combined treatment of mice with piroxicam plus DFMO was much more effective than either

55 een rats to test the impact of nonselective (Piroxicam), preferential (Meloxicam), and selective COX-

56 tion of glutathione (GSH) in the presence of piroxicam (PXM) for the first time.

57 m treatment with this chemopreventive agent, piroxicam, reduced colon carcinoma incidence and multipl

58 PC-3 cells with a COX-1 selective inhibitor, piroxicam, reduced TXA(2) synthesis by approximately 40%

59 Furthermore, treatment with piroxicam results in significantly lower [Ca(2+)](i) in

60 ations due to toxicity occurred earlier with piroxicam than with other NSAIDs.

61 other drug substances, namely sparfloxacin, piroxicam, theophylline, caffeine, ibuprofen, acetaminop

62 known but may be related to the inability of piroxicam to modulate other biochemical pathways involve

63 ctivated cathepsins to the inflamed colon of piroxicam-treated il10(-/-) mice.

64 ves of the well-known anti-inflammatory drug Piroxicam using THz spectroscopy and employed Principal

65 reatment and for the remainder of the study, piroxicam was administered in the diet at 200 and 400 pp

66 tion applications, fluorescence quenching by piroxicam was not affected by pH variation, elevated tem

67 Of these drugs, only one, piroxicam, was found to quench luminescence.

68 Other compounds of piroxicam, which are yellow, are known to contain zwitte

69 In contrast to the significant toxicity of piroxicam, which caused ulcers complicated by perforatio

70 ress, these crystals become yellow amorphous piroxicam, which has a strong propensity to recrystalliz