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 For the slow absorption group, piroxicam, 25%-75%, was separated by a 3-hours interval.

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

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

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

14 igated disease in both the Cox2 MKO/CCHF and piroxicam-accelerated Il10-/- models of inflammatory bow

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

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

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

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

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

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

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

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

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

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

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

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

27 Crystalline piroxicam anhydrate exists as colorless single crystals

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

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

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

31 -type NSAIDs tenoxicam (TNX), meloxicam, and piroxicam, but not other types of NSAIDs, exhibit an inh

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

33 ermine the crystal structures of ampicillin, piroxicam, cocaine, and two polymorphs of the drug molec

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

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

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

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

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

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

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

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

42 Administration of piroxicam in the diet produced no significant reductions

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

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

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

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

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

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

49 amorphous piroxicam is attributed to charged piroxicam molecules.

50 of the polymorphic form and contains neutral piroxicam molecules.

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

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

53 case studies of commercially available APIs: piroxicam, naproxen sodium, and benzocaine.

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

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

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

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

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

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

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

61 intestinal mucus using carvedilol (CVDL) and piroxicam (PXM) as model drugs.

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

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

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

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

66 etone, Naproxen, Nimesulide, Phenylbutazone, Piroxicam, Salicylamide, and Tolmetin.

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

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

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

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

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

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

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

74 icles, the release kinetics of a model drug (piroxicam) was quantified showing that release was more

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

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

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

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