ライフサイエンスコーパス: COX inhibitor

1 ive COX-2 inhibitor) and indomethacin (a pan-COX inhibitor).

2 profen (800 mg 3 times a day), a nonspecific COX inhibitor.

3 or of COX-2, with diclofenac, a non-specific COX inhibitor.

4 by treatment with sulindac sulfide, a known COX inhibitor.

5 vity in this example of a diaryl-heterocycle COX inhibitor.

6 e experiments does not involve its role as a COX inhibitor.

7 or cells may be a direct target of action by COX inhibitors.

8 ltured ex vivo with or without IL-1 beta and COX inhibitors.

9 or to intracellular Ca(2+) were inhibited by COX inhibitors.

10 PGE2 should prove useful for identifying new COX inhibitors.

11 were more potent growth inhibitors than the COX inhibitors.

12 s 11-dehydro metabolite are depressed by the COX inhibitors.

13 ed mode-of-action such as PPARa agonists and COX inhibitors.

14 A binding to Eallo also affects responses to COX inhibitors.

15 ould be optimized by the further addition of COX inhibitors.

16 e-line prostanoid synthesis and responses to COX inhibitors.

17 ulating PGHS-2 activity and its responses to COX inhibitors.

18 effects typically associated with the use of COX inhibitors.

19 re enhanced by prostaglandins and reduced by COX inhibitors.

20 and PGE2 production and their regulation by COX inhibitors.

21 nary NO(x) and PGE(2) were corrected by both COX inhibitors.

22 activity, was added simultaneously with the COX inhibitors.

23 f a NO donor with those of a cyclooxygenase (COX) inhibitor.

24 an macrophages compared with cyclooxygenase (COX) inhibitors.

25 nd evaluation of 18F-labeled cyclooxygenase (COX) inhibitors.

26 ry reactions to nonselective cyclooxygenase (COX) inhibitors.

27 Unlike the selective COX inhibitors 1-[(4-methylsulfonyl)phenyl]-3-trifluorom

28 Using COX inhibitors, a sequential increase of posttransplanta

29 o increase Ecat activity; and (c) allosteric COX inhibitors act by preventing FA binding to Eallo and

30 mode by analyzing the action of a series of COX inhibitors against site-directed mutants of COX-2 be

31 Although neither estradiol nor the COX inhibitors alone had an effect on PGD2 serum levels,

32 Pretreatment of tumor cells with COX inhibitors also reduces metastatic success, indicati

33 d TNF-alpha production, whereas experimental COX inhibitors and antipyretics used during human malari

34 Thus, a major effect of COX inhibitors and COX-deficiency is the induction of ke

35 on previously shown in the mice treated with COX inhibitors and in COX-deficient mice and suggest tha

36 f a chiral antifungal azole pharmacophore to COX inhibitors and the evaluation of activity of 24 hybr

37 Hence, concomitant therapy with COX inhibitors and/or IL-6R antibodies might increase th

38 Experiments using specific cyclooxygenase (COX) inhibitors and genetic knockdown approaches indicat

39 a baicalensis), indomethacin (a nonselective COX inhibitor), and celecoxib (a selective COX-2 inhibit

40 tudy we found that both piroxicam, a general COX inhibitor, and NS-398, a COX-2 selective inhibitor,

41 ty compared with rofecoxib, the nonselective COX inhibitors, and control animals.

42 (2) inhibited MMP-1, reversed the effects of COX inhibitors, and inhibited ERK activation, suggesting

43 to standard anti-pyretic medications such as COX inhibitors, and lack of good medical therapy has led

44 COX inhibitors are also frequent cofactors in anaphylaxi

45 e for testing potential benefits from common COX inhibitors as a part of AML treatments.

46 disease processes and the widespread use of COX inhibitors as therapeutic agents.

47 (NS398) and nonselective (sulindac sulfide) COX inhibitors, as well as 5-fluorouracil (5-FU), induce

48 prevented this effect, and the non-specific COX inhibitor aspirin (1 mM) also alleviated the damage.

49 each at 60 s intervals) before and after the COX inhibitor aspirin (600 mg p.o.).

50 Developmental exposure to the COX inhibitor aspirin results in mild impairment of sexu

51 celecoxib or rofecoxib, and the nonspecific COX inhibitors, aspirin, naproxen, ibuprofen, or indomet

52 Pretreatment with ibuprofen, a nonspecific COX inhibitor, attenuated the febrile and systemic respo

53 tment of bFGF- or VEGF-stimulated HMECs with COX inhibitors blocked tubular formation by about 50% to

54 -specific inhibitor, and indomethacin, a pan-COX inhibitor, but not by SC-560, a COX-1-specific inhib

55 lly treated with opioids and cyclooxygenase (COX) inhibitors, but both are limited by side effects.

56 ase from FLSCs via inhibition of ERK, and 3) COX inhibitors, by attenuating PGE inhibition of ERK, en

57 Although COX inhibitors can be used to close the PDA by lowering

58 All of the COX inhibitors caused dose-dependent decreases in IL-1be

59 Crystallographic analysis of selective COX inhibitors complexed with either isoform provides so

60 Our data indicate that COX inhibitor coprescription among aspirin users is freq

61 nducing eradication of tumors, implying that COX inhibitors could be useful adjuvants for immune-base

62 Identification of genes regulated by COX inhibitors could lead to a better understanding of t

63 this study was to analyze if cyclooxygenase (COX) inhibitors could improve the early posttransplant o

64 Cyclooxygenase (COX) inhibitors decrease tumor multiplicity in the Min m

65 Studies in COX-deficient cells and using COX inhibitors demonstrated that COX-2 mediated the high

66 e FAs can potentiate or attenuate actions of COX inhibitors depending on the FA and whether the inhib

67 In contrast, the slow, time-dependent COX inhibitors (diclofenac, indomethacin, and flurbiprof

68 cations included coculture plus or minus the COX-inhibitor, Diclofenac, or synthetic PGE(2) in the ab

69 oncentrations of salicylate, while selective Cox inhibitors did not inhibit angiogenesis in this assa

70 Ibuprofen, a structurally dissimilar COX inhibitor, did not activate Slo2.1.

71 treatment with indomethacin, a non-selective COX inhibitor, did not prevent BAT thermogenesis or cuta

72 However, COX inhibitors do not eliminate IL-1beta-induced fever,

73 5-LO knockout mice that were treated with a COX inhibitor during allergic sensitization and challeng

74 and nonsubstrate fatty acids (FAs) and some COX inhibitors (e.g. naproxen) preferentially bind to th

75 Furthermore, multiple distinct classes of COX inhibitors efficiently blocked neurite loss in prima

76 t in which the R120Q subunit cannot bind the COX inhibitor flurbiprofen, was inhibited by flurbiprofe

77 raise concern regarding the use of selective COX inhibitors for the management of preterm labor.

78 This study established that azole-COX inhibitor hybrids are a novel class of potent antifu

79 Some COX inhibitors (i.e. nonsteroidal anti-inflammatory drug

80 -overexpressing cells with the non-selective COX inhibitor ibuprofen (1 microM, 48 h) or with the spe

81 4-bromophenacyl bromide (4-BPB), the general COX inhibitor ibuprofen (IB), and the highly selective C

82 d significantly not only by the nonselective COX inhibitor ibuprofen but also by the COX-2 selective

83 Furthermore, the well tolerated COX inhibitor ibuprofen was protective against IL-1beta-

84 Treatment with the cyclooxygenase (COX) inhibitor ibuprofen restores RSV clearance, indicat

85 hosphonovalerate as well the cyclooxygenase (COX) inhibitor ibuprofen.

86 The inhibitory activity of rapid, reversible COX inhibitors (ibuprofen, naproxen, mefenamic acid, and

87 However, medical use of COX inhibitors in glioblastoma treatment has been limite

88 Furthermore, COX inhibitors in humans, as well as platelet depletion,

89 c desensitization to aspirin by nonselective COX inhibitors in patients with AERD.

90 nimals are spared the hemorrhaging caused by COX inhibitors in the gut, where prostaglandins are inst

91 77 may represent more effective therapy than COX inhibitors in treating uveitis and ocular diseases w

92 , markedly enhanced, whereas cyclooxygenase (COX) inhibitors including aspirin, piroxicam, and NS398

93 COX inhibitors, including coxibs, nonselective nonsteroi

94 1.7 nmol OH(-) min(-1)) by the non-specific COX inhibitor indomethacin (5 mg kg(-1) I.P.).

95 nist collagen-related peptide along with the COX inhibitor indomethacin did not result in phosphoryla

96 tube formation by EPCs were inhibited by the COX inhibitor indomethacin or by genetic inactivation of

97 as an adjuvant and treated the mice with the COX inhibitor indomethacin or vehicle for analyses of th

98 The COX inhibitor indomethacin or vehicle was administered i

99 aglandin synthesis in newborn males with the COX inhibitor indomethacin permanently downregulates mar

100 e GPCR agonist AYPGKF in the presence of the COX inhibitor indomethacin, we found that PTPN7 KO mouse

101 beta-casein gene, which was inhibited by the Cox inhibitor indomethacin.

102 Mice were treated with the COX inhibitors indomethacin, flurbiprofen, or vehicle an

103 200 (5 mg kg(-1)) or by the cyclo-oxygenase (COX) inhibitor indomethacin (20 mg kg(-1)).

104 completely abolished by the cyclooxygenase (COX) inhibitor indomethacin or by selective antagonism o

105 of coinfected mice with the cyclooxygenase (COX) inhibitor indomethacin reduces the infectious burde

106 Treatment with the COX-inhibitor indomethacin and/or the clinical monoclona

107 ly blocked in the presence of a nonselective COX inhibitor (indomethacin) or a selective COX-2 inhibi

108 Administration of a nonselective COX inhibitor (indomethacin), selective COX-1 (valeryl s

109 A non-selective COX inhibitor (indomethacin, 15 mg kg(-1) I.P.), a selec

110 (NS-398; 1 mg/kg x 7 days; N = 16), general COX inhibitor (indomethacin; 1 mg/kg x 7 days; N = 16),

111 OX-2 inhibitor, SC58238, and the nonspecific COX inhibitor, indomethacin, effectively inhibited the e

112 791, as well as the traditional nonsteroidal COX inhibitor, indomethacin.

113 atment of platelets with the cyclooxygenase (COX) inhibitor, indomethacin (20 microM), the thromboxan

114 Cyclooxygenase (COX) inhibitors, indomethacin and NS-398, did not reduce

115 tment of W256 cells with various LOX but not COX inhibitors induced apoptotic cell death, which could

116 ophils to aspirin or sodium salicylate (poor COX inhibitor) inhibited Erk activity and adhesiveness o

117 Sulindac sulfide, a COX inhibitor, inhibited the growth of non-small-cell lu

118 m contribute to anaphylaxis independently of COX inhibitor intake is unclear.

119 were associated with data indicating that a COX inhibitor is not preventive in NMBA-induced rat esop

120 n response to administration of nonselective COX inhibitors is a cardinal feature of aspirin-exacerba

121 t of combined therapy with aspirin and other COX inhibitors is not yet clear.

122 inflammatory drugs (NSAIDs), cyclooxygenase (COX) inhibitors, is well established, but responsible mo

123 The pan-COX inhibitor ketorolac continuously and significantly d

124 Sodium salicylate, a poor COX inhibitor, likewise enhanced IL-1-mediated COX-2 gen

125 proapoptotic protein, and its regulation by COX inhibitors may provide new clues for explaining thei

126 (PLA2) inhibitor], ibuprofen [a nonselective COX inhibitor], neomycine [a phospholipase C (PLC) inhib

127 motes CRC progression, and both nonselective COX inhibitors (NSAIDs) and selective COX-2 inhibitors (

128 tes to the proapoptotic effects of high-dose COX inhibitors (NSAIDs) by serving as a downstream media

129 We evaluated the effect of cyclooxygenase (COX) inhibitors (NSAIDs) on human colon carcinoma cells

130 o compare the activity of target ligands and COX inhibitors on PGE2 synthesis and release, the respon

131 the pharmacologic effects of specific spinal COX inhibitors on uterine cervical distention induced no

132 The beneficial effects of Cyclooxygenases (COX) inhibitors on human health have been known for thou

133 cific NO synthase inhibitor, a non-selective COX inhibitor or combined inhibition during perfusion of

134 Treatment with COX inhibitors or albumin restored immune competence and

135 ere exposed to low doses of the nonselective COX inhibitor piroxicam and the ornithine decarboxylase

136 th was unaffected by either the nonselective COX inhibitor piroxicam or the selective COX-2 inhibitor

137 this study, we determined the effects of the cox inhibitor, piroxicam, on tumor response, apoptotic i

138 Cyclooxygenase (COX) inhibitors, present during incubation with endotoxi

139 xplain a component of the mechanism by which COX inhibitors prevent colorectal cancer in humans.

140 patients with AERD react to all nonselective COX inhibitors regardless of their chemical structure, t

141 s are among the most potent multitarget FAAH/COX inhibitors reported so far in the literature and thu

142 d the well-known side effects of opioids and COX inhibitors, resolvins may represent new analgesics f

143 2 production with diclofenac, a nonselective COX inhibitor, resulted in reduced tumor growth in an in

144 r reversed by addition of the nonfluorescent COX inhibitor (S)-flurbiprofen.

145 The nonselective COX inhibitors salicylate and indomethacin enhanced the

146 etylated form of aspirin), and the selective Cox inhibitors SC560 and Celecoxib on endothelial cell p

147 hough sharing a common response with AERD to COX inhibitors, seems to have a distinctive phenotype, b

148 Furthermore, COX inhibitors significantly decreased PG production.

149 First, the non-COX inhibitor, sodium salicylate, was as potent as aspir

150 ic effects than those seen with nonselective COX inhibitors such as acetylsalicylic acid (aspirin).

151 levels were increased in cells treated with COX inhibitors such as NS-398, nimesulide, SC-58125, and

152 with azole antifungal drugs, cyclooxygenase (COX) inhibitors such as ibuprofen improve antifungal eff

153 Classical cyclooxygenase (COX) inhibitors, such as indomethacin, which inhibit bot

154 ppaB translocation inhibitor), or ibuprofen (COX inhibitor) suppressed molecular changes and inhibite

155 ts into the mechanism of negative effects of COX inhibitors that may influence the treatment of sever

156 ture of T. suis with several cyclooxygenase (COX) inhibitors that inhibit mammalian prostaglandin syn

157 pment of a new class of dual cyclooxygenase (COX) inhibitors/thromboxane receptor antagonists (COXTRA

158 We used nonselective and selective COX inhibitors to determine the role of COX on inducible

159 may be an alternative approach to the use of COX inhibitors to prevent tumor metastasis.

160 hifted focus away from these cyclooxygenase (COX) inhibitors to seek additional therapeutic targets i

161 evaluated the ability of piroxicam, a potent COX inhibitor, to prevent postinitiation events of NMBA-

162 e observed in COX-deficient keratinocytes or COX-inhibitor treated wild-type cells.

163 lpha formation is substantially depressed by COX inhibitors, urinary excretion of the compound is una

164 However, the COX inhibitors used were shown to cause relevant hepatot

165 Indomethacin, a nonselective cyclooxygenase (COX) inhibitor, was modified in three distinct regions i

166 COX inhibitors were prescribed to the majority of aspiri

167 of xenograft tumor volume when nonselective COX inhibitors were used in combination with erlotinib.

168 ation that may guide the design of dual FAAH-COX inhibitors with superior analgesic efficacy.

169 alicylic acid (aspirin) is a cyclooxygenase (COX) inhibitor, yet some of its therapeutic effects are