ライフサイエンスコーパス: COX-2 inhibitor

1 or =18 years who were prescribed a selective COX-2 inhibitor.

2 nullified by treatment with NS398, specific COX-2 inhibitor.

3 at were suppressed by celecoxib, a selective COX-2 inhibitor.

4 y before initiating therapy with a selective COX-2 inhibitor.

5 ha) (PGI-M), only PGI-M was depressed by the COX-2 inhibitor.

6 reated with PGE(2) or rofecoxib, a selective COX-2 inhibitor.

7 s blocked by NS-398 (15-150 ng), a selective COX-2 inhibitor.

8 -staphylococcal activity when treated with a Cox-2 inhibitor.

9 the presence of nonspecific NSAIDs and of a COX-2 inhibitor.

10 rdiovascular side effects seen with systemic COX-2 inhibitors.

11 itivity are often able to tolerate selective COX-2 inhibitors.

12 ncluded 171,645 patients receiving selective COX-2 inhibitors.

13 roidal anti-inflammatory drugs and selective COX-2 inhibitors.

14 d that this phenomenon can be prevented with COX-2 inhibitors.

15 ase-2 (COX-2) upregulation and is ablated by COX-2 inhibitors.

16 er low-dose aspirin is cardioprotective with COX-2 inhibitors.

17 e in NHL risk associated with regular use of COX-2 inhibitors.

18 combined, aspirin, nonselective NSAIDs, and COX-2 inhibitors.

19 strength of stimulation and is reversible by COX-2 inhibitors.

20 , and this was reduced in cells treated with COX-2 inhibitors.

21 via S-nitrosylation of COX-2 and reduced by COX-2 inhibitors.

22 elp explain the cancer prevention effects of COX-2 inhibitors.

23 ti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors.

24 ch to inhibit STIM1-mediated metastasis with COX-2 inhibitors.

25 s of cardiovascular events among patients on COX-2 inhibitors.

26 c COX-2(-/-) mice or in WT mice treated with COX-2 inhibitors.

27 herothrombotic complications associated with COX-2 inhibitors.

28 rognosis overall or predict effectiveness of COX-2 inhibitors.

29 l antiinflammatory drugs and cyclooxygenase (COX) 2 inhibitors.

30 placebo controlled trials of cyclooxygenase (COX)-2 inhibitors.

31 ase, gamma-tocopherol, and cyclooxygenase-2 (COX-2) inhibitors.

32 r nonselective NSAIDs, and cyclooxygenase-2 (COX-2) inhibitors.

33 When given a choice between NSAIDs and COX-2 inhibitors, 57% of patients preferred COX-2 inhibi

34 COX-2-transgenic mice, and treatment with a COX-2 inhibitor abrogated the upregulation of (pro)renin

35 n mouse models of glioma, treatment with the COX-2 inhibitors acetylsalicylic acid (ASA) or celecoxib

36 Patients receiving selective COX-2 inhibitors after September 2004 were younger and i

37 0%) and/or SC560 (COX-1 inhibitor) or NS398 (COX-2 inhibitor) after intraplantar carrageenan administ

38 ng skin cancer development in mice; however, COX-2 inhibitors alone are not effective as chemotherape

39 (1) Indomethacin, but not selective COX-1 or COX-2 inhibitors alone or in combination, reduces surviv

40 Furthermore, a selective COX-2 inhibitor also diminished toxin A-associated ileal

41 cell infiltration to the lymph nodes, and a COX-2 inhibitor, an SDF-1 antagonist, and a CXCR4 neutra

42 lopment of fibrosis we have used a selective COX-2 inhibitor and COX-2-deficient ((-/-) and (+/-)) mi

43 fen arginate provides, in one preparation, a COX-2 inhibitor and NOS substrate that could act to nega

44 We show that traditional COX-2 inhibitors and a newly developed substrate-selecti

45 strointestinal events in patients using both COX-2 inhibitors and aspirin than in those using non-sel

46 R-Profens are substrate selective COX-2 inhibitors and block the oxygenation of endocannab

47 ective small molecule cyclooxygenase (Cox)-1/Cox-2 inhibitors and by Cox-2 selective inhibitors.

48 sms responsible for the antitumor effects of COX-2 inhibitors and how COX-2 modulates apoptotic signa

49 Regular use of selective cox-2 inhibitors and nonselective NSAIDs with cox-2>cox-

50 fully understand the spectrum of effects of COX-2 inhibitors and potential differences among them.

51 established evidence that cyclooxygenase-2 (COX-2) inhibitors and statins [hydroxy-3-methylglutaryl

52 d cells was abrogated by NS 398 (a selective COX-2 inhibitor) and indomethacin (a pan-COX inhibitor).

53 cts were prevented by rofecoxib (a selective COX-2 inhibitor) and rescued by exogenous PGE2.

54 mg of indomethacin (non-selective COX-1 and COX-2 inhibitor), and another HS group subset received 2

55 IDs, cyclooxygenase -2 selective inhibitors (COX-2 inhibitors), and low-dose aspirin with other drugs

56 moter activity were significantly reduced by COX-2 inhibitors, and this inhibition was relieved by ex

57 ikely to use methotrexate, cyclooxygenase 2 (COX-2) inhibitors, and corticosteroids than those in oth

58 epileptic neuronal injury and that selective COX-2 inhibitors are neuroprotective.

59 Selective COX-2 inhibitors are non-steroidal anti-inflammatory dru

60 NSAIDs, particularly sulindac, and selective COX-2 inhibitors are now given to patients at high risk

61 indings may explain the enigma regarding why COX-2 inhibitors are palliative rather than curative in

62 Data support the conclusion that COX-2 inhibitors are preferable to non-selective NSAIDs

63 Although cyclooxygenase-2 (COX-2) inhibitors are effective chemopreventive agents a

64 Cyclooxygenase 2 (COX-2) inhibitors are promising antiangiogenic agents in

65 Cyclooxygenase-2 (COX-2) inhibitors are promising anticancer agents but th

66 Selective cyclooxygenase-2 (COX-2) inhibitors are widely prescribed for severe arthr

67 drugs, including selective cyclooxygenase-2 (COX-2) inhibitors, are among the most promising chemopre

68 -DR5 antibodies in combination with low-dose COX-2 inhibitors as a rational approach for cancer preve

69 rns regarding the safety of long-term use of COX-2 inhibitors as well as a desire to seek more effect

70 yl)methanesulfonamide; 10 mg/kg] a selective COX-2 inhibitor, as well as by an anti-prostaglandin (PG

71 ial utility of SSCIs, as well as traditional COX-2 inhibitors, as novel treatment approaches for stre

72 compared with rofecoxib and the nonselective COX-2 inhibitors at 10 days.

73 ced acute hypertension, whereas celecoxib, a COX-2 inhibitor, augmented and sustained higher BP in mi

74 Should selective cyclo-oxygenase (COX) 2 inhibitors be used?

75 n exogenous PGE2 was added concurrently with COX-2 inhibitors before addition of IL-1beta, IL-6 produ

76 was used to compare patients using selective COX-2 inhibitors before and after September 2004.

77 bset received 200 mg of celecoxib (selective COX-2 inhibitor) before repeating laser Doppler flowmetr

78 or inhibition of the catalytic activity by a COX-2 inhibitor blocked prostanoid production.

79 COX-2 activity is preferentially blocked by COX-2 inhibitors called coxibs.

80 rtant question if other structurally related COX-2 inhibitors can affect ion channels in similar fash

81 ase and NIUA, and thus only use of selective COX-2 inhibitors can replace the culprit drug if the chr

82 Recent clinical studies have revealed that COX-2 inhibitors cause adverse cardiovascular side effec

83 Neither NS-398 nor celecoxib, selective COX-2 inhibitors, caused gastric damage in either SO or

84 B (CALGB) 30203, we found that the selective COX-2 inhibitor celecoxib in addition to chemotherapy in

85 On short-term administration, the selective COX-2 inhibitor celecoxib inhibits adenoma growth in ani

86 The selective COX-2 inhibitor celecoxib reduces COX-2 and prostaglandi

87 that the adenoma prevention activity of the COX-2 inhibitor celecoxib requires the concomitant prese

88 Importantly, treatment with the COX-2 inhibitor celecoxib significantly inhibited the gr

89 In the present work, the EPI activity of the COX-2 inhibitor celecoxib was confirmed and a new class

90 nfusion and the effect of treatment with the COX-2 inhibitor celecoxib was examined when initiated at

91 Analogues of the sulfonamide-containing COX-2 inhibitor Celecoxib were prepared and evaluated.

92 her, our observations support the use of the COX-2 inhibitor celecoxib, in combination with paclitaxe

93 ith either of two angiogenic inhibitors, the COX-2 inhibitor celecoxib, or the VEGFR2 inhibitor ZD647

94 alylation could be reversed by the selective COX-2 inhibitor celecoxib.

95 , and resistant to a high concentration of a COX-2 inhibitor celecoxib.

96 The selective cyclooxygenase-2 (COX-2) inhibitor celecoxib (Celebrex) causes ER stress t

97 , we demonstrated that the cyclooxygenase-2 (COX-2) inhibitor celecoxib acts to significantly suppres

98 The cyclooxygenase-2 (COX-2) inhibitor celecoxib is an approved drug in the cl

99 al analog of the selective cyclooxygenase-2 (COX-2) inhibitor celecoxib that lacks COX-2 inhibitory f

100 The effects of a selective COX-2 inhibitor, celecoxib, on these markers were also i

101 A COX-2 inhibitor class effect was not evident.

102 nd led to the rapid development of selective COX-2 inhibitors, collectively called coxibs.

103 COX-1 and COX-2 inhibitor combination caused injury in vivo and in

104 Thus COX-2 inhibitors could be used in patients with AERD or

105 SLE spontaneously hyperexpressed COX-2, and COX-2 inhibitors could cause cell apoptosis.

106 studies have demonstrated that high doses of COX-2 inhibitors could inhibit the growth of rodent and

107 Although cyclooxygenase (COX)-2 inhibitors (coxibs) are effective in controlling

108 ti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors (COXIBs) on CRC.

109 c administration of high levels of selective COX-2 inhibitors (coxibs), particularly rofecoxib, valde

110 Apc with either retinoic acid or a selective COX-2 inhibitor decreased beta-catenin protein levels an

111 er interstitial fibrosis, whereas ketamine + Cox-2 inhibitor decreased the intensity of fibrosis.

112 COX-2 inhibitors decreased the hypoxic induction of Ang2

113 Although COX-2 inhibitors diminished both AID expression and IgG

114 Although COX-2 inhibitors diminished daughter cell viability, exo

115 yses considered the association of selective cox-2 inhibitors (eg, celecoxib), nonselective agents wi

116 5% CI, -0.04 to 0.02; P = .42) occurred with COX-2 inhibitors (eg, celecoxib).

117 ermore, blocking arginase I expression using COX-2 inhibitors elicited a lymphocyte-mediated antitumo

118 Our results also show that administration of COX-2 inhibitors enhance in vitro photosensitization by

119 Celecoxib, a selective COX-2 inhibitor, exacerbated the disease, suggesting a p

120 mals treated with selective and nonselective COX-2 inhibitors, except aspirin, had significantly fewe

121 in and SC-236, a selective cyclooxygenase-2 (COX-2) inhibitor, exerted a similar effect as sulindac.

122 l trials evaluating acute selective NSAID or COX-2 inhibitor exposure in patients with AERD.

123 nary function after acute selective NSAID or COX-2 inhibitor exposure in patients with the AERD pheno

124 Combination with the COX-2 inhibitor failed to augment the impact of TP antag

125 nfortunately, randomised trials of selective COX-2 inhibitors for cancer prevention have shown that b

126 es for the development of (18)F-radiolabeled COX-2 inhibitors for imaging purposes with positron emis

127 erest waning in the use of cyclooxygenase-2 (COX-2) inhibitors for inflammatory disease, prostaglandi

128 Animals fed the COX-2 inhibitor had significantly fewer PanIN-2 and PanI

129 Selective COX-2 inhibitors had a concentration-dependent effect on

130 Only 20% of patients receiving selective COX-2 inhibitors had GI risk factors but low Framingham

131 Selective COX-2 inhibitors had opposite effects on growth and angi

132 Selective COX-2 inhibitors have been approved for use as adjunctiv

133 COX-2 inhibitors have been associated with colonic anast

134 Because COX-2 inhibitors have been shown to prevent cancer in ot

135 his context, both selective and nonselective COX-2 inhibitors have been used in clinical trials to de

136 Exploratory analyses of studies that used COX-2 inhibitors have demonstrated potentially superior

137 s regarding the adverse effects of selective COX-2 inhibitors have stimulated intense debate.

138 s angiogenesis, and cyclooxygenase-2 enzyme (COX-2) inhibitors have antiendothelial activity, we test

139 Cyclooxygenase-2 (COX-2) inhibitors have been shown to reduce colorectal a

140 Selective cyclooxygenase-2 (COX-2) inhibitors have come under scrutiny because of re

141 hough randomized trials of cyclooxygenase-2 (COX-2) inhibitors have shown increased cardiovascular ri

142 by intrathecal pretreatment with a selective COX-2 inhibitor immediately before formalin injection, c

143 , we examined how the combination of PDT and COX-2 inhibitors improve treatment responsiveness.

144 might reveal an antiinflammatory effect of a COX-2 inhibitor in this disease.

145 ors have antiendothelial activity, we tested COX-2 inhibitors in a murine model of intra-abdominal ad

146 the biological rationale for using selective COX-2 inhibitors in cancer chemoprevention, and outline

147 ffers a potential therapeutic alternative to COX-2 inhibitors in chemoprevention strategies.

148 ounds proved to be very potent and selective COX-2 inhibitors in in vitro experimental models.

149 se, and to examine the therapeutic effect of COX-2 inhibitors in mice prone to spontaneously develop

150 further study of the therapeutic efficacy of COX-2 inhibitors in postpartum breast cancer is warrante

151 rovide a molecular basis for the efficacy of COX-2 inhibitors in the treatment of colon cancer.

152 ptors and strengthen the rationale for using COX-2 inhibitors in the treatment of neurological diseas

153 chemopreventive and therapeutic efficacy of COX-2 inhibitors in this population.

154 ster intermediates were potent and selective COX-2 inhibitors in vitro, showed equipotent anti-inflam

155 Selective COX-2 inhibitors, in particular celecoxib, provide durab

156 n of celecoxib, a specific cyclooxygenase-2 (COX-2) inhibitor, in combination with a dendritic cell-b

157 the allosteric effects of FAs and allosteric COX-2 inhibitors, including naproxen and flurbiprofen.

158 However, COX-2 inhibitors increase the risk of cardiovascular com

159 als removed, we must seek new answers to why COX-2 inhibitors increase the risk of cardiovascular eve

160 cular effects with chronic administration of COX-2 inhibitors, indicating that specific PG signaling

161 parable to that observed with the dual COX-1/COX-2 inhibitor indomethacin.

162 3) to a greater extent than monotherapy with COX-2 inhibitors (IRR, 2.9) or low-dose aspirin (IRR, 3.

163 The role of COX-2 inhibitors is currently being evaluated for use in

164 The study suggests that short-term use of COX-2 inhibitors is safe in subjects with asthma.

165 moderate asthma with AERD, acute exposure to COX-2 inhibitors is safe, and selective NSAIDs exhibit a

166 roidal anti-inflammatory drugs and selective COX-2 inhibitors, is importantly involved in these respo

167 ial success of the selective cyclooxygenase (COX)-2 inhibitors, known as the coxibs, with second-gene

168 increased cardiovascular risks of selective COX-2 inhibitors limit their use in chemoprevention of C

169 n hBD production and suggest that the use of Cox-2 inhibitors may adversely influence the risk for ba

170 familial adenomatous polyposis suggest that COX-2 inhibitors may also prevent sporadic colorectal ne

171 Combining 4-HPR with COX-2 inhibitors may be a novel chemopreventive strategy

172 ses in patients with breast cancer, and that COX-2 inhibitors may be useful in halting this process.

173 ach other to maintain homeostasis, selective COX-2 inhibitors may disrupt this balance, thereby resul

174 ata provide further evidence that the use of COX-2 inhibitors may increase the risk of serious cardio

175 Chronic use of high doses of COX-2 inhibitors may induce side effects, and combining

176 MTX also negated COX-2 inhibitor-mediated down-regulation of ABCA1.

177 In vivo depletion of IFN-gamma abrogated the COX-2 inhibitor-mediated enhancement of the vaccination

178 tudy, the administration of the preferential COX-2 inhibitor Meloxicam via histidine-tryptophan-ketog

179 of COX-2 expression in CSCs we utilized the COX-2 inhibitors meloxicam and mavacoxib.

180 IDs, ibuprofen and naproxen, and a selective COX-2 inhibitor, MF-tricyclic, each restored memory func

181 Next, we found that a COX-2 inhibitor, MF-tricyclic, inhibited bone metastasis

182 COX-2 inhibitors might improve patient response to radio

183 ed to a diet supplemented with the selective COX-2 inhibitor nimesulide (400 ppm) or a control diet.

184 In summary, we found that the selective COX-2 inhibitor nimesulide delays the progression of pan

185 kb1(-/-) mice with the Mas antagonist A-779, COX-2 inhibitor nimesulide, or Sirt1 inhibitor splitomic

186 anticancer agents based on cyclooxygenase-2 (COX-2) inhibitor nimesulide as a lead compound.

187 P) or suppression of PGI2 with the selective COX-2 inhibitor, nimesulide, both augment intimal hyperp

188 Pretreatment with either of the selective COX-2 inhibitors, nimesulide or DuP 697, prevents the de

189 In addition, through the use of the specific COX-2 inhibitor NS 398, we show that when PGE(2) product

190 Treatment with the COX-2 inhibitor NS-398 and the AhR antagonist 3'-methoxy

191 The selective COX-2 inhibitor NS-398 was protective against cellular D

192 epithelial cell line, were treated with the COX-2 inhibitor NS-398, PGD(2), or vehicle and stimulate

193 Pretreatment with a COX-2 inhibitor (NS-398) or an EGFR inhibitor (AG1478) e

194 ose) and daily intraperitoneal injections of COX-2 inhibitor (NS-398; 1 mg/kg x 7 days; N = 16), gene

195 ranial window model where treatment with the COX-2 inhibitor, NS-398 (0.1 microM), or the NF-kappaB i

196 we demonstrated that pre-treatment with the Cox-2 inhibitor NS398 could inhibit Cox-2 expression dur

197 cerbated gastric injury, while the selective COX-2 inhibitor NS398 had no effect on iNOS expression o

198 We found that the COX-2 inhibitor NS398 inhibited specifically alpha(v)bet

199 ms of NIHL and the therapeutic effect of the Cox-2 inhibitor NS398 on NIHL using a mouse model.

200 incubated in the presence or absence of the COX-2 inhibitor NS398 or IFNgamma, with and without MTX.

201 Treatment with anti-PGE2 antiserum or the COX-2 inhibitor NS398 reversed the inhibitory effects of

202 We used cox-2 inhibitors, NS398 and celecoxib, and neutralizing

203 miracoxib is the first example of a marketed COX-2 inhibitor of the arylacetic acid class, and it is

204 us PGE2 prevented the restorative effects of COX-2 inhibitors on LTP.

205 of the lupus immune system and the effect of COX-2 inhibitors on the function of these cells in vitro

206 tudy was to evaluate the effect of selective COX-2 inhibitors on vascular endothelial growth factor (

207 nd the mechanisms of unanticipated action of COX-2 inhibitors on voltage-activated potassium channels

208 verse effects of selective cyclooxygenase 2 (COX-2) inhibitors on renal events and arrhythmia have be

209 tudied effects of SC-791, a highly selective COX-2 inhibitor, on K(v)2.1 channels expressed in HEK-29

210 t that COX-2-selective celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 (DR5

211 f PGE2 production was blocked by a selective Cox-2 inhibitor or small interfering RNA against MyD88.

212 be blocked by treatment with antioxidants or COX-2 inhibitors or by depletion of regulatory T cells.

213 CHS was also blocked by a cyclooxygenase-2 (COX-2) inhibitor or a neutralizing antibody directed aga

214 e treated with either celecoxib (a selective COX-2 inhibitor) or erlotinib (Tarceva, an EGFR inhibito

215 lished when cells were treated with NS398 (a COX-2 inhibitor) or L-798,106 (a PGE2-EP3 receptor antag

216 ndomethacin (10 mg/kg), a nonselective COX-1/COX-2 inhibitor, or NS398 [N-(2-cyclohexyloxy-4-nitrophe

217 eries analysis, concomitant use of nsNSAIDs, COX-2 inhibitors, or low-dose aspirin with SSRIs signifi

218 termined based on prescriptions of nsNSAIDs, COX-2 inhibitors, or low-dose aspirin, alone and in comb

219 COX-2 inhibitors, 57% of patients preferred COX-2 inhibitors over NSAIDs.

220 However, the administration of selective COX-2 inhibitors paradoxically increases the frequency o

221 ek and were treated daily with the selective COX-2 inhibitor parecoxib (25 mg/kg) or vehicle (control

222 nt with ketamine or ketamine combined with a Cox-2 inhibitor (parecoxib).

223 am), preferential (Meloxicam), and selective COX-2 inhibitors (Parecoxib).

224 nd valdecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor; PIO+ATV and zileuton, a selective 5-li

225 Cyclooxygenase (COX)-2 inhibitors pose a cardiovascular risk by potentia

226 Treatment with ketamine + COX-2 inhibitor prevented these bladder dysfunctions.

227 Inhibition of PGE2 synthesis by COX-2 inhibitors prevented IVIg-mediated Treg expansion

228 reveal that 2-AG functions as an endogenous COX-2 inhibitor protecting neurons from harmful insults

229 While both nonselective NSAIDs and selective COX-2 inhibitors reduce disease burden, their adverse ga

230 Zinc replenishment, but not a COX-2 inhibitor, reduced the overexpression of these 4 p

231 nticancer or toxic cardiovascular effects of COX-2 inhibitors remain unknown.

232 hazard and if so, at what cost; (c) whether COX-2 inhibitors result in cardiovascular risk transform

233 The administration of a COX-2 inhibitor resulted in compromised PMN infiltration

234 Treatment with COX-2 inhibitors resulted in decreased autoantibody prod

235 Importantly, treatment with celecoxib, a COX-2 inhibitor, resulted in significantly lower PGE2 an

236 t utilization of either an ENaC blocker or a COX-2 inhibitor results in a marked reduction in scarrin

237 other non-steroidal anti-inflammatory drugs, COX-2 inhibitors, retinoids, rexinoids, and dietary comp

238 or administration of PGE2 to mice receiving COX-2 inhibitors reversed these effects.

239 urpose of this study was to test whether the COX-2 inhibitor rofecoxib could reduce recurrence and im

240 mes associated with the use of the selective COX-2 inhibitor rofecoxib in a long-term, multicenter, r

241 trial to assess whether use of the selective COX-2 inhibitor rofecoxib would reduce the risk of color

242 sembly by testing the effect of the specific COX-2 inhibitor SC-236 in an orthotopic xenograft model

243 The selective cyclooxygenase-2 (COX-2) inhibitor (SC-236) was used to differentiate betw

244 Treatment of naive mice with the COX-2 inhibitor, SC-58236, skewed splenocytes toward a t

245 The selective COX-2 inhibitor, SC236, reduced PG-G and PG production b

246 g seizures, and treatment with the selective COX-2 inhibitor SC58125, 3 mg/kg p.o., attenuated the in

247 The effects of a specific COX-2 inhibitor, SC58125, on neuronal survival and PGE2

248 effects associated with NSAIDs and selective COX-2 inhibitors (see the related article beginning on p

249 Cardiovascular effects among the COX-2 inhibitors seem different, but further studies, pr

250 These data emphasize that COX-2 inhibitors should be avoided after colonic surgery

251 -2 in the genesis of CSFTCs and suggest that COX-2 inhibitors should be investigated in patients with

252 ial showed that celecoxib, a cyclooxygenase (COX)-2 inhibitor, significantly reduced the number of co

253 rs and a newly developed substrate-selective COX-2 inhibitor (SSCI) reduce a variety of stress-induce

254 Clinical data show that mixed COX-1/COX-2 inhibitors such as aspirin, but not COX-2 selectiv

255 COX-2 inhibitors such as celecoxib are widely used for p

256 ective COX inhibitors (NSAIDs) and selective COX-2 inhibitors (such as glucocorticoids) reduce the nu

257 settings; they were also less likely to use COX-2 inhibitors than those in fee-for-service settings.

258 less distal gastrointestinal blood loss with COX-2 inhibitors than with non-selective NSAIDs.

259 GE2, and this enhancement was inhibited by a COX-2 inhibitor that inhibited production of PGE2.

260 Celecoxib is a COX-2 inhibitor that reduces the risk of colon cancer.

261 Most NSAIDs function as COX-2 inhibitors that prevent production of prostaglandi

262 e chrysin, indole, and barbituric acid based COX-2 inhibitors, the new compounds have displayed signi

263 Approximately 80% stopped selective COX-2 inhibitor therapy within 6 months.

264 Feeding a COX-2 inhibitor to nursing mothers partially prevents de

265 was to evaluate the efficacy of a selective COX-2 inhibitor to prevent the progression of PanINs in

266 for additional evaluation of the capacity of COX-2 inhibitors to enhance vaccination responses agains

267 Targeting delivery of COX-2 inhibitors to macrophages may conserve their effic

268 resistance to TRAIL-mediated apoptosis using COX-2 inhibitors to manipulate the lipid metabolism with

269 nistration of 3 mg of celecoxib (a selective COX-2 inhibitor) to Brown Norway (BN) rats.

270 Administration of celecoxib, a selective COX-2 inhibitor, to tumor-bearing mice decreased xenogra

271 was no channeling in the usage of selective COX-2 inhibitors toward patients with a high risk of GI

272 C3H backgrounds to confirm the findings from COX-2 inhibitor-treated mice.

273 In COX-2 inhibitor-treated or COX-2-/- C3H mice, arthritis

274 interfering RNA inhibition of HIF-1alpha and COX-2 inhibitor treatment had no effect on PDT induction

275 These findings indicate that COX-2 inhibitor treatment initiated after formation of A

276 Cessation of COX-2 inhibitor treatment on day 14 postinfection did no

277 umor-free survival when compared with PDT or COX-2 inhibitor treatments alone.

278 Among aspirin users, concomitant selective cox-2 inhibitor use was no longer associated with increa

279 vals were wide, the adjusted odds ratios for COX-2 inhibitor use were nearly twofold for women, indic

280 ent effects of the selective cyclooxygenase (COX)-2 inhibitor, valdecoxib, were investigated in a rat

281 To determine whether the effect of COX-2 inhibitors was mediated by peroxisome proliferator

282 d clinical trial, the efficacy of celecoxib (COX-2 inhibitor) was evaluated in conjunction with scali

283 me contributing to this release, SC 58236, a COX-2 inhibitor, was given and found to reduce prostagla

284 f treatment, patients who received selective COX-2 inhibitors were 1.3-3.4-times more likely to have

285 COX-2 inhibitors were administered daily, and their effe

286 Selective cox-2 inhibitors were associated with a modest increased

287 bservations with IP receptor antagonists and COX-2 inhibitors were confirmed with IP receptor or COX-

288 The selective COX-2 inhibitors were more effective at suppressing bFGF

289 COX-2 inhibitors, which block the formation of prostagla

290 explored for anti-inflammatory therapy with COX-2 inhibitors, which proved to be effective in reduci

291 as in conjunction with--a cyclooxygenase-2 (COX-2) inhibitor, which suggests that targeting both TRP

292 ofenac are clinically used cyclooxygenase-2 (COX-2) inhibitors, which have been under intense scrutin

293 of nsNSAIDs with anticoagulants was 2.4, of COX-2 inhibitors with anticoagulants was 0.1, and of low

294 Comparisons of COX-2 inhibitors with nonselective NSAIDs were the follo

295 f NOS activity, and that coadministration of Cox-2 inhibitors with sanguinarine may be developed as a

296 rs (SSRIs) was 1.6, whereas that from use of COX-2 inhibitors with SSRIs was 1.9 and that for use of

297 derivative of celecoxib, a cyclooxygenase-2 (COX-2) inhibitor with anticancer activity in both precli

298 use of nsNSAIDs or low-dose aspirin, but not COX-2 inhibitors, with corticosteroids, aldosterone anta

299 ences between individuals in the response to COX-2 inhibitors would be expected to influence their su

300 ttent pulse therapy with low doses of select COX-2 inhibitors would be of value in the treatment of l