ライフサイエンスコーパス: celecoxib

1 P = .42) occurred with COX-2 inhibitors (eg, celecoxib).

2 hamide followed by docetaxel with or without celecoxib).

3 h the MDSC-diminishing drugs cabozantinib or celecoxib.

4 be reversed by the selective COX-2 inhibitor celecoxib.

5 to a high concentration of a COX-2 inhibitor celecoxib.

6 bited in a concentration-dependent manner by celecoxib.

7 steroidal anti-inflammatory blockbuster drug celecoxib.

8 in/+ mice receiving long-term treatment with celecoxib.

9 ministration of the selective COX2 inhibitor celecoxib.

10 esponse or toxicity in a randomized trial of celecoxib.

11 e are associated with impaired metabolism of celecoxib.

12 ity to the potential benefits and hazards of celecoxib.

13 celecoxib, or 150 ppm CP-31398 plus 300 ppm celecoxib.

14 ardiovascular status to risk associated with celecoxib.

15 05 for index = 9) for patients not receiving celecoxib.

16 by the cycolooygenase 2 selective inhibitor celecoxib.

17 was significantly reduced by treatment with celecoxib.

18 ly characterized PDK1 inhibitor derived from celecoxib.

19 inhibitor with potency in HWB comparable to celecoxib.

20 edematogenic effects than the reference drug Celecoxib.

21 e found that this pathway can be targeted by celecoxib.

22 effect neutralized by COX-2 inhibition with celecoxib.

23 tive activity of the anti-inflammatory agent celecoxib.

24 availability expressed as percentage (F%) of celecoxib (10 mg/kg BW), mavacoxib (4 mg/kg BW) and melo

25 enhanced by PGE(2) (10 muM) and reversed by celecoxib (2 muM).

26 utes: for diclofenac 5%-15%-30%-50%, and for celecoxib, 20%-80%.

27 aily, the combination of glucosamine and CS, celecoxib 200 mg daily, or placebo over 24 months.

28 administered erlotinib 150 mg once per day, celecoxib 200 mg twice per day, and methotrexate per wee

29 ts were randomized to receive SRP and either celecoxib (200 mg) or placebo every day for 6 months.

30 Open-label oral celecoxib (200 mg, twice daily) was administered for 8 w

31 Suspension of celecoxib (3 mg/rat) was injected periocularly into one

32 assigned to: (a) zileuton 600 mg PO qid, (b) celecoxib 400 mg PO bid, or (c) celecoxib and zileuton a

33 We caution against using celecoxib 400 mg twice daily as a preventive agent for p

34 Celecoxib 400 mg twice daily for up to 1 year is insuffi

35 atients randomly allocated to arm D received celecoxib 400 mg twice daily, given orally, until 1 year

36 Patients were randomly assigned to celecoxib (400 mg twice per day; arm A) or placebo (arm

37 d after periocular administration of 3 mg of celecoxib (a selective COX-2 inhibitor) to Brown Norway

38 edly alleviated pressure hyperalgesia, while celecoxib (a selective inhibitor of cyclooxygenase 2 [CO

39 (Ang II)-induced acute hypertension, whereas celecoxib, a COX-2 inhibitor, augmented and sustained hi

40 Importantly, treatment with celecoxib, a COX-2 inhibitor, resulted in significantly

41 A clinical trial showed that celecoxib, a cyclooxygenase (COX)-2 inhibitor, significa

42 -Dimethyl-celecoxib (DMC) is a derivative of celecoxib, a cyclooxygenase-2 (COX-2) inhibitor with ant

43 Administration of celecoxib, a selective COX-2 inhibitor, to tumor-bearing

44 is, while treatment with the COX-2 inhibitor celecoxib abrogates prolactin secretion by fibroblasts a

45 In this study, we defined a mechanism of celecoxib action based on degradation of cellular FLICE-

46 ptor signaling are controlled by GSK3, which celecoxib acts at an upstream level to control independe

47 it appears that a comparatively low dose of celecoxib administered to low-risk subjects is associate

48 Celecoxib administration in the presence of gliosis labe

49 of depressive symptoms following open-label celecoxib administration in treatment-resistant major de

50 has better apoptosis-inducing activity than celecoxib, albeit with undefined mechanisms, and exhibit

51 Although ibuprofen, naproxen, and celecoxib all had the potential to compete with the acce

52 The effects of celecoxib alone and in combination with gamma-aminobutyr

53 Celecoxib alone significantly inhibited xenograft progre

54 Mice treated with celecoxib also showed significantly reduced aortic ruptu

55 Alternatively, celecoxib, an inhibitor of prostaglandin-endoperoxide sy

56 A celecoxib analog, 2,5-dimethyl-celecoxib, which does not

57 ctive C-H bonds to synthesize directly novel celecoxib analogues as potential cyclooxygenase-II (COX-

58 cosanoid pathways (cyclooxygenase-2 [COX-2], celecoxib and 5-lipoxygenase [5-LOX], zileuton) added to

59 ntermittent feeding, with the combination of celecoxib and aspirin delayed development of nephritis t

60 In preclinical models, both Celecoxib and aspirin reduced tumor development.

61 studies of anti-inflammatory agents, such as celecoxib and aspirin, in patients with SCZ have provide

62 between naproxen and aspirin but not between celecoxib and aspirin.

63 ed subset analysis suggests an advantage for celecoxib and chemotherapy for patients with moderate to

64 tural melanin was estimated by co-incubating celecoxib and melanin in isotonic phosphate-buffered sal

65 dosing of mavacoxib is proposed compared to celecoxib and meloxicam.

66 e, we report the surprising observation that celecoxib and other coxibs bind tightly to a subunit of

67 te (CS), alone or in combination, as well as celecoxib and placebo on progressive loss of joint space

68 We found that a combined treatment with celecoxib and rapamycin markedly reduces EMC progression

69 geous, helping to avoid systemic exposure to celecoxib and related side effects.

70 idemiological cohort receiving aspirin, both celecoxib and rofecoxib reduced risk of admission for ga

71 ed a 4-drug oral metronomic regimen of daily celecoxib and thalidomide with alternating periods of et

72 ith surface plasmon resonance, that dimethyl celecoxib and the anti-inflammatory agent celecoxib can

73 Combined celecoxib and TNF-alpha blockade more effectively suppre

74 otrexate when given along with erlotinib and celecoxib and to assess the efficacy of this three-drug

75 ice daily) or high-dose (400 mg twice daily) celecoxib and underwent follow-up colonoscopies at 1 and

76 -e were designed as constrained analogues of celecoxib and valdecoxib.

77 cyclic sulfonamides, different from those of celecoxib and valdecoxib.

78 PO qid, (b) celecoxib 400 mg PO bid, or (c) celecoxib and zileuton at the same doses.

79 e that ON09310 is generally more potent than celecoxib and, at lower concentration, strongly cooperat

80 mbination with a cyclooxygenase-2 inhibitor (celecoxib), and low-dose chemotherapy (gemcitabine) was

81 In this study, we used a Cox2 inhibitor, celecoxib, and an mTORC1 inhibitor, rapamycin, in mouse

82 h cytokine antagonists, omega-3 fatty acids, celecoxib, and exercise is that anti-inflammatory interv

83 ls with a combination of MUC1-based vaccine, celecoxib, and gemcitabine for the treatment of pancreat

84 2) channels reproduced the cardiac effect of celecoxib, and the drug was unable to further enhance th

85 tumors were given vehicle (controls), PGE2, celecoxib, and/or Ono-AE3-208.

86 COX-2 specific inhibitor, celecoxib, apart from its anticancer properties was show

87 COX-2 inhibitors such as celecoxib are widely used for pain relief.

88 S2-low group (n = 100), EFS was lower in the celecoxib arm (HR, 3.01; 95% CI, 1.45 to 6.24; P = .002)

89 iate analysis comparing hormone therapy plus celecoxib (arm D) with hormone therapy alone (control ar

90 m A) and 291 to receive hormone therapy plus celecoxib (arm D).

91 enhanced tumor malignancy was assessed using celecoxib as a COX-2 specific inhibitor in a murine mode

92 hat regulates DR5 expression primarily using celecoxib as a DR5 inducer.

93 or RSK2 siRNA abrogated DR5 up-regulation by celecoxib as well as other agents.

94 The cardiovascular safety of celecoxib, as compared with nonselective nonsteroidal an

95 strates, as well as certain inhibitors (e.g. celecoxib), bind the COX site of E(cat).

96 Although celecoxib binding to one monomer of COX-1 does not affec

97 2) production in response to Ang II, whereas celecoxib blocked both PGE(2) and PGI(2) production.

98 ive of the cyclooxygenase-2 (COX2) inhibitor celecoxib but lacking COX2 inhibitory activity, kills tr

99 4-155, TG6-10-1 or COX-2 selective inhibitor celecoxib, but not by GW627368X.

100 Celecoxib, but not rofecoxib or diclofenac, dramatically

101 Celecoxib, but not rofecoxib, also inhibited calcium res

102 Celecoxib, but not rofecoxib, is shown to act as an "ope

103 receptor (EP4 antagonist, AH23848) mimicked celecoxib by inhibiting MMP-13, ADAMST-5 expression, and

104 Celecoxib can be an effective adjunctive treatment to SR

105 yl celecoxib and the anti-inflammatory agent celecoxib can bind cadherin-11, an adhesion molecule imp

106 ined with a celecoxib/COX-1 complex show how celecoxib can bind to one of the two available COX sites

107 n that clinically relevant concentrations of celecoxib can cause inhibition or augmentation of variou

108 We report survival data for two celecoxib (Cel)-containing comparisons, which stopped ac

109 selective cyclooxygenase-2 (COX-2) inhibitor celecoxib (Celebrex) causes ER stress through a differen

110 genase-2 (COX-2), such as rofecoxib (Vioxx), celecoxib (Celebrex), and valdecoxib (Bextra), have been

111 cular morbidity; however, another such drug, celecoxib (Celebrex), suffers far less from this side ef

112 The greater efficacy of high-dose celecoxib, compared with the low-dose, in preventing col

113 Tissue celecoxib concentrations also were measured.

114 The predicted celecoxib concentrations from this model also showed ver

115 mmittee recommended stopping accrual to both celecoxib-containing arms on grounds of lack of benefit

116 We found that celecoxib controlled c-FLIP ubiquitination through Akt-i

117 , randomized clinical trial, the efficacy of celecoxib (COX-2 inhibitor) was evaluated in conjunction

118 ray crystallographic results obtained with a celecoxib/COX-1 complex show how celecoxib can bind to o

119 Systemic administration of indomethacin or celecoxib (cyclo-oxygenase inhibitors), pyrilamine, apre

120 ow micromolar range (abiratone, candesartan, celecoxib, dasatinib, nilvadipine, nimodipine, and regor

121 The models were validated by using the celecoxib data from a prior study in Sprague-Dawley (SD)

122 By contrast, celecoxib decreased TXA2 levels but had no significant e

123 t anti-inflammatory treatment, in particular celecoxib, decreases depressive symptoms without increas

124 of gefitinib or erlotinib with OSU-03012, a celecoxib-derived antitumor agent, to overcome EGFR inhi

125 SC-791 modified K(v)2.1 gating, but, unlike celecoxib, did not induce channel block.

126 2,5-Dimethyl-celecoxib (DMC) is a derivative of celecoxib, a cyclooxy

127 on-coxib analogue of this drug, 2,5-dimethyl-celecoxib (DMC), faithfully and more potently mimicked t

128 essing of AA by the second, partner subunit, celecoxib does interfere with the inhibition of COX-1 by

129 ability to assess the relationship of either celecoxib dose or pretreatment cardiovascular status to

130 rential cardiovascular risk as a function of celecoxib dose regimen and baseline cardiovascular risk.

131 brogated by a PGE2-neutralizing antibody and celecoxib drug-mediated blockade of PGE2 signalling.

132 ion of the cyclooxygenase-2 (COX2) inhibitor celecoxib effectively abolishes a PGE2- and COX2-mediate

133 -1 expression was inhibited by PGE(2), while celecoxib enhanced both spontaneous and IL-1-induced exp

134 able of potentiating the biologic effects of celecoxib, etoposide, and TRAIL.

135 as observed following oral administration of celecoxib (F% = 56-110%) and mavacoxib (F% = 111-113%),

136 grounds of lack of benefit and discontinuing celecoxib for patients currently on treatment, which was

137 tance to chemotherapy drugs or resistance to celecoxib, further supporting a linkage between cellular

138 utcome event occurred in 134 patients in the celecoxib group (1.7%), 144 patients in the naproxen gro

139 utcome event occurred in 188 patients in the celecoxib group (2.3%), 201 patients in the naproxen gro

140 ollow-up, EFS was significantly lower in the celecoxib group (hazard ratio [HR], 1.7; 95% CI, 1 to 2.

141 4,081 patients were randomly assigned to the celecoxib group (mean [+/-SD] daily dose, 209+/-37 mg),

142 The celecoxib group also exhibited a greater percentage of s

143 D reduction and CAL gain were greater in the celecoxib group, primarily in moderate and deep sites, t

144 d COX-2 expression (index >or= 4), receiving celecoxib had better survival than did COX-2-expressing

145 Treatment with 4 to 6 weeks of celecoxib had no effect on intermediate biomarkers of pr

146 Celecoxib has low aqueous solubility, which may limit it

147 In conclusion, we show that celecoxib has marked antiproliferative activity against

148 metabolite of prostaglandin E2 who received celecoxib (HR = 1.57; 95% CI, 0.87 to 2.84; P = .13).

149 cular risk were randomly assigned to receive celecoxib, ibuprofen, or naproxen.

150 c acid and docetaxel, or zoledronic acid and celecoxib) improves survival in men starting first-line,

151 sess the cardiovascular risk associated with celecoxib in 3 dose regimens and to assess the relations

152 Patients were administered celecoxib in 3 dose regimens: 400 mg QD, 200 mg BID, or

153 we found that the selective COX-2 inhibitor celecoxib in addition to chemotherapy in advanced NSCLC

154 Celecoxib in addition to docetaxel enhanced cell viabili

155 We found that DMC was more potent than celecoxib in decreasing the survival and inducing apopto

156 oxib, which does not inhibit COX-2, mimicked celecoxib in its enhancement of vascular KCNQ5 currents,

157 (P = 0.001) and vitreal (P = 0.001) AUCs of celecoxib in the treated eyes were approximately 1.5-fol

158 tions support the use of the COX-2 inhibitor celecoxib, in combination with paclitaxel, for the manag

159 Additionally, celecoxib increased CHOP promoter activity in an ATF4-de

160 volunteers also revealed that the NSAID drug celecoxib increased LPS-induced TNF production in whole

161 regulated protein, we accordingly found that celecoxib increased the levels of phosphorylated ERK1/2,

162 Celecoxib increased the levels of phosphorylated GSK3, i

163 ly, we conclude that small molecules such as celecoxib induce DR5 expression through activating ERK/R

164 hase-specific cytometric sorting showed that celecoxib induced clonogenic toxicity preferentially to

165 Celecoxib induced p21(waf1/cip1) at the transcriptional

166 NSCC) and explored the relationships between celecoxib-induced cell cycle inhibition and toxicity in

167 ulation, indicating that ATF4 is involved in celecoxib-induced CHOP and DR5 expression.

168 Moreover, these inhibitions suppressed celecoxib-induced CHOP up-regulation.

169 The celecoxib-induced downregulation of COX-2 protein and p-

170 ous protein (CHOP) and Elk1 are required for celecoxib-induced DR5 expression based on promoter delet

171 protein kinase C (PKC) inhibitors abolished celecoxib-induced GSK3 phosphorylation, implying that ce

172 phorylation as expected but had no effect on celecoxib-induced GSK3 phosphorylation.

173 -induced GSK3 phosphorylation, implying that celecoxib influenced GSK3 phosphorylation through a mech

174 X-2 inhibitors acetylsalicylic acid (ASA) or celecoxib inhibited systemic PGE(2) production and delay

175 Celecoxib inhibited the proliferation of UM-SCC-1 and UM

176 We conclude that celecoxib inhibits calcium responses in VSMCs by enhanci

177 Celecoxib inhibits proliferation and induces apoptosis i

178 Celecoxib is a COX-2 inhibitor that reduces the risk of

179 rate that the adenoma-preventive activity of celecoxib is abrogated in mice genetically lacking 15-PG

180 emotherapy with erlotinib, methotrexate, and celecoxib is efficacious in platinum-refractory oral cav

181 inal and vitreal drug delivery of lipophilic celecoxib is significantly lower in pigmented rats than

182 Celecoxib kinetics in the BN rat cornea can be described

183 2 hours after the drug was administered, and celecoxib levels in ocular tissues (sclera, choroid-RPE,

184 nistered periocularly in SD and BN rats, and celecoxib levels in these eye tissues were assessed on d

185 Celecoxib loaded nanoemulsions showed a dose dependent u

186 mportant relationship between sensitivity to celecoxib, LY-294002 (PI3kinase inhibitor), retinol, and

187 with the loss of tumor prevention activity, celecoxib-mediated suppression of colonic PGE(2) levels

188 rats treated with periocularly administered celecoxib microparticles served as the positive control,

189 GDH null animals develop more tumors than do celecoxib naive WT mice.

190 Here we report multifunctional celecoxib nanoemulsions that can be imaged by both near-

191 sociation of selective cox-2 inhibitors (eg, celecoxib), nonselective agents with cox-2>cox-1 inhibit

192 either a drug treatment group that received celecoxib on a daily basis for 7 days or a control group

193 ating agent CP-31398 alone and combined with celecoxib on azoxymethane-induced aberrant crypt foci (A

194 n baseline cardiovascular risk and effect of celecoxib on cardiovascular events.

195 servations reveal an unanticipated effect of celecoxib on Drosophila hearts and on heart cells from r

196 double-blind trial to examine the effect of celecoxib on drug-specific biomarkers from prostate tiss

197 lysis confirmed the interaction of COX-2 and celecoxib on survival.

198 e, memantine, N-acetylcysteine, lamotrigine, celecoxib, ondansetron) either in combination with selec

199 (hazard ratio, 1.13; 1.04-1.23; P=0.004 and celecoxib only: HR, 1.13; 1.01-1.27; P=0.031).

200 results show that combining bortezomib with celecoxib or DMC very potently triggers the ER stress re

201 ly assigned to a double-blind treatment with celecoxib or placebo.

202 and the COX-2-specific inhibitors NS-398 and celecoxib or siRNAs targeting COXs, inhibited PSaV repli

203 ferent doses of the COX-2-specific inhibitor celecoxib or the nonspecific inhibitor aspirin, or a com

204 Furthermore, treatment with celecoxib or ZD6474 substantially decreased the incidenc

205 ssing germinal matrix angiogenesis, prenatal celecoxib or ZD6474 treatment may be able to reduce both

206 taining 0, 150, or 300 ppm CP-31398, 300 ppm celecoxib, or 150 ppm CP-31398 plus 300 ppm celecoxib.

207 o angiogenic inhibitors, the COX-2 inhibitor celecoxib, or the VEGFR2 inhibitor ZD6474, could suppres

208 nce of an advantage for hormone therapy plus celecoxib over hormone therapy alone: HR 0.94 (95% CI 0.

209 Thus, large porous celecoxib-PLGA microparticles prepared using supercritic

210 In addition, celecoxib-poly(lactide) microparticles (750 microg drug/

211 With celecoxib-poly(lactide) microparticles, choroid-RPE, ret

212 Chemopreventive potential of celecoxib porous particles was assessed in a benzo[a]pyr

213 Treatment with celecoxib prevented IH-induced adverse tumor outcomes by

214 In FVB mice, celecoxib prevents 85% of azoxymethane-induced tumors >1

215 Specific inhibition of COX-2 by celecoxib, promoted apoptosis through activation of casp

216 Importantly, the FDA-approved drug celecoxib re-establishes the AKT/miR-199a-5p/CAV1 axis i

217 of patients on treatment, demonstrating that celecoxib reached its target.

218 s isolated from IH-exposed mice treated with celecoxib reduced the proliferation of LLC1 naive cells,

219 The selective COX-2 inhibitor celecoxib reduces COX-2 and prostaglandin E(2) (PGE(2))

220 The Ptgs2 inhibitor celecoxib reduces dsRNA-induced WIHN and Wnt7b, and exog

221 t rapamycin reduces Cox2 expression, whereas celecoxib reduces mTORC1 activity.

222 onstrated disproportionately greater risk of celecoxib-related adverse events (P for interaction=0.03

223 By further clarifying the extent of celecoxib-related cardiovascular risk, these findings ma

224 s for each dose regimen and examined whether celecoxib-related risk was associated with baseline card

225 COX-2 inhibition with the specific inhibitor celecoxib represses PGE2 secretion, presenting a feasibl

226 a prevention activity of the COX-2 inhibitor celecoxib requires the concomitant presence of the 15-hy

227 Our findings argue that celecoxib resistance is an acquired adaptation to change

228 with low colonic 15-PGDH levels also exhibit celecoxib resistance.

229 oses were 400 and 3,000 ppm for CP-31398 and celecoxib, respectively.

230 ways with a neutralizing antibody to HGF and celecoxib resulted in enhanced anti-invasion effects in

231 C tone is shown to be selectively reduced by celecoxib, resulting in dilation of blood vessels and re

232 Celecoxib, rofecoxib, and diclofenac are clinically used

233 We investigated the effects of celecoxib, rofecoxib, and diclofenac on ionic currents a

234 of 15-PGDH expression imparts resistance to celecoxib's anti-tumor effects.

235 The r(max) and k for celecoxib's binding to natural melanin were (3.92 +/- 0.

236 The affinity and the extent of celecoxib's binding to natural melanin were not signific

237 d another HS group subset received 200 mg of celecoxib (selective COX-2 inhibitor) before repeating l

238 98 or a combination of low-dose CP-31398 and celecoxib showed considerable enhancement of p53 and p21

239 al treatment with the anti-inflammatory drug celecoxib significantly decreased tumor numbers in both

240 that a combination of low-dose CP-31398 and celecoxib significantly enhanced colon cancer chemopreve

241 Treatment with a cyclooxygenase 2 inhibitor celecoxib significantly improved renal fibrosis in CLOCK

242 ortantly, treatment with the COX-2 inhibitor celecoxib significantly inhibited the growth of NF2-null

243 of the selective cyclooxygenase 2 inhibitor celecoxib (SMD, -0.29; 95% CI, -0.49 to -0.08; I2=73%) o

244 iovascular events when given with rofecoxib, celecoxib, sulindac, meloxicam, and indometacin but not

245 Dietary celecoxib suppressed colon adenocarcinoma incidence (60%

246 tantly, combination of low-dose CP-31398 and celecoxib suppressed colon adenocarcinoma incidence by 7

247 by the cyclooxygenase inhibitors aspirin and celecoxib suppressed M2 macrophage polarization and decr

248 bution compartment or a dissolution step for celecoxib suspension did not lead to an overall improvem

249 time profiles for animals administered with celecoxib suspension was not significantly different bet

250 es being greater than those recorded for the celecoxib suspension.

251 In contrast to celecoxib (T1/2el = 0.88 h) and meloxicam (T1/2el = 0.90

252 of renal events was significantly lower with celecoxib than with ibuprofen (P=0.004) but was not sign

253 testinal events was significantly lower with celecoxib than with naproxen (P=0.01) or ibuprofen (P=0.

254 =0.004) but was not significantly lower with celecoxib than with naproxen (P=0.19).

255 AR-12 is an IND-approved derivative of celecoxib that demonstrated preclinical activity against

256 Treatment with celecoxib that was started at a late stage of AAA develo

257 d by certain small molecule drugs, including celecoxib, through mechanisms that have not been fully e

258 ity (k) and the maximum binding (r(max)) for celecoxib to both natural and synthetic melanin were est

259 Finally, we find that administration of celecoxib to dogs interferes with the ability of a low d

260 In this study, we evaluated the ability of celecoxib to induce toxicity in head and neck squamous c

261 ay be attributable to significant binding of celecoxib to melanin and its accumulation/retention in t

262 oxide solubilization METHOD: The affinity of celecoxib to synthetic and natural melanin was estimated

263 the ability of the anti-inflammatory agent, celecoxib, to suppress hyperemia formation during photoc

264 nly consumed NSAIDs-ibuprofen, naproxen, and celecoxib-to cause a drug-drug interaction with aspirin

265 ective role for p21(waf1/cip1) expression in celecoxib toxicity.

266 Indeed, celecoxib treated 15-PGDH null animals develop more tumo

267 Celecoxib treatment decreased angiopoietin-2 and VEGF le

268 Celecoxib treatment significantly increased smooth muscl

269 Celecoxib treatment that was started 1 week after initia

270 s who developed new adenomas while receiving celecoxib treatment were also found as having low coloni

271 In ileum subjected to long-term celecoxib treatment, we noted relatively higher expressi

272 riant allele) in the Adenoma Prevention with Celecoxib trial.

273 When combined, bortezomib and celecoxib triggered elevated expression of the ER stress

274 Celecoxib use during chemotherapy adversely affected sur

275 the relationships between PTGS2 expression, celecoxib use during neoadjuvant chemotherapy (NAC), and

276 Celecoxib use was an independent predictor of poor EFS,

277 ant interaction between PTGS2 expression and celecoxib use was detected ( P(interaction) = .01).

278 ctide-co-glycolide) (PLGA) microparticles of celecoxib using supercritical fluid pressure-quench tech

279 r = 0.99) and SD (r = 0.99) rats for retinal celecoxib using the same model; however, the parameter e

280 Here we show a novel effect of celecoxib via a mechanism that is independent of COX-2 i

281 0.90; 95% CI, 0.71 to 1.15; hazard ratio for celecoxib vs. ibuprofen, 0.81; 95% CI, 0.65 to 1.02; P<0

282 nterval [CI], 0.76 to 1.13; hazard ratio for celecoxib vs. ibuprofen, 0.85; 95% CI, 0.70 to 1.04; P<0

283 the ibuprofen group (1.9%) (hazard ratio for celecoxib vs. naproxen, 0.90; 95% CI, 0.71 to 1.15; haza

284 the ibuprofen group (2.7%) (hazard ratio for celecoxib vs. naproxen, 0.93; 95% confidence interval [C

285 Overall, celecoxib was associated with a dose-dependent reduction

286 ork, the EPI activity of the COX-2 inhibitor celecoxib was confirmed and a new class of pyrazolo[4,3-

287 effect of treatment with the COX-2 inhibitor celecoxib was examined when initiated at different stage

288 At moderate doses, celecoxib was found to be noninferior to ibuprofen or na

289 The contribution of celecoxib was independent of the inhibition of COX-2 bec

290 Celecoxib was measurable in prostate tissue of patients

291 Celecoxib was safe and resulted in only grade 1 toxiciti

292 The chemopreventive activity of celecoxib was shown to correlate with its ability to red

293 ibrary, including ingliforib, furosemide and celecoxib, we successfully prepared stable solid nanodis

294 The effects of celecoxib were concentration-dependent within the therap

295 f the sulfonamide-containing COX-2 inhibitor Celecoxib were prepared and evaluated.

296 A celecoxib analog, 2,5-dimethyl-celecoxib, which does not inhibit COX-2, mimicked celeco

297 Combining celecoxib with GSK3 inhibition enhanced attenuation of c

298 nts in 6 placebo-controlled trials comparing celecoxib with placebo for conditions other than arthrit

299 he trial was to assess the noninferiority of celecoxib with regard to the primary composite outcome o

300 ne or two drugs (docetaxel, zoledronic acid, celecoxib, zoledronic acid and docetaxel, or zoledronic