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1 P = .42) occurred with COX-2 inhibitors (eg, celecoxib).
2 bited in a concentration-dependent manner by celecoxib.
3 steroidal anti-inflammatory blockbuster drug celecoxib.
4 in/+ mice receiving long-term treatment with celecoxib.
5 ministration of the selective COX2 inhibitor celecoxib.
6 esponse or toxicity in a randomized trial of celecoxib.
7 e are associated with impaired metabolism of celecoxib.
8 ity to the potential benefits and hazards of celecoxib.
9 celecoxib, or 150 ppm CP-31398 plus 300 ppm celecoxib.
10 ardiovascular status to risk associated with celecoxib.
11 05 for index = 9) for patients not receiving celecoxib.
12 by the cycolooygenase 2 selective inhibitor celecoxib.
13 was significantly reduced by treatment with celecoxib.
14 ly characterized PDK1 inhibitor derived from celecoxib.
15 inhibitor with potency in HWB comparable to celecoxib.
16 e found that this pathway can be targeted by celecoxib.
17 effect neutralized by COX-2 inhibition with celecoxib.
18 tive activity of the anti-inflammatory agent celecoxib.
19 be reversed by the selective COX-2 inhibitor celecoxib.
20 to a high concentration of a COX-2 inhibitor celecoxib.
21 availability expressed as percentage (F%) of celecoxib (10 mg/kg BW), mavacoxib (4 mg/kg BW) and melo
24 ts were randomized to receive SRP and either celecoxib (200 mg) or placebo every day for 6 months.
27 assigned to: (a) zileuton 600 mg PO qid, (b) celecoxib 400 mg PO bid, or (c) celecoxib and zileuton a
30 atients randomly allocated to arm D received celecoxib 400 mg twice daily, given orally, until 1 year
33 intermittent therapy with the lowest dose of celecoxib (500 parts per million), approximating <100 mg
34 lyps in APC(min+/-) mice treated with either celecoxib (a selective COX-2 inhibitor) or erlotinib (Ta
35 d after periocular administration of 3 mg of celecoxib (a selective COX-2 inhibitor) to Brown Norway
36 edly alleviated pressure hyperalgesia, while celecoxib (a selective inhibitor of cyclooxygenase 2 [CO
37 (Ang II)-induced acute hypertension, whereas celecoxib, a COX-2 inhibitor, augmented and sustained hi
40 -Dimethyl-celecoxib (DMC) is a derivative of celecoxib, a cyclooxygenase-2 (COX-2) inhibitor with ant
42 In this study, we defined a mechanism of celecoxib action based on degradation of cellular FLICE-
43 ptor signaling are controlled by GSK3, which celecoxib acts at an upstream level to control independe
44 it appears that a comparatively low dose of celecoxib administered to low-risk subjects is associate
45 has better apoptosis-inducing activity than celecoxib, albeit with undefined mechanisms, and exhibit
52 ctive C-H bonds to synthesize directly novel celecoxib analogues as potential cyclooxygenase-II (COX-
53 cosanoid pathways (cyclooxygenase-2 [COX-2], celecoxib and 5-lipoxygenase [5-LOX], zileuton) added to
55 ntermittent feeding, with the combination of celecoxib and aspirin delayed development of nephritis t
57 studies of anti-inflammatory agents, such as celecoxib and aspirin, in patients with SCZ have provide
59 ed subset analysis suggests an advantage for celecoxib and chemotherapy for patients with moderate to
60 tural melanin was estimated by co-incubating celecoxib and melanin in isotonic phosphate-buffered sal
62 e, we report the surprising observation that celecoxib and other coxibs bind tightly to a subunit of
63 te (CS), alone or in combination, as well as celecoxib and placebo on progressive loss of joint space
66 idemiological cohort receiving aspirin, both celecoxib and rofecoxib reduced risk of admission for ga
68 ed a 4-drug oral metronomic regimen of daily celecoxib and thalidomide with alternating periods of et
69 ith surface plasmon resonance, that dimethyl celecoxib and the anti-inflammatory agent celecoxib can
71 ice daily) or high-dose (400 mg twice daily) celecoxib and underwent follow-up colonoscopies at 1 and
75 e that ON09310 is generally more potent than celecoxib and, at lower concentration, strongly cooperat
76 mbination with a cyclooxygenase-2 inhibitor (celecoxib), and low-dose chemotherapy (gemcitabine) was
78 h cytokine antagonists, omega-3 fatty acids, celecoxib, and exercise is that anti-inflammatory interv
79 ls with a combination of MUC1-based vaccine, celecoxib, and gemcitabine for the treatment of pancreat
81 2) channels reproduced the cardiac effect of celecoxib, and the drug was unable to further enhance th
85 iate analysis comparing hormone therapy plus celecoxib (arm D) with hormone therapy alone (control ar
87 enhanced tumor malignancy was assessed using celecoxib as a COX-2 specific inhibitor in a murine mode
89 ndently of cyclooxygenase-2 (COX-2), we used celecoxib as a scaffold to develop a COX-2-inactive PDK-
94 2) production in response to Ang II, whereas celecoxib blocked both PGE(2) and PGI(2) production.
95 ive of the cyclooxygenase-2 (COX2) inhibitor celecoxib but lacking COX2 inhibitory activity, kills tr
100 receptor (EP4 antagonist, AH23848) mimicked celecoxib by inhibiting MMP-13, ADAMST-5 expression, and
102 yl celecoxib and the anti-inflammatory agent celecoxib can bind cadherin-11, an adhesion molecule imp
103 ined with a celecoxib/COX-1 complex show how celecoxib can bind to one of the two available COX sites
104 n that clinically relevant concentrations of celecoxib can cause inhibition or augmentation of variou
107 selective cyclooxygenase-2 (COX-2) inhibitor celecoxib (Celebrex) causes ER stress through a differen
108 genase-2 (COX-2), such as rofecoxib (Vioxx), celecoxib (Celebrex), and valdecoxib (Bextra), have been
109 cular morbidity; however, another such drug, celecoxib (Celebrex), suffers far less from this side ef
113 mmittee recommended stopping accrual to both celecoxib-containing arms on grounds of lack of benefit
115 , randomized clinical trial, the efficacy of celecoxib (COX-2 inhibitor) was evaluated in conjunction
116 ray crystallographic results obtained with a celecoxib/COX-1 complex show how celecoxib can bind to o
117 Systemic administration of indomethacin or celecoxib (cyclo-oxygenase inhibitors), pyrilamine, apre
118 ow micromolar range (abiratone, candesartan, celecoxib, dasatinib, nilvadipine, nimodipine, and regor
122 t anti-inflammatory treatment, in particular celecoxib, decreases depressive symptoms without increas
123 of gefitinib or erlotinib with OSU-03012, a celecoxib-derived antitumor agent, to overcome EGFR inhi
126 on-coxib analogue of this drug, 2,5-dimethyl-celecoxib (DMC), faithfully and more potently mimicked t
127 essing of AA by the second, partner subunit, celecoxib does interfere with the inhibition of COX-1 by
128 ability to assess the relationship of either celecoxib dose or pretreatment cardiovascular status to
129 rential cardiovascular risk as a function of celecoxib dose regimen and baseline cardiovascular risk.
130 In the current study, we further show that celecoxib down-regulated the expression of cellular FLIC
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
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 4,081 patients were randomly assigned to the celecoxib group (mean [+/-SD] daily dose, 209+/-37 mg),
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
149 c acid and docetaxel, or zoledronic acid and celecoxib) improves survival in men starting first-line,
150 sess the cardiovascular risk associated with celecoxib in 3 dose regimens and to assess the relations
152 we found that the selective COX-2 inhibitor celecoxib in addition to chemotherapy in advanced NSCLC
154 oxib, which does not inhibit COX-2, mimicked celecoxib in its enhancement of vascular KCNQ5 currents,
155 (P = 0.001) and vitreal (P = 0.001) AUCs of celecoxib in the treated eyes were approximately 1.5-fol
156 tions support the use of the COX-2 inhibitor celecoxib, in combination with paclitaxel, for the manag
158 volunteers also revealed that the NSAID drug celecoxib increased LPS-induced TNF production in whole
159 regulated protein, we accordingly found that celecoxib increased the levels of phosphorylated ERK1/2,
161 ntive efficacy of atorvastatin (Lipitor) and celecoxib individually or in combination in an animal mo
162 ly, we conclude that small molecules such as celecoxib induce DR5 expression through activating ERK/R
163 hase-specific cytometric sorting showed that celecoxib induced clonogenic toxicity preferentially to
165 NSCC) and explored the relationships between celecoxib-induced cell cycle inhibition and toxicity in
169 ous protein (CHOP) and Elk1 are required for celecoxib-induced DR5 expression based on promoter delet
170 protein kinase C (PKC) inhibitors abolished celecoxib-induced GSK3 phosphorylation, implying that ce
172 -induced GSK3 phosphorylation, implying that celecoxib influenced GSK3 phosphorylation through a mech
173 X-2 inhibitors acetylsalicylic acid (ASA) or celecoxib inhibited systemic PGE(2) production and delay
178 rate that the adenoma-preventive activity of celecoxib is abrogated in mice genetically lacking 15-PG
179 inal and vitreal drug delivery of lipophilic celecoxib is significantly lower in pigmented rats than
181 2 hours after the drug was administered, and celecoxib levels in ocular tissues (sclera, choroid-RPE,
182 nistered periocularly in SD and BN rats, and celecoxib levels in these eye tissues were assessed on d
184 mportant relationship between sensitivity to celecoxib, LY-294002 (PI3kinase inhibitor), retinol, and
185 with the loss of tumor prevention activity, celecoxib-mediated suppression of colonic PGE(2) levels
187 rats treated with periocularly administered celecoxib microparticles served as the positive control,
190 sociation of selective cox-2 inhibitors (eg, celecoxib), nonselective agents with cox-2>cox-1 inhibit
191 either a drug treatment group that received celecoxib on a daily basis for 7 days or a control group
192 ating agent CP-31398 alone and combined with celecoxib on azoxymethane-induced aberrant crypt foci (A
194 servations reveal an unanticipated effect of celecoxib on Drosophila hearts and on heart cells from r
195 double-blind trial to examine the effect of celecoxib on drug-specific biomarkers from prostate tiss
196 , and the selective Cox inhibitors SC560 and Celecoxib on endothelial cell proliferation, viability,
198 The effects of a selective COX-2 inhibitor, celecoxib, on these markers were also investigated in di
199 e, memantine, N-acetylcysteine, lamotrigine, celecoxib, ondansetron) either in combination with selec
201 results show that combining bortezomib with celecoxib or DMC very potently triggers the ER stress re
203 and the COX-2-specific inhibitors NS-398 and celecoxib or siRNAs targeting COXs, inhibited PSaV repli
204 ferent doses of the COX-2-specific inhibitor celecoxib or the nonspecific inhibitor aspirin, or a com
206 ssing germinal matrix angiogenesis, prenatal celecoxib or ZD6474 treatment may be able to reduce both
207 taining 0, 150, or 300 ppm CP-31398, 300 ppm celecoxib, or 150 ppm CP-31398 plus 300 ppm celecoxib.
208 o angiogenic inhibitors, the COX-2 inhibitor celecoxib, or the VEGFR2 inhibitor ZD6474, could suppres
209 nce of an advantage for hormone therapy plus celecoxib over hormone therapy alone: HR 0.94 (95% CI 0.
210 significantly after 7 days of treatment with celecoxib (P < .05), but it was not significantly change
218 formation about the cardiovascular safety of celecoxib prompted review of ongoing clinical studies.
221 s isolated from IH-exposed mice treated with celecoxib reduced the proliferation of LLC1 naive cells,
225 onstrated disproportionately greater risk of celecoxib-related adverse events (P for interaction=0.03
227 s for each dose regimen and examined whether celecoxib-related risk was associated with baseline card
228 COX-2 inhibition with the specific inhibitor celecoxib represses PGE2 secretion, presenting a feasibl
229 a prevention activity of the COX-2 inhibitor celecoxib requires the concomitant presence of the 15-hy
233 ways with a neutralizing antibody to HGF and celecoxib resulted in enhanced anti-invasion effects in
234 C tone is shown to be selectively reduced by celecoxib, resulting in dilation of blood vessels and re
240 d another HS group subset received 200 mg of celecoxib (selective COX-2 inhibitor) before repeating l
241 98 or a combination of low-dose CP-31398 and celecoxib showed considerable enhancement of p53 and p21
242 al treatment with the anti-inflammatory drug celecoxib significantly decreased tumor numbers in both
243 that a combination of low-dose CP-31398 and celecoxib significantly enhanced colon cancer chemopreve
244 Treatment with a cyclooxygenase 2 inhibitor celecoxib significantly improved renal fibrosis in CLOCK
245 ortantly, treatment with the COX-2 inhibitor celecoxib significantly inhibited the growth of NF2-null
246 of the selective cyclooxygenase 2 inhibitor celecoxib (SMD, -0.29; 95% CI, -0.49 to -0.08; I2=73%) o
247 iovascular events when given with rofecoxib, celecoxib, sulindac, meloxicam, and indometacin but not
249 tantly, combination of low-dose CP-31398 and celecoxib suppressed colon adenocarcinoma incidence by 7
250 by the cyclooxygenase inhibitors aspirin and celecoxib suppressed M2 macrophage polarization and decr
251 bution compartment or a dissolution step for celecoxib suspension did not lead to an overall improvem
252 time profiles for animals administered with celecoxib suspension was not significantly different bet
255 of renal events was significantly lower with celecoxib than with ibuprofen (P=0.004) but was not sign
256 testinal events was significantly lower with celecoxib than with naproxen (P=0.01) or ibuprofen (P=0.
260 d by certain small molecule drugs, including celecoxib, through mechanisms that have not been fully e
261 ity (k) and the maximum binding (r(max)) for celecoxib to both natural and synthetic melanin were est
262 Finally, we find that administration of celecoxib to dogs interferes with the ability of a low d
263 In this study, we evaluated the ability of celecoxib to induce toxicity in head and neck squamous c
264 ay be attributable to significant binding of celecoxib to melanin and its accumulation/retention in t
265 oxide solubilization METHOD: The affinity of celecoxib to synthetic and natural melanin was estimated
266 the ability of the anti-inflammatory agent, celecoxib, to suppress hyperemia formation during photoc
267 nly consumed NSAIDs-ibuprofen, naproxen, and celecoxib-to cause a drug-drug interaction with aspirin
273 s who developed new adenomas while receiving celecoxib treatment were also found as having low coloni
277 ctide-co-glycolide) (PLGA) microparticles of celecoxib using supercritical fluid pressure-quench tech
278 r = 0.99) and SD (r = 0.99) rats for retinal celecoxib using the same model; however, the parameter e
280 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
281 nterval [CI], 0.76 to 1.13; hazard ratio for celecoxib vs. ibuprofen, 0.85; 95% CI, 0.70 to 1.04; P<0
282 the ibuprofen group (1.9%) (hazard ratio for celecoxib vs. naproxen, 0.90; 95% CI, 0.71 to 1.15; haza
283 the ibuprofen group (2.7%) (hazard ratio for celecoxib vs. naproxen, 0.93; 95% confidence interval [C
285 ork, the EPI activity of the COX-2 inhibitor celecoxib was confirmed and a new class of pyrazolo[4,3-
286 effect of treatment with the COX-2 inhibitor celecoxib was examined when initiated at different stage
293 ibrary, including ingliforib, furosemide and celecoxib, we successfully prepared stable solid nanodis
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
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