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1 ly inhibit only COX-2 (such as celecoxib and rofecoxib).
2 45.8% (P < 0.001, ibuprofen vs. 25 and 50 mg rofecoxib).
3 the cyclooxygenase inhibitors diclofenac and rofecoxib.
4 d adenomas to receive daily placebo or 25 mg rofecoxib.
5 mokers and nonsmokers and were unaffected by rofecoxib.
6 celecoxib was the most common alternative to rofecoxib.
7 ge 34 to 125 pg/mg creatinine (P=0.001) with rofecoxib.
8 n cyclooxygenase-2 inhibitors, in particular rofecoxib.
9 early because of the worldwide withdrawal of rofecoxib.
10 ctive COX-2 inhibitors NS-398, celecoxib, or rofecoxib.
11 other COX-2 inhibitors such as celecoxib and rofecoxib.
12 taking naproxen and 42.7% among those taking rofecoxib.
13 ith the use of the selective COX-2 inhibitor rofecoxib.
14 dverse cardiovascular events associated with rofecoxib.
15 vascular disease following the withdrawal of rofecoxib.
16 prematurely owing to worldwide withdrawal of rofecoxib.
17 ition in humans in response to celecoxib and rofecoxib.
18 tively, whereas no such effect was seen with rofecoxib.
20 Patients were randomly assigned to receive rofecoxib, 12.5 mg/d (n = 96); rofecoxib, 25 mg/d (n = 9
21 0 mL/s were observed after multiple doses of rofecoxib, 12.5 mg/d (P = 0.019); rofecoxib, 25 mg (P =
22 b and P =.006 vs acetaminophen and P =.02 vs rofecoxib, 12.5 mg/d), composite pain subscale (P</=.03
23 response to rofecoxib, 25 mg/d, followed by rofecoxib, 12.5 mg/d, celecoxib, and acetaminophen, resp
26 lcer rates were 25 mg rofecoxib, 9.6%; 50 mg rofecoxib, 14.7%; and ibuprofen, 45.8% (P < 0.001, ibupr
27 0.001, respectively) and were noninferior to rofecoxib (-2 mm [-8, 4], P < 0.001 and -3 mm [-9, 3], P
29 o placebo, enteric-coated aspirin 81 mg/day, rofecoxib 25 mg combined with aspirin 81 mg/day, or ibup
30 D3582 125 mg, 375 mg, or 750 mg twice a day; rofecoxib 25 mg once a day; naproxen 500 mg twice a day;
32 eived either celecoxib 200 mg/day (n = 189), rofecoxib 25 mg/day (n = 190), or placebo (n = 96) for 6
35 were superior to placebo and as effective as rofecoxib 25 mg/day in treating the signs and symptoms o
36 oses), 1.59 (95% CI 1.10-2.32, p=0.015); for rofecoxib 25 mg/day or less, 1.47 (0.99-2.17, p=0.054);
37 hours before the cyclooxygenase-2 inhibitor rofecoxib (25 mg every morning) and the same medications
38 thesized that COX-2-specific inhibition with rofecoxib (25 mg once daily) in the treatment of patient
39 common (P < 0.001) following treatment with rofecoxib (25 mg or 50 mg) than with ibuprofen after 12
40 Fifty healthy volunteers received placebo, rofecoxib (25 mg), and celecoxib (200 mg), randomized by
41 reatment with a cyclo-oxygenase-2 inhibitor, rofecoxib (25 mg), on recurrence of neoplastic polyps of
42 idence of gastroduodenal ulcers >/=3 mm with rofecoxib (25 or 50 mg once daily) was significantly (P
43 endoscopy were randomly assigned to receive rofecoxib (25 or 50 mg once daily), ibuprofen (800 mg 3
44 e doses of rofecoxib, 12.5 mg/d (P = 0.019); rofecoxib, 25 mg (P = 0.029), and indomethacin (P = 0.08
45 in a randomized, placebo-controlled trial of rofecoxib, 25 mg daily, started after potentially curati
47 ed to receive rofecoxib, 12.5 mg/d (n = 96); rofecoxib, 25 mg/d (n = 95); celecoxib, 200 mg/d (n = 97
48 days of therapy showed greatest response to rofecoxib, 25 mg/d, followed by rofecoxib, 12.5 mg/d, ce
52 2, - 22.0, - 18.7, and - 18.8 mm; P =.04 for rofecoxib, 25 mg/d, vs both acetaminophen and celecoxib)
53 56%, 46%, and 39%, respectively; P</=.03 for rofecoxib, 25 mg/d, vs celecoxib and acetaminophen; P =.
54 of rofecoxib vs acetaminophen and P =.02 for rofecoxib, 25 mg/d, vs celecoxib), night pain (-25.2, -
55 ts with osteoarthritis treated for 12 weeks, rofecoxib, 25 mg/d, was as effective as naproxen, 500 mg
57 reports including 127 trial populations (40 rofecoxib, 37 celecoxib, 29 valdecoxib + parecoxib, 15 e
58 ysis, the 12-week ulcer incidence with 25 mg rofecoxib (4.7%) and with placebo (7.3%) satisfied presp
60 to placebo at week 12 (placebo, 9.9%; 25 mg rofecoxib, 4.1%; 50 mg rofecoxib, 7.3%; and ibuprofen, 2
61 costeroid therapy) were randomly assigned to rofecoxib 50 mg daily or naproxen 500 mg twice daily for
64 cipants treated with naproxen (5.8 [8.0]) or rofecoxib (7.6 [7.7]) was not significantly different fr
67 clinB1 since these effects were prevented by rofecoxib (a selective COX-2 inhibitor) and rescued by e
68 -receptor deficient mice treated with either rofecoxib (a selective cyclooxygenase-2 inhibitor) or in
69 ouble-blind study tested the hypothesis that rofecoxib, a drug that specifically inhibits cyclooxygen
71 and BBB integrity, mice were pretreated with rofecoxib, a specific inhibitor of COX-2, prior to Tat t
72 comitant administration of ibuprofen but not rofecoxib, acetaminophen, or diclofenac antagonizes the
74 d that the shortened bleeding time following rofecoxib administration is attributable, in part, to th
75 P4A-like immune reactivity was increased by rofecoxib administration, but 20-HETE production increas
76 usted odds ratios versus celecoxib were: for rofecoxib (all doses), 1.59 (95% CI 1.10-2.32, p=0.015);
77 he cyclooxygenase (COX)-2-specific inhibitor rofecoxib, alone or in combination with the standard ant
81 GI events per 100 patient-years was 0.41 for rofecoxib and 0.89 for naproxen (relative risk, 0.46; 95
82 At this point, 1,167 patients had received rofecoxib and 1,160 patients had received placebo for me
83 o, the average selectivity attained by 25 mg rofecoxib and 200 mg celecoxib in vivo were not differen
87 s-Webster mice were dosed with celecoxib and rofecoxib and challenged with CT in ligated small intest
88 COX-2-selective agents, including celecoxib, rofecoxib and diisopropyl fluorophosphate, demonstrate a
91 emonstrated a significant difference between rofecoxib and its NSAID comparator (naproxen) in the ris
93 CHD) in non-users (n=202916) and in users of rofecoxib and other NSAIDs (rofecoxib n=24 132, other n=
96 eduction in adhesion formation compared with rofecoxib and the nonselective COX-2 inhibitors at 10 da
97 omparisons were made between patients taking rofecoxib and those taking either placebo, naproxen (an
99 inhibited by the cyclooxygenase-2 inhibitor rofecoxib and was restored by the stable PGI(2) analogue
103 We investigated the effects of celecoxib, rofecoxib, and diclofenac on ionic currents and calcium
104 l infarction (AMI) among users of celecoxib, rofecoxib, and NSAIDs in Medicare beneficiaries with a c
106 ith the selective COX-2 agents, celecoxib or rofecoxib, and the nonspecific COX inhibitors, aspirin,
107 such as celecoxib, etoricoxib, lumiracoxib, rofecoxib, and valdecoxib have been developed and the gr
108 n the US during the study period (celecoxib, rofecoxib, and valdecoxib), as well as oral formulations
113 e randomly assigned to receive 50 mg of oral rofecoxib at 24 hours and at 1 to 2 hours before TKA, 50
114 prominent apoptosis in these cells, whereas rofecoxib at 50 microM was without effect in either supp
115 th osteoarthritis were randomized to receive rofecoxib at a dosage of 25 mg or 50 mg once daily, ibup
119 vidence of raised risk of CHD among users of rofecoxib at doses of 25 mg or less or among users of ot
120 ought to establish if risk was enhanced with rofecoxib at either high or standard doses compared with
125 When mice were fed chow containing 0.01% rofecoxib beginning on day 0 after tumor cell implantati
128 -4 times the therapeutically effective dose, rofecoxib caused fewer endoscopically detected ulcers th
129 ies highlight the cardiovascular toxicity of rofecoxib, celecoxib, parecoxib, valdecoxib and naproxen
130 isk of cardiovascular events when given with rofecoxib, celecoxib, sulindac, meloxicam, and indometac
132 etary groups: control chow, low-dose (0.01%) rofecoxib chow, and high-dose (0.025%) rofecoxib chow.
134 cebo (N = 381) 5.8%, aspirin (N = 387) 7.3%, rofecoxib combined with aspirin (N = 377) 16.1%, and ibu
135 0.17, aspirin 0.85 (P = 0.002 vs. placebo), rofecoxib combined with aspirin 1.67, and ibuprofen 1.91
136 and ibuprofen (N = 374) 17.1% (P < 0.001 for rofecoxib combined with aspirin and for ibuprofen vs. ea
137 he relative risk of AMI in patients who used rofecoxib compared with persons taking no NSAID, taking
138 consumption were less in the group receiving rofecoxib compared with the group receiving placebo (P<.
139 V thrombotic events in patients treated with rofecoxib compared with those treated with placebo or no
140 tudy was to test whether the COX-2 inhibitor rofecoxib could reduce recurrence and improve survival w
145 I within 180 days after initiation of NSAID (rofecoxib, diclofenac, ibuprofen, and naproxen compared
146 ated therapy in the adjuvant setting of CRC, rofecoxib did not improve OS or protect from recurrence
148 ed larger effect sizes versus placebo in the rofecoxib/etoricoxib trials than in the celecoxib/valdec
149 ersus placebo, as determined using data from rofecoxib/etoricoxib trials, were consistently higher th
150 These data suggest 20-HETE as a marker of rofecoxib exposure and that inhibition of 20-HETE's degr
152 , we demonstrate that oral administration of rofecoxib for 3 mo results in a greater than 120-fold hi
153 ZD3582 with placebo for superiority and with rofecoxib for noninferiority using a predefined margin o
155 ically relevant doses of the COX-2 inhibitor rofecoxib given orally were effective in inhibiting the
156 or less, 1.47 (0.99-2.17, p=0.054); and for rofecoxib greater than 25 mg/day, 3.58 (1.27-10.11, p=0.
157 There was less postoperative vomiting in the rofecoxib group (6%) compared with the placebo group (26
158 , 59 individuals had an APTC endpoint in the rofecoxib group and 34 in the placebo group (hazard rati
159 ing the follow-up period, one patient in the rofecoxib group and five patients in the placebo group d
162 0-10) achieved for the knee was lower in the rofecoxib group compared with the placebo group during h
163 scular thrombotic events, 16 occurred in the rofecoxib group during or within 14 days after the treat
165 ere statistically significantly lower in the rofecoxib group than in the naproxen group (5.9% vs. 8.1
167 lure (hazard ratio for the comparison of the rofecoxib group with the placebo group, 4.61; 95 percent
168 cardiovascular thrombotic events, six in the rofecoxib group, were reported within the 2 years after
170 OR, 1.21; 95% CI, 1.01 to 1.44; P=0.036) and rofecoxib >25 mg versus celecoxib >200 mg (OR, 1.70; 95%
173 strumental variable analysis, diclofenac and rofecoxib had the least favorable benefit-risk balance a
176 ith the use of the selective COX-2 inhibitor rofecoxib in a long-term, multicenter, randomized, place
177 presented mortality findings associated with rofecoxib in clinical trials of patients with Alzheimer
178 eraction by revacept was more effective than rofecoxib in preventing platelet-induced mRNA changes of
181 rounded the question about whether high-dose rofecoxib increases or naproxen decreases the risk of se
182 , but not COX-2 selective inhibitors such as rofecoxib, induce bronchoconstriction and asthma in sens
184 ecame available during litigation related to rofecoxib involving Merck & Co, including internal compa
185 2 articles concluded that regarding safety, rofecoxib is "well tolerated." In contrast, in April 200
186 that inhibition of 20-HETE's degradation by rofecoxib is a partial explanation for its dramatic incr
191 also elevated in dose-specific comparisons: rofecoxib < or =25 mg versus celecoxib < or =200 mg (OR,
192 omparisons of efficacy between celecoxib and rofecoxib met the predefined criteria for noninferiority
194 the effect of three years of treatment with rofecoxib on the risk of recurrent neoplastic polyps of
195 mized to 1 of 3 treatment groups: 12.5 mg of rofecoxib once daily, 25 mg of rofecoxib once daily, and
196 s: 12.5 mg of rofecoxib once daily, 25 mg of rofecoxib once daily, and 50 mg of diclofenac 3 times da
197 to inform our patients of the withdrawal of rofecoxib, one of the largest drug withdrawals in United
198 , controlled trials with the COX-2 inhibitor rofecoxib, one study demonstrated a significant differen
201 male LDLR-/- mice fed the Western diet with rofecoxib or indomethacin for 6 weeks resulted in signif
203 The results of this study indicate that rofecoxib or low-dose naproxen does not slow cognitive d
204 of the cyclo-oxygenase-2 selective inhibitor rofecoxib or the mixed cyclo-oxygenase-1/cyclo-oxygenase
206 oduced cyclo-oxygenase-2 selective inhibitor rofecoxib, owe part of their inhibitory actions to effec
207 factors, ischemic stroke was associated with rofecoxib (P = 0.060, OR 2.27 [95% CI 0.97-5.28]), and p
208 rimary prevention trials (0.52%): 0.74% with rofecoxib (P =.04 compared with the placebo group of the
209 an 206, range 154 to 383 pg/mg creatinine by rofecoxib (P=0.04) but was not changed in nonsmokers.
210 th overall mortality of 34 deaths among 1069 rofecoxib patients and 12 deaths among 1078 placebo pati
211 ithin 14 days of the last dose (24 among 725 rofecoxib patients and 15 among 732 placebo patients) an
212 ods and reported 29 deaths (2.7%) among 1067 rofecoxib patients and 17 deaths (1.6%) among 1075 place
213 ed deaths" were reported (9 deaths among 346 rofecoxib patients and 2 deaths among 346 placebo patien
219 cohort receiving aspirin, both celecoxib and rofecoxib reduced risk of admission for gastrointestinal
220 s no evidence for an excess of CV events for rofecoxib relative to either placebo or the non-naproxen
221 posure showed an increase in the MI risk for rofecoxib (risk difference [RD] 1.40, 95% confidence int
222 significant elevation in the event rate for rofecoxib (RR 1.15, 95% confidence interval [95% CI] 1.0
223 ts for new users of each agent increased for rofecoxib (RR 1.22, 95% confidence interval [95% CI] 1.1
228 nhibition of COX-2 by oral administration of Rofecoxib significantly slowed but did not cure the grow
230 omethacin, lumiracoxib, meloxicam, naproxen, rofecoxib, sodium salicylate, and SC560 as inhibitors of
233 Adenoma recurrence was less frequent for rofecoxib subjects than for those randomized to placebo
234 en but also by the COX-2 selective inhibitor rofecoxib, suggesting that the majority of PGE2 formed i
237 Time-cumulative analyses indicated that for rofecoxib the adverse risks for peripheral edema and hyp
238 ad reduced microvessel density compared with rofecoxib, the nonselective COX inhibitors, and control
239 e-free survival and overall survival between rofecoxib therapy and placebo and between the use and no
241 e 85 to 390 pg/mg creatinine) was reduced by rofecoxib to 78+/-27, median 71.5, range 50 to 135 pg/mg
242 ascular adverse events in patients receiving rofecoxib to reduce rates of recurrence of colorectal ca
244 cal analyses of the primary splenic tumor in rofecoxib-treated mice showed no alteration in COX-1 exp
245 stroke, and transient ischemic attacks) with rofecoxib treatment compared with naproxen was 2.38 (95%
246 found no evidence of a greater benefit from rofecoxib treatment compared with placebo in patients wh
248 IK3CA mutation does not predict benefit from rofecoxib treatment, it merits further evaluation as a p
251 justed relative risks of AMI associated with rofecoxib use of 1 to 30 days (OR, 1.40; 95% CI, 1.12 to
254 aration of the event curves) among long-term rofecoxib users at low or high baseline cardiovascular r
256 cal trials of coxibs (etoricoxib, celecoxib, rofecoxib, valdecoxib) in patients with hip and/or knee
257 tive COX-2 inhibitors (coxibs), particularly rofecoxib, valdecoxib, and parecoxib, increases risk for
259 with nonselective NSAIDs were the following: rofecoxib versus naproxen (odds ratio, 3.39 [CI, 1.37 to
260 genase-2 inhibition led to the withdrawal of rofecoxib (Vioxx) and valdecoxib (Bextra), but the mecha
261 ibitors of cyclooxygenase-2 (COX-2), such as rofecoxib (Vioxx), celecoxib (Celebrex), and valdecoxib
262 hibitors, including celecoxib (Celebrex) and rofecoxib (Vioxx), produced two unanticipated findings.
263 l anti-inflammatory drugs until one of them, rofecoxib (Vioxx), was found to be associated with incre
264 een under intense scrutiny because long-term rofecoxib (Vioxx; Merck, Whitehouse Station, NJ) treatme
265 idal anti-inflammatory drugs (NSAIDs) (e.g., rofecoxib [Vioxx]) increase the risk of heart attack and
266 5, and - 12.5 mm; P</=.02 for either dose of rofecoxib vs acetaminophen and P =.02 for rofecoxib, 25
268 ll others vs acetaminophen; P =.05 for 25-mg rofecoxib vs celecoxib), rest pain (-21.8, - 18.6, - 15.
269 he use of celecoxib (adjusted odds ratio for rofecoxib vs. celecoxib, 2.72 [CI, 1.24 to 5.95]; P = 0.
273 a history of colorectal adenomas, the use of rofecoxib was associated with an increased cardiovascula
274 randomized trials with 116,094 participants, rofecoxib was associated with increased renal and arrhyt
287 s that clinical trial manuscripts related to rofecoxib were authored by sponsor employees but often a
288 g division to promote prescription of Vioxx (rofecoxib) when it became available on the market in 199
289 , which blocks COX-1 selectively, but not by rofecoxib, which is a selective inhibitor of COX-2.
292 bo; 0.79 (95% CI: 0.40, 1.55) when comparing rofecoxib with non-naproxen NSAIDs; and 1.69 (95% CI: 1.
293 R) trial, a large randomized trial comparing rofecoxib with placebo after primary CRC resection.
294 was 0.84 (95% CI: 0.51, 1.38) when comparing rofecoxib with placebo; 0.79 (95% CI: 0.40, 1.55) when c
295 ed that COX-2 inhibitor drugs, celecoxib and rofecoxib, with similar COX-2-selectivity and clinical e
296 whether use of the selective COX-2 inhibitor rofecoxib would reduce the risk of colorectal adenomas.
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