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1 dentical design (lumiracoxib vs ibuprofen or naproxen).
2 Thus, SCC-25 cells possess transporters for naproxen.
3 h as hydroxylating the antiinflammatory drug naproxen.
4 ecoxib, celecoxib, parecoxib, valdecoxib and naproxen.
5 assigned to receive celecoxib, ibuprofen, or naproxen.
6 te the evident macroscopic damage induced by naproxen.
7 events compared with the nonselective NSAID naproxen.
8 s been interpreted as a protective effect of naproxen.
9 I: 1.07, 2.69) when comparing rofecoxib with naproxen.
10 00 mg/day or to begin placebo in addition to naproxen.
11 hanges in basal firing and was unaffected by naproxen.
12 mg twice per day, respectively; and 31 % for naproxen.
13 incidence of endoscopic ulcers compared with naproxen.
14 with her rheumatoid arthritis and was taking naproxen.
15 out 20x at little expense of the activity of naproxen.
16 for the development of pain and response to naproxen.
17 group (1.9%) (hazard ratio for celecoxib vs. naproxen, 0.90; 95% CI, 0.71 to 1.15; hazard ratio for c
18 group (2.7%) (hazard ratio for celecoxib vs. naproxen, 0.93; 95% confidence interval [CI], 0.76 to 1.
20 ts with painful OA of the knee responding to naproxen 1,000 mg/day, the addition of tramadol 200 mg/d
26 king the nonsteroidal anti-inflammatory drug naproxen (3 cases) or acetaminophen (2 cases) but in who
28 ADAS-Cog scores in participants treated with naproxen (5.8 [8.0]) or rofecoxib (7.6 [7.7]) was not si
29 values for endothelial cells vs. platelets: naproxen -5.59+/-0.07 vs. -4.81+/-0.04; rofecoxib -4.93+
30 bable membrane plus twice daily postsurgical naproxen 500 mg for one week (test or GPN group) or with
32 d to lumiracoxib 400 mg once daily (n=9156), naproxen 500 mg twice daily (4754), or ibuprofen 800 mg
33 d to lumiracoxib 400 mg once daily (n=9156), naproxen 500 mg twice daily (4754), or ibuprofen 800 mg
34 andomly assigned to rofecoxib 50 mg daily or naproxen 500 mg twice daily for a median of 9 months.
35 1 year or greater were randomly assigned to naproxen 500 mg twice daily or rofecoxib 50 mg daily.
36 ed to receive lumiracoxib 400 mg once daily, naproxen 500 mg twice daily, or ibuprofen 800 mg 3 times
39 eks, rofecoxib, 25 mg/d, was as effective as naproxen, 500 mg twice daily, but had statistically sign
41 r day (n = 240, 235, and 218, respectively); naproxen, 500 mg twice per day (n = 225); or placebo (n
45 I endoscopy study, 19% of subjects receiving naproxen (6 of 32) developed gastric ulcers, whereas no
46 0.1-4.8 days), sulfamethoxazole (2-33 days), naproxen (6-19 days), carbamazepine (355-1,624 days), an
47 For example, after 120 h, the metabolites of naproxen accounted for >90% of the extractable chemical
48 ritis patients taking the nonselective NSAID naproxen, accounting for nearly 40% of the serious GI ev
50 elated NSAIDs, niflumic acid, ibuprofen, and naproxen, acutely increase intracellular zinc stores fro
52 yclobenzaprine or oxycodone/acetaminophen to naproxen alone did not improve functional outcomes or pa
54 g rofecoxib and those taking either placebo, naproxen (an NSAID with near-complete inhibition of plat
59 Treatments more used to migraine, such as naproxen and a calcitonin gene-related peptide receptor
60 on between ibuprofen and aspirin and between naproxen and aspirin but not between celecoxib and aspir
61 ng were monitored during coincubation of (S)-naproxen and CYP2C9 over a range of P450 reductase conce
66 ddition, tert-butyl esters, such as those of Naproxen and Flurbiprofen, were prepared from tert-butyl
69 these results, the binding properties toward naproxen and ibuprofen were measured for two combinatori
74 tive agents with cox-2>cox-1 inhibition (eg, naproxen), and nonselective agents with cox-1>cox-2 inhi
75 reatment of migraine, including sumatriptan, naproxen, and a calcitonin gene-related peptide antagoni
78 mmatory drugs including ibuprofen, fenbupen, naproxen, and acetaminophen also up-regulated ACOX::CAT.
79 l C-H oxidation methods using oxcarbazepine, naproxen, and an early compound hit (phthalazine 1).
81 nsity of commonly consumed NSAIDs-ibuprofen, naproxen, and celecoxib-to cause a drug-drug interaction
85 observed bile concentrations of diclofenac, naproxen, and ibuprofen in bream ranged from 6 to 95 ng
86 cyclooxygenase inhibitors such as ibuprofen, naproxen, and indomethacin were used as orally bioavaila
87 * have been determined by energy transfer to naproxen, and it has been found that its energy is lower
91 arated a standard mixture of 1 mM ibuprofen, naproxen, and phenylbutazone using a commercially availa
92 a40 aggregation inhibitor than ibuprofen and naproxen, and prevented Abeta42 oligomer formation and t
93 ation of the biphasic kinetics substrate (S)-naproxen, and the CYP2C9*2 (R144C) and CYP2C9*3 (I359L)
97 Differences observed between rofecoxib and naproxen are likely the result of the antiplatelet effec
98 bservations reveals potential limitations of naproxen as an effective therapeutic agent in the treatm
100 -controlled clinical trial demonstrated that naproxen at a dose of 500 mg twice per day is effective
104 NSAID (rofecoxib, diclofenac, ibuprofen, and naproxen compared with celecoxib) therapy was assessed u
106 The MEND was defined as 250 mg above the naproxen daily dosage at which pain relief was no longer
108 out whether high-dose rofecoxib increases or naproxen decreases the risk of serious coronary heart di
110 d the effects of naproxcinod, an NO-donating naproxen derivative, on the skeletal and cardiac disease
113 of salicylic acid, bisphenol A, gemfibrozil, naproxen, diclofenac, technical 4-nonylphenol, and 4-ter
114 n-steroidal anti-inflammatory drugs, such as naproxen, dicofenac and ibuprofen, might differ in their
115 In contrast, the non-RhoA-inhibiting NSAID naproxen does not have the axon growth-promoting effects
116 is study indicate that rofecoxib or low-dose naproxen does not slow cognitive decline in patients wit
121 ts (5596 patient-years) received etodolac or naproxen during a 3-year period without concurrent use o
125 can produce metabolites of acetaminophen and naproxen for which certain drug-dependent antibodies are
126 in the presence of a known drug metabolite (naproxen glucuronide or acetaminophen sulfate) were iden
127 celecoxib group (1.7%), 144 patients in the naproxen group (1.8%), and 155 patients in the ibuprofen
128 celecoxib group (2.3%), 201 patients in the naproxen group (2.5%), and 218 patients in the ibuprofen
129 tly lower in the rofecoxib group than in the naproxen group (5.9% vs. 8.1%; relative risk, 0.74 [95%
130 (mean [+/-SD] daily dose, 209+/-37 mg), the naproxen group (852+/-103 mg), or the ibuprofen group (2
132 was the CSUGI event rate of the etodolac and naproxen groups without concomitant low-dose aspirin.
134 prostaglandin E2 (PGE2), in the presence of naproxen, had no direct effect on afferent activity, but
135 Similarly, the cyclooxygenase inhibitor, naproxen, had no effect on the ischaemic afferent respon
137 the covalent conjugation of d-amino acids to naproxen (i.e., a NSAID) not only affords supramolecular
140 SAIDs (nonsteroidal anti-inflammatory drugs) naproxen, ibuprofen, flurbiprofen, ketoprofen, and fenop
142 that cultured gingival fibroblasts transport naproxen in a saturable, temperature-dependent manner wi
144 lating anti-inflammatory agents (aspirin and naproxen) in these polymeric nanomicelles and by applyin
145 , acetaminophen, and other NSAID (ibuprofen, naproxen, indomethacin) use were based on a self-adminis
146 spirin, ibuprofen, sulindac, phenylbutazone, naproxen, indomethacin, diclofenac, resveratrol, curcumi
147 spirin, ibuprofen, sulindac, phenylbutazone, naproxen, indomethacin, diclofenac, resveratrol, curcumi
150 udy evaluated if rebamipide protects against naproxen-induced gastric damage in healthy volunteers.
152 By comparing the free-energy landscapes of naproxen interactions with Abeta dimers and fibrils, we
155 that the nonsteroidal antiinflammatory drug naproxen may be useful in the treatment of Alzheimer's d
156 d that other nonselective agents, especially naproxen, may provide some lesser degree of cardioprotec
157 rapid, reversible COX inhibitors (ibuprofen, naproxen, mefenamic acid, and lumiracoxib) demonstrated
160 e proposed biosensor was employed to monitor Naproxen (NAP), a well-known anti-inflammatory compound,
163 ays confirmed that AK transforms galaxolide, naproxen, nonylphenol, octylphenol, ibuprofen, diclofena
164 mmatory drugs (NSAIDs), diclofenac (Dic) and naproxen (Nps), were studied by X-ray crystallography an
166 .40, 1.55) when comparing rofecoxib with non-naproxen NSAIDs; and 1.69 (95% CI: 1.07, 2.69) when comp
167 NSAIDs were the following: rofecoxib versus naproxen (odds ratio, 3.39 [CI, 1.37 to 8.40]) and celec
169 effect of a one week course of postsurgical naproxen on the osseous healing in intrabony defects.
170 o measure the effects of NANSAIDs, including naproxen, on risk of serious coronary heart disease.
174 ine, the nonsteroidal anti-inflammatory drug naproxen or the steroidal antiinflammatory drug dexameth
175 ibuprofen (OR = 0.41, 95% CI: 0.2, 0.8), and naproxen/other NSAIDs (OR = 0.34, 95% CI: 0.1, 0.8).
176 erall effect size for NSAIDs (P = 0.007) and naproxen (P = 0.04) groups based on data available from
177 significantly lower with celecoxib than with naproxen (P=0.01) or ibuprofen (P=0.002); the risk of re
180 ty acids (FAs) and some COX inhibitors (e.g. naproxen) preferentially bind to the COX site of E(allo)
183 nt-years was 0.41 for rofecoxib and 0.89 for naproxen (relative risk, 0.46; 95% confidence interval [
184 1 years; 147 females), 90 were stratified as naproxen responders and 146 as naproxen nonresponders.
185 = 0.040) in the treatment effect between the naproxen responders and nonresponders, thus demonstratin
188 fenac, indomethacin, lumiracoxib, meloxicam, naproxen, rofecoxib, sodium salicylate, and SC560 as inh
191 Comparison of the NANSAID rofexocib with naproxen showed a substantial difference in acute myocar
193 dontal treatment (scaling, root planing) and naproxen sodium (275 mg) administration daily for 6 week
196 ausea for the comparison between sumatriptan-naproxen sodium and placebo, and the percentages of pati
198 onotherapy (16% and 14% in studies 1 and 2), naproxen sodium monotherapy (10% and 10% in studies 1 an
199 onducted to determine the possible effect of naproxen sodium on clinical status and the enzymatic pro
201 tablet containing sumatriptan succinate and naproxen sodium relative to efficacy and safety of each
202 urs after dosing was higher with sumatriptan-naproxen sodium than placebo in study 1 (71% vs 65%; P =
204 ur sustained pain-free response, sumatriptan-naproxen sodium was superior at P<.01 (25% and 23% in st
206 m, 500 mg; sumatriptan, 85 mg (monotherapy); naproxen sodium, 500 mg (monotherapy); or placebo, to be
208 le tablet containing sumatriptan, 85 mg, and naproxen sodium, 500 mg; sumatriptan, 85 mg (monotherapy
212 th lumiracoxib (18 events) versus 0.21% with naproxen (ten) and 0.11% with lumiracoxib (five) versus
213 iinflammatory drug derivatives such as (+/-)-naproxen tert-butyl ester and (+/-)-flurbiprofen tert-bu
214 er needed to treat with rofecoxib instead of naproxen to avert 1 GI event was 10-12 in highest risk p
217 Power analysis to determine superiority of naproxen treatment showed that a 12 per group sample siz
220 ntiinflammatory drugs aspirin, ibuprofen and naproxen, used as positive controls in the assay at 108,
221 erence between the risk of toxicity with OTC naproxen versus OTC ibuprofen (adjusted OR, 0.84; 95% CI
224 acks) with rofecoxib treatment compared with naproxen was 2.38 (95% confidence interval, 1.39-4.00; P
228 es of the nonsteroidal antiinflammatory drug naproxen was designed to have both antiinflammatory and
230 ng this unbiased scanning method except that naproxen was not detected due to low sensitivity at nega
231 utanoic acid (in which the methyl group of R-naproxen was replaced by an ethyl group) acts as a poten
235 onsteroidal antiinflammatory drugs [NSAIDs], naproxen) were determined by the mean changes from basel
236 Bay x 1005, and the cyclooxygenase inhibitor naproxen, were evaluated individually and in combination
237 ointestinal event rates between etodolac and naproxen when low-dose aspirin was taken concomitantly.
239 trated that SCC-25 cell monolayers transport naproxen with a Michaelis constant (K(m)) and maximum ve
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