ライフサイエンスコーパス: naproxen

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.

19 The remaining patients received naproxen 1,000 mg/day for 3 weeks.

20 ts with painful OA of the knee responding to naproxen 1,000 mg/day, the addition of tramadol 200 mg/d

21 mization was stratified based on response to naproxen 1,000 mg/day.

22 Naproxen (10 mg kg-1, I.V.), but not a cocktail of omega

23 Inhibition of cyclo-oxygenase with naproxen (10 microM) prevented sensitization after hista

24 ng blockade of cyclo-oxygenase activity with naproxen (10 microM).

25 low-dose aspirin increased event rates with naproxen 2-fold and etodolac 9-fold.

26 king the nonsteroidal anti-inflammatory drug naproxen (3 cases) or acetaminophen (2 cases) but in who

27 mong the target compounds (63%), followed by naproxen (43%).

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

31 mg twice a day; rofecoxib 25 mg once a day; naproxen 500 mg twice a day; or placebo for 6 weeks.

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

37 1-week medication washout were treated with naproxen 500 mg/day for 1 week.

38 Naproxen, 500 mg twice daily, and coxib, once daily.

39 eks, rofecoxib, 25 mg/d, was as effective as naproxen, 500 mg twice daily, but had statistically sign

40 Rofecoxib, 25 mg/d, or naproxen, 500 mg twice daily.

41 r day (n = 240, 235, and 218, respectively); naproxen, 500 mg twice per day (n = 225); or placebo (n

42 All participants were given 20 tablets of naproxen, 500 mg, to be taken twice a day.

43 One group received sodium naproxen 550 mg b.i.d. plus placebo for 7 days, while th

44 days, while the other group received sodium naproxen 550 mg b.i.d. plus rebamipide 100 mg b.i.d.

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

49 Naproxen accumulation was more efficient at acidic pH th

50 elated NSAIDs, niflumic acid, ibuprofen, and naproxen, acutely increase intracellular zinc stores fro

51 (adjusted OR 0.52; 95% CI: 0.39 to 0.69) and naproxen (adjusted OR 0.48; 95% CI: 0.28 to 0.82).

52 yclobenzaprine or oxycodone/acetaminophen to naproxen alone did not improve functional outcomes or pa

53 Naproxen also reduced overall pain incidence from 71.3%

54 g rofecoxib and those taking either placebo, naproxen (an NSAID with near-complete inhibition of plat

55 We examined a series of naproxen analogues and find that (R)-2-(6-methoxynaphtha

56 ationic thioflavin T, or the hydrophobic (S)-naproxen and (R)-ibuprofen molecules.

57 ent or lower GI event) among patients taking naproxen and 42.7% among those taking rofecoxib.

58 xtracellular concentration ratio was 1.9 for naproxen and 7.2 for ibuprofen.

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

62 A selective response to naproxen and dexketoprofen with tolerance to ibuprofen w

63 A was observed in animals that received both naproxen and either Bay y 1015 or Bay x 1005.

64 idence of CSUGI events was .78% and .24% for naproxen and etodolac, respectively.

65 idence of CSUGI events was .99% and .24% for naproxen and etodolac, respectively.

66 ddition, tert-butyl esters, such as those of Naproxen and Flurbiprofen, were prepared from tert-butyl

67 s and allosteric COX-2 inhibitors, including naproxen and flurbiprofen.

68 copy was performed for microcrystals of both naproxen and glucose isomerase.

69 these results, the binding properties toward naproxen and ibuprofen were measured for two combinatori

70 Naproxen and ibuprofen, in their parent form, were conju

71 Here, we evaluated the metabolism of naproxen and ibuprofen, two of the most-used human drugs

72 h two non-steroidal anti-inflammatory drugs, naproxen and ibuprofen.

73 2-lowering agent (SALA), over the non-SALAs, naproxen and MF-tricyclic.

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

76 oral formulations of diclofenac, ibuprofen, naproxen, and a composite of all other NSAIDs.

77 The non-selective NSAIDs, ibuprofen and naproxen, and a selective COX-2 inhibitor, MF-tricyclic,

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).

80 Although ibuprofen, naproxen, and celecoxib all had the potential to compete

81 nsity of commonly consumed NSAIDs-ibuprofen, naproxen, and celecoxib-to cause a drug-drug interaction

82 ory drugs (NSAIDs) (indomethacin, ibuprofen, naproxen, and flurbiprofen).

83 nsteroidal antiinflammatory drugs ibuprofen, naproxen, and flurbiprofen.

84 and roach living in a lake where diclofenac, naproxen, and ibuprofen are present as pollutants.

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

88 teroidal anti-inflammatory drugs: ibuprofen, naproxen, and ketoprofen.

89 rbiprofen, ibuprofen, oxaprozin, fenoprofen, naproxen, and ketoprofen.

90 trin with benzene, resorcinol, flurbiprofen, naproxen, and nabumetone.

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)

94 usly been implicated, ibuprofen, nabumetone, naproxen, and tolmetin were found to be associated.

95 e, primidone, DEET, carbamazepine, dilantin, naproxen, and triclosan.

96 f a variety of drugs, including propranolol, naproxen, and warfarin.

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

99 The RD for naproxen as well as its upper 95% CI was the lowest of a

100 -controlled clinical trial demonstrated that naproxen at a dose of 500 mg twice per day is effective

101 In humans, systemically administered naproxen attained steady-state levels of 61.9 mug/mL in

102 l biosensor for the continuous monitoring of Naproxen based on cytochrome P450.

103 The analysis of naproxen binding energetics shows that the location of l

104 NSAID (rofecoxib, diclofenac, ibuprofen, and naproxen compared with celecoxib) therapy was assessed u

105 The anti-inflammatory drug naproxen could be detected in all the six bream and roac

106 The MEND was defined as 250 mg above the naproxen daily dosage at which pain relief was no longer

107 Patients were stabilized with 1,000 mg naproxen/day and then began a 6-week, double-blind trial

108 out whether high-dose rofecoxib increases or naproxen decreases the risk of serious coronary heart di

109 iants are associated with lower rates of (S)-naproxen demethylation.

110 d the effects of naproxcinod, an NO-donating naproxen derivative, on the skeletal and cardiac disease

111 Thus, the antioxidant-naproxen derivatives represent a novel series of agents

112 Inhibitors of COX (naproxen, diclofenac, or ibuprofen) increased bronchocon

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

117 ers and nonresponders react to a decrease in naproxen dosage after the addition of tramadol.

118 efficacy end point was the minimum effective naproxen dose (MEND).

119 icacy were assigned a MEND equal to the last naproxen dose received.

120 During the double-blind phase, the naproxen dose was reduced by 250 mg every 2 weeks.

121 ts (5596 patient-years) received etodolac or naproxen during a 3-year period without concurrent use o

122 luronic F-127, and glucosylceramide enhanced naproxen entry.

123 Compared with naproxen, etodolac was associated with a reduction in up

124 The administration of postsurgical naproxen failed to produce osseous healing that was stat

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

131 7.71 for the placebo group and 6.04 for the naproxen group (P = .037).

132 was the CSUGI event rate of the etodolac and naproxen groups without concomitant low-dose aspirin.

133 Naproxen had an average market share of less than 10%.

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

136 acute myocardial infarction, and studies of naproxen have found a possible protective effect.

137 the covalent conjugation of d-amino acids to naproxen (i.e., a NSAID) not only affords supramolecular

138 s with documented harmful effects, including naproxen, ibuprofen and rubella live vaccine.

139 Rate ratios for naproxen, ibuprofen, and other NANSAIDs were 0.95 (0.82-

140 SAIDs (nonsteroidal anti-inflammatory drugs) naproxen, ibuprofen, flurbiprofen, ketoprofen, and fenop

141 and the nonspecific COX inhibitors, aspirin, naproxen, ibuprofen, or indomethacin.

142 that cultured gingival fibroblasts transport naproxen in a saturable, temperature-dependent manner wi

143 between rofecoxib and its NSAID comparator (naproxen) in the risk of CV thrombotic events.

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

148 Sodium naproxen induced gastric damage in both groups.

149 Rebamipide does not protect against naproxen-induced gastric damage in healthy volunteers.

150 udy evaluated if rebamipide protects against naproxen-induced gastric damage in healthy volunteers.

151 As a result naproxen induces a destabilizing effect on Abeta dimer.

152 By comparing the free-energy landscapes of naproxen interactions with Abeta dimers and fibrils, we

153 between lumiracoxib and either ibuprofen or naproxen, irrespective of aspirin use.

154 We show that naproxen ligands bind to Abeta dimer and penetrate its v

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

158 Naphthalene metabolism by CYP3A4 and naproxen metabolism by CYP2C9 demonstrated nonhyperbolic

159 4 and dapsone activation of flurbiprofen and naproxen metabolism by CYP2C9 were also observed.

160 e proposed biosensor was employed to monitor Naproxen (NAP), a well-known anti-inflammatory compound,

161 For the naproxen nonresponders, the mean MEND was 419 mg in the

162 stratified as naproxen responders and 146 as naproxen nonresponders.

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

165 ecoxib relative to either placebo or the non-naproxen NSAIDs that were studied.

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

168 Diclofenac was listed on 74 national EMLs, naproxen on just 27.

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.

171 inhibition (HR, 1.17; 1.10-1.24; P<0.001 and naproxen only: HR, 1.22; 1.12-1.34; P<0.001).

172 Prophylaxis against gout flares with naproxen or colchicine was provided during weeks 1 throu

173 Absence of a protective effect of naproxen or other NANSAIDs on risk of coronary heart dis

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

178 significantly lower with celecoxib than with naproxen (P=0.19).

179 ile inverse to that of a weakly acidic drug (naproxen; pK(a) = 4.15).

180 ty acids (FAs) and some COX inhibitors (e.g. naproxen) preferentially bind to the COX site of E(allo)

181 Naproxen produced a moderate attenuation of carrageenan

182 Naproxen reduced maximum pain from 3.40 to 2.59 (P = .00

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

186 Among naproxen responders, the MEND was significantly lower in

187 The potencies of diclofenac, naproxen, rofecoxib, and salicylate, but not aspirin, ce

188 fenac, indomethacin, lumiracoxib, meloxicam, naproxen, rofecoxib, sodium salicylate, and SC560 as inh

189 and a significant reduction in the rate for naproxen (RR 0.75, 95% CI 0.62-0.92).

190 erval [95% CI] 1.14, 1.30) and decreased for naproxen (RR 0.79, 95% CI 0.67, 0.93).

191 Comparison of the NANSAID rofexocib with naproxen showed a substantial difference in acute myocar

192 All dosages of celecoxib and naproxen significantly improved the signs and symptoms o

193 dontal treatment (scaling, root planing) and naproxen sodium (275 mg) administration daily for 6 week

194 ponse for the comparison between sumatriptan-naproxen sodium and each monotherapy.

195 of nausea did not differ between sumatriptan-naproxen sodium and placebo (65% vs 64%; P = .71).

196 ausea for the comparison between sumatriptan-naproxen sodium and placebo, and the percentages of pati

197 verse events was similar between sumatriptan-naproxen sodium and sumatriptan monotherapy.

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

200 nd divided into two groups to receive either naproxen sodium or placebo.

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 =

203 Sumatriptan-naproxen sodium was more effective than placebo for head

204 ur sustained pain-free response, sumatriptan-naproxen sodium was superior at P<.01 (25% and 23% in st

205 Once-daily rofecoxib, 25 mg, or twice-daily naproxen sodium, 220 mg, or placebo.

206 m, 500 mg; sumatriptan, 85 mg (monotherapy); naproxen sodium, 500 mg (monotherapy); or placebo, to be

207 Sumatriptan, 85 mg, plus naproxen sodium, 500 mg, as a single tablet for acute tr

208 le tablet containing sumatriptan, 85 mg, and naproxen sodium, 500 mg; sumatriptan, 85 mg (monotherapy

209 reatment except placebo was given instead of naproxen sodium.

210 In the naproxen substudy, rates of myocardial infarction (clini

211 lofenac, gemfibrozil, ibuprofen, ketoprofen, naproxen, sulfamethoxazole, and sildenafil).

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

215 Naproxen transport was most efficient at neutral pH and

216 ointestinal (GI) system, with the background naproxen treatment possibly contributing.

217 Power analysis to determine superiority of naproxen treatment showed that a 12 per group sample siz

218 Naproxen use does not protect against serious coronary h

219 sers of rofecoxib, and a decreased rate with naproxen use.

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

222 The effect sizes for NSAIDs or naproxen versus placebo, as determined using data from r

223 For naproxen versus remote NSAID use the adjusted odds ratio

224 acks) with rofecoxib treatment compared with naproxen was 2.38 (95% confidence interval, 1.39-4.00; P

225 In contrast, the incidence with naproxen was 36 (26%) of 137, significantly greater than

226 olymeric nanomicelles containing aspirin and naproxen was 62 and 64%, respectively.

227 Naproxen was associated with a low risk.

228 es of the nonsteroidal antiinflammatory drug naproxen was designed to have both antiinflammatory and

229 When naproxen was directly compared with ibuprofen, the curre

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

232 inhibitors (flufenamic acid, ibuprofen, and naproxen) was also readily evaluated.

233 1/cyclo-oxygenase-2 inhibitors ibuprofen and naproxen were significant reduced by t-butylOOH.

234 Patients intolerant of naproxen were switched to a coxib.

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.

238 Patients administered naproxen who had prior upper GI complications or who wer

239 trated that SCC-25 cell monolayers transport naproxen with a Michaelis constant (K(m)) and maximum ve

240 To investigate the interactions of naproxen with Abeta dimers, which are the smallest cytot

241 was found to be noninferior to ibuprofen or naproxen with regard to cardiovascular safety.

242 ows a significant reduction in the dosage of naproxen without compromising pain relief.