ライフサイエンスコーパス: fenofibrate

1 cipants, 74 had complete data (35 niacin, 39 fenofibrate).

2 e were orally treated with PPARalpha agonist fenofibrate.

3 onditions and by lipid-lowering fish oil and fenofibrate.

4 ole was predicted for the antilipidemic drug Fenofibrate.

5 e up-regulated in aortas from mice receiving fenofibrate.

6 compared to the effect of the standard drug fenofibrate.

7 te hind-paw perfusion recovery after feeding fenofibrate.

8 6 weeks of oral administration of vehicle or fenofibrate.

9 Most patients (91%) were prescribed fenofibrate.

10 mal abrogated the potent antitumor effect of fenofibrate.

11 .5 mg/dL (34.9% to 41.7%) but was similar to fenofibrate.

12 -induced diabetes and ameliorated by feeding fenofibrate.

13 wer than the marketed weak PPARalpha agonist fenofibrate.

14 therosclerosis drugs such as simvastatin and fenofibrate.

15 seen in patients with diabetes treated with fenofibrate.

16 lic acid and an increase after they were fed fenofibrate.

17 pharmaceutical drugs, such as pitofenone and fenofibrate.

18 sed in diabetic mice, which was prevented by fenofibrate.

19 toma cells treated with the anticancer agent fenofibrate.

20 s, as demonstrated by the rapid synthesis of fenofibrate.

21 reduced inducibility of the MDR3 promoter by fenofibrate.

22 iferator-activated receptor-alpha activators fenofibrate (100 micromol/L) and Wy-14649 (100 micromol/

23 Fenofibrate (145 mg tablet) was self-administered daily

24 g, or a combination of simvastatin 20 mg and fenofibrate 160 mg daily.

25 domly assigned to receive simvastatin 20 mg, fenofibrate 160 mg, or a combination of simvastatin 20 m

26 tients with baseline hsCRP levels >2.0 mg/l (fenofibrate = -18.9%, p = 0.002 vs. baseline; simvastati

27 iacin 1500 mg/day with aspirin 325 mg/day or fenofibrate 200 mg/day for 24 weeks.

28 Dyslipidemia study: placebo, fenofibrate (200 mg), or LY518674 (10, 25, 50, or 100 mi

29 Fenofibrate (30 mg/kg) increased mRNA levels of all thre

30 A(2) greater than the median of 320.9 ng/ml (fenofibrate = -41.3%, p < 0.0001; simvastatin = -47.5%,

31 Additionally, treating mice with fenofibrate, a clinical PPARalpha agonist used for hypol

32 ased by treatment of glioblastoma cells with fenofibrate, a lipid-lowering drug with multiple antican

33 Fenofibrate, a peroxisome proliferator-activated recepto

34 ependent clinical studies have reported that fenofibrate, a peroxisome proliferator-activated recepto

35 Fenofibrate, a peroxisome proliferator-activated recepto

36 Fenofibrate, a peroxisome proliferator-activated recepto

37 Fenofibrate, a PPARa agonist and lipid-lowering agent, d

38 Fenofibrate, a PPARalpha agonist and lipid-lowering agen

39 Additionally, we show that fenofibrate, a PPARalpha agonist, increased the expressi

40 Activating PPARalpha by fenofibrate, a PPARalpha agonist, restores lipid homeost

41 a-deficient tumors were still susceptible to fenofibrate, absence of PPARalpha in the host animal abr

42 Functionally, fenofibrate acted as an agonist at the CB2 receptor (pEC

43 igated the cellular/molecular mechanisms for fenofibrate action.

44 inally, treatment with the PPARalpha agonist fenofibrate activated the integrated stress response and

45 rol Cardiovascular Risk in Diabetes trial of fenofibrate added to baseline simvastatin therapy in dia

46 19 were given 145 mg/day of nanocrystallized fenofibrate added to the standard of care.

47 Fenofibrate also ameliorated retinal NV in the oxygen-in

48 Fenofibrate also attenuated overexpression of intercellu

49 PPARalpha WT mice fed fenofibrate also had a fivefold increase in LPS-induced

50 Fenofibrate also induced autophagy and promoted beta-oxi

51 Fenofibrate also reduced %LDLIII from 60 to 33% (P: < 0.

52 Fenofibrate also reduced electrically induced contractio

53 Fenofibrate also repressed the expression of the genes e

54 Fenofibrate also restored hepatic Sort1 protein levels i

55 However, fenofibrate, an activator of PPARalpha, aggravated liver

56 potent Abeta42-raising agents identified are fenofibrate, an antilipidemic agent, and celecoxib, a CO

57 Fenofibrate and bezafibrate are reasonable second-line t

58 Fenofibrate and bezafibrate are reasonable second-line t

59 Fenofibrate and gemfibrozil, previously reported to indu

60 micked by the PPAR-alpha synthetic agonists, fenofibrate and GW7647, and were prevented by PPAR-alpha

61 Fenofibrate and LY518674 (50 microg and 100 microg) incr

62 Fenofibrate and LY518674 both raised safety concerns.

63 Also, lipid-lowering drugs fenofibrate and niacin reduced liver KC content, accompa

64 The PPARalpha agonist fenofibrate and overexpression of PPARalpha both attenua

65 rthermore, neuroprotective agents, including fenofibrate and simvastatin, induced NEAT1 up-regulation

66 fatty acid catabolism, which is promoted by fenofibrate and synergistic with immune checkpoint block

67 hat influences the cardiovascular effects of fenofibrate and that could be used to identify patients

68 by Med1 and also by the PPARalpha activators fenofibrate and Wy-14,643.

69 ed that the decrease in insulin secretion by fenofibrate and Wy14643 is accompanied by reduction in i

70 Simvastatin, fenofibrate, and combination therapy each lowered hsCRP

71 ure present in a common lipid-lowering drug, fenofibrate, and in our first prototype glioblastoma dru

72 -activated receptor alpha (PPARalpha) ligand fenofibrate, and the PPARdelta ligand GW0742, in IL-10(-

73 To examine the effect of discontinuation of fenofibrate, another animal group treated with fenofibra

74 The present findings suggest that fenofibrate antagonizes AngII-induced AAA and atheroscle

75 n patients with PBC, whereas bezafibrate and fenofibrate are available as off-label therapies.

76 Because gemfibrozil and fenofibrate are known to activate peroxisome proliferato

77 st and consistent clinical data to recommend fenofibrate as an adjunctive treatment for early diabeti

78 d material (beeswax) as the drug carrier and fenofibrate as the drug.

79 (during the whole treatment) and ranitidine-fenofibrate (at short periods) in the BTV biopiles in re

80 Notably, liganding PPARalpha through fenofibrate attenuated hepatic inflammation in both MCD-

81 Fenofibrate but not cerivastatin reduces remnant lipopro

82 osphorylation in ECs, which was rescued with fenofibrate but not PC16:0/18:1.

83 osphorylation in ECs, which was rescued with fenofibrate but not PC16:0/18:1.

84 Fenofibrate, but not LY518674, increased creatine phosph

85 These findings show that fenofibrate can rapidly decrease hepatic glycogen and tr

86 25 657 in the TZDs cohort, and 18 606 in the fenofibrates cohort.

87 ificantly increased in PPARalpha KO mice fed fenofibrate compared to those in control-fed animals.

88 itched from beneficial to deleterious as the fenofibrate concentration increased leading to liver inj

89 nt safety profile, our findings suggest that fenofibrate could be a potential pharmacological therapy

90 In DR management, fenofibrate could be a useful adjunctive treatment to mo

91 Our results showed that fenofibrate could potentially be a novel treatment for p

92 Five-day administration of fenofibrate decreased the elevated hepatic and renal tri

93 In patients with dyslipidemia, LY518674 and fenofibrate decreased triglycerides and increased HDL-C

94 Treatment of C3H.IL-10(-/-) mice with fenofibrate delayed the onset of colitis, decreased the

95 automated parallel synthesis of a library of Fenofibrate derivatives.

96 ith type 2 diabetes mellitus, and found that fenofibrate did not affect any of the adverse cardiovasc

97 pled with cell surface biotinylation assays, fenofibrate did not inhibit SR-BI trafficking to the pla

98 Our results show that OM-3CA and fenofibrate differentially modulate the plasma mediator

99 Surprisingly, fenofibrate does not repress LXR-induced transcription o

100 ARalpha-knockout mice, indicating that these fenofibrate effects are largely PPARalpha independent.

101 from fenofibrate-fed mice demonstrated that fenofibrate enhanced the degradation of SR-BI in a post-

102 Together, the data support a model in which fenofibrate enhances the degradation of SR-BI in a post-

103 Here we show that fenofibrate ester, but not fenofibric acid, functions as

104 The PPAR-alpha agonist fenofibrate exhibited submicromolar affinity for both re

105 In the United States, crude fenofibrate expenditures increased from $11,535/100,000

106 Fenofibrate exposure significantly increased liver but n

107 h fructose (HFru) diet with the treatment of fenofibrate (FB) 100 mg/kg/day, a peroxisome proliferato

108 In vivo studies of fenofibrate-fed Berkeley sickle mice resulted in increas

109 ling experiments in primary hepatocytes from fenofibrate-fed mice demonstrated that fenofibrate enhan

110 acebo (PLA) or 5 mg/kg of PPAR-alpha agonist fenofibrate (FEN) treatment, within 3 weeks of injury.

111 -term safety and efficacy of co-administered fenofibrate (FENO) and ezetimibe (EZE) in patients with

112 Fenofibrate (FF) is a common lipid-lowering drug and a p

113 nation of rosiglitazone (RGZ) (8 mg/day) and fenofibrate (FFB) (160 mg/day) in a single-blind placebo

114 study participants continued treatment with fenofibrate following completion of ACCORD.

115 study reveals a novel use of gemfibrozil and fenofibrate, Food and Drug Administration-approved lipid

116 type and D2-deficient mice were treated with fenofibrate for 14 days.

117 schemic brain, separate animals treated with fenofibrate for 7 days were subjected to 60 minutes of f

118 The benefits of fenofibrate for microvascular disease and its potential

119 Unexpected benefits were seen with fenofibrate for microvascular endpoints including microa

120 y-14,643 or the clinically used fibrate drug fenofibrate, fully protects mice from APAP-induced hepat

121 Mice receiving fenofibrate had reduced suprarenal aortic diameter, redu

122 The drug fenofibrate has received major attention as a novel medi

123 Fenofibrate has the potential to be an effective therape

124 pha agonists, gemfibrozil, ciprofibrate, and fenofibrate, have an excellent track history as oral age

125 analysis parameters, specifically niacin and fenofibrate, have not been shown to additionally reduce

126 erienced a 51% MACE reduction in response to fenofibrate (hazard ratio 0.49; 95% CI 0.34-0.72), where

127 Further, fenofibrate improves retinal outcomes in rodent models o

128 ials are needed to establish the benefits of fenofibrate in other forms of diabetes, including type 1

129 ned with higher potency and selectivity than fenofibrate in PPARalpha agonism.

130 the second study to confirm the benefits of fenofibrate in reducing diabetic retinopathy progression

131 primary male T cells abolished the effect of fenofibrate in reducing IFN-gamma production.

132 yl-CoA transporter that is highly induced by fenofibrate in the livers of mice.

133 f action will help to refine how best to use fenofibrate in the management of diabetic retinopathy.

134 ants confirms the original neutral effect of fenofibrate in the overall study cohort.

135 The novel therapeutic activity of fenofibrate in this mouse model suggests that it may als

136 Interestingly, fenofibrate in vivo and FFA in vitro reversed high gluco

137 the use of PPARalpha ligand therapy, such as fenofibrate, in various cholestatic liver disorders.

138 Dyslipidemia study: LY518674 (25 mug) and fenofibrate increased HDL-C by 5.9 and 5.5 mg/dL (15.8%

139 amine and docosapentaenoyl ethanolamine, and fenofibrate increased palmitoleoyl ethanolamine, the eff

140 ich cultured rat hepatocytes, treatment with fenofibrate increased secretion of fluorescent PC into b

141 de, prescriptions for fibrates (particularly fenofibrate) increased in the United States, while presc

142 LY518674, but not fenofibrate, increased LDL-C.

143 le CD4(+) T cells with the PPARalpha agonist fenofibrate induced the recruitment of PPARalpha and the

144 Moreover, fenofibrate-induced degradation of SR-BI was independent

145 e lysosome, and antioxidants did not inhibit fenofibrate-induced degradation of SR-BI.

146 urthermore, Pparalpha knockout abolished the fenofibrate-induced downregulation of VEGF and reduction

147 ide a potential therapeutic approach whereby fenofibrate-induced miR-199a2 expression can ameliorate

148 erol response to a high-fat meal and greater fenofibrate-induced reduction of fasting triacylglycerol

149 Oral administration of gemfibrozil and fenofibrate inhibited clinical signs of experimental aut

150 Fenofibrate inhibited Wnt signaling in the kidney of dia

151 de not only an unexpected mechanism by which fenofibrate inhibits lipogenesis but also the basis for

152 ophoretic mobility shift assays suggest that fenofibrate inhibits VCAM-1 transcription in part by inh

153 ne also known as eotaxin (P for rs6008845-by-fenofibrate interaction = 0.003).

154 The rs6008845-by-fenofibrate interaction on MACE was replicated in Africa

155 jor randomized controlled trials: the FIELD (Fenofibrate Intervention and Event Lowering in Diabetes)

156 In the Fenofibrate Intervention in Endpoint Lowering in Diabete

157 The Fenofibrate Intervention in Endpoint Lowering in Diabete

158 ions and the response to a high-fat meal and fenofibrate interventions.

159 chanisms implicated in the mode of action of fenofibrate involve lipid and nonlipid pathways, includi

160 Fenofibrate is a peroxisome proliferator-activated recep

161 Fenofibrate is a peroxisome proliferator-activated recep

162 However, fenofibrate is also associated with adverse effects, inc

163 could account for these findings given that fenofibrate is an AMPK activator.

164 Moreover, since fenofibrate is an FDA-approved drug that has an excellen

165 Fenofibrate is clinically successful in treating hypertr

166 Fenofibrate is thus identified as an example of a new cl

167 the combination of low-dose simvastatin and fenofibrate is well tolerated, and is potentially cardio

168 that the activation of PPAR-alpha action via fenofibrate leads to neuroprotection by both reducing ne

169 Fenofibrate lowered cholesterol (19%), triglyceride (41%

170 ntial effects on chronic inflammation, while fenofibrate mainly reducing ceramides.

171 in liver or in macrophages, suggesting that fenofibrate manifests variable biocharacter in the conte

172 In this study, we demonstrate that fenofibrate markedly attenuates diabetes-related impairm

173 Fenofibrate may be a potential new therapeutic option fo

174 ate on diabetic retinopathy, and showed that fenofibrate may be used to reduce the risk of progressio

175 PPAR alpha agonists such as gemfibrozil and fenofibrate, may be attractive candidates for use in hum

176 ), the role of PPARalpha in gemfibrozil- and fenofibrate-mediated up-regulation of TPP1 was investiga

177 bel, randomized clinical trial of once-daily fenofibrate monotherapy administered for 2- (Mo2) and 4-

178 Fenofibrate monotherapy for Mo2 and Mo4 initiated in per

179 61.1%] male; 3024 [51.8%] White) and 144 417 fenofibrate nonusers (mean [SD] age, 65.7 [12.3] years;

180 present study aimed to assess the effects of fenofibrate on aortic dilatation in a mouse model of AAA

181 Effects of fenofibrate on cytokine and chemokine gene expression we

182 tiple mechanisms may underpin the benefit of fenofibrate on diabetic microvascular end points.

183 st partially, for the therapeutic effects of fenofibrate on diabetic nephropathy.

184 to the sparse clinical data on the effect of fenofibrate on diabetic retinopathy, and showed that fen

185 e results demonstrate therapeutic effects of fenofibrate on DR in type 1 diabetes and support the exi

186 This study evaluated the efficacy of fenofibrate on DR in type 1 diabetes models and determin

187 kout (KO) mice, we showed that the effect of fenofibrate on LPS-induced TNF expression was indeed med

188 -wide significant influence on the effect of fenofibrate on major cardiovascular events (MACE) among

189 efinitively demonstrating that the effect of fenofibrate on SR-BI is PDZK1-independent.

190 ts of a statin (cerivastatin) and a fibrate (fenofibrate) on LDLIII and RLP in 12 patients with nephr

191 oliferated activated receptor alpha agonist, fenofibrate, on liver and kidney autophagy and lipid met

192 e also achieved by intravitreal injection of fenofibrate or another specific PPARalpha agonist.

193 tration of either of the PPARalpha agonists, fenofibrate or clofibric acid, increases hepatic and ren

194 ARalpha null mice that had been treated with fenofibrate or gemfibrozil for 7 days.

195 The effect of fenofibrate or GW0742 on the progression of colitis in C

196 f study participants previously treated with fenofibrate or masked placebo.

197 s treated with simvastatin and randomized to fenofibrate or placebo in the ACCORD-Lipid trial.

198 among participants originally randomized to fenofibrate or placebo.

199 CD-1 mice treated with dietary fenofibrate or Wy-14,643 had fivefold-higher lipopolysac

200 ured human ECs with the PPARalpha activators fenofibrate or WY14643 inhibited TNF-alpha-induced VCAM-

201 ice a high fat diet supplemented with either fenofibrate or Wy14643, a selective PPARalpha agonist, a

202 an of 3 mg/dL with niacin and 6.5 mg/dL with fenofibrate (P < .001 for both).

203 ian of 16 mg/dL with niacin and 8 mg/dL with fenofibrate (P = .08 for both).

204 iacin (P = .28) and +0.5% (-1.0 to 3.0) with fenofibrate (P = .19).

205 from pyruvate increased significantly after fenofibrate (P = 0.001) and was accompanied by maintaine

206 for the 100-mug dose vs 0.3 mg/dL (2.3%) for fenofibrate (P< or =.01).

207 The dyslipidemia trial compared fenofibrate plus simvastatin with placebo plus simvastat

208 (ACCORD) trial, which assessed therapy with fenofibrate plus statins.

209 nsistent with its LXR antagonistic activity, fenofibrate potently represses LXR agonist-induced trans

210 Surprisingly, the PPARalpha agonist fenofibrate potently suppressed primary tumor growth in

211 The target for fenofibrate, PPARalpha, was expressed in lymphocytes, ma

212 In the United States, fenofibrate prescriptions dispensed increased from 150 p

213 In Canada, fenofibrate prescriptions increased from 321 prescriptio

214 Cerivastatin and fenofibrate reduce LDLIII concentration in nephrotic-ran

215 Instead, fish oil and fenofibrate reduced circulating and hepatic fatty acids

216 A 3-week course of fenofibrate reduced fasting interstitial glucose and inf

217 Fenofibrate reduced first laser treatment by 31% (P = .0

218 Fenofibrate reduced IEL density in the duodenum of dogs

219 heral blood cells (PBMC), and, as predicted, Fenofibrate reduced IL17 and IFN-gamma gene expression i

220 Fenofibrate reduced infarct size measured at 24 hours af

221 Fenofibrate reduced plasma concentrations of vasoactive

222 Fenofibrate reduced the use of glucose by tumor and stro

223 To determine whether fenofibrate reduces CVD risk in statin-treated patients

224 In addition, how fenofibrate regulates lipid metabolism differently in th

225 Here we examined the mechanism by which fenofibrate regulates MDR3 gene expression.

226 Fenofibrate regulates the expression of many different g

227 scovered a potential off-target liability of fenofibrate-related compounds, and in a comprehensive pr

228 s compared with control IL-10(-/-) mice, and fenofibrate repressed interferon-gamma and IL-17 express

229 and tissue recovery after ischemia and that fenofibrate rescues CEPT1-mediated activation of PPARalp

230 We conclude that fenofibrate rescues diabetic impairment in ischemia-medi

231 The PPARalpha agonist fenofibrate rescues the impaired axon regeneration in mi

232 re we show that feeding PDZK1-deficient mice fenofibrate resulted in the near absence of SR-BI in liv

233 Metabolism-focused drug screen showed that fenofibrate reversed lipid accumulation and blocked SARS

234 ctivating PPARalpha, the lipid-lowering drug fenofibrate reverses dyslipidemia and improves insulin s

235 Fenofibrate's beneficial effects were blocked by a speci

236 ducing diabetic retinopathy progression, and fenofibrate should be considered for treatment of diabet

237 Oral administration of fenofibrate significantly ameliorated retinal vascular l

238 Fenofibrate significantly reduced superoxide production

239 y demonstrated that the lipid-lowering agent fenofibrate significantly reduces the development and pr

240 Fenofibrate significantly up-regulated MDR3 messenger RN

241 p analysis showed a significant benefit from fenofibrate-simvastatin combination therapy over simvast

242 tes mellitus, of whom 5701 were treated with fenofibrate (+/- statin) for up to 5 years.

243 In addition, fenofibrate suppressed endothelial cell proliferation an

244 alpha) by the PPAR-alpha agonists GW7647 and fenofibrate synergizes with the glucocorticoid receptor

245 In contrast to the beneficial effect of fenofibrate, the PPARdelta ligand GW0742 accelerated the

246 D Lipid trial studied the additive effect of fenofibrate therapy along with low-dose simvastatin ther

247 results, we continued to find evidence that fenofibrate therapy effectively reduced CVD in study par

248 Fenofibrate therapy in 9795 patients comprising a mixed

249 that may contribute to the beneficial use of fenofibrate therapy in human cholestatic liver disease.

250 nt response by baseline lipids suggests that fenofibrate therapy may reduce CVD in patients with diab

251 ed primary and secondary prevention cohorts, fenofibrate therapy resulted in an 11% reduction in coro

252 Fenofibrate therapy upregulated the peroxisome prolifera

253 In this study fenofibrate therapy was associated with reduced progress

254 investigating the systemic administration of fenofibrate, this ligand for peroxisome proliferator-act

255 trial, in our view, supports the addition of fenofibrate to statin therapy in patients with T2DM and

256 provide support for the general addition of fenofibrate to statin-treated patients with type 2 diabe

257 , endpoint trials of adding either niacin or fenofibrate to statins have not shown any benefit, excep

258 We administered fenofibrate to superoxide dismutase 1 (SOD1(G93A)) mice

259 for all covariates, Cox model results showed fenofibrates to be associated with a decreased risk of V

260 Fenofibrate transactivates MDR3 gene transcription by wa

261 ased by more than 75% in colonic sections of fenofibrate-treated as compared with control IL-10(-/-)

262 euronal loss was significantly attenuated in fenofibrate-treated mice.

263 of DME (HR: 0.77, 95% CI: 0.70-0.85), as did fenofibrate-treated patients (HR: 0.83, 95% CI: 0.68-0.9

264 Serum creatinine increased with fenofibrate treatment (14%, P: < 0.01); however, creatin

265 to insulin increased significantly following fenofibrate treatment (P = 0.04 for both).

266 o suppress hepatic glucose release following fenofibrate treatment (P = 0.06).

267 Early fenofibrate treatment 3 days after vaccination improved

268 ction in LDLIII concentration and RLP-C with fenofibrate treatment correlated with plasma triglycerid

269 ducing glucose-stimulated insulin secretion, fenofibrate treatment does not result in insulin insuffi

270 Despite improvements in lipids, niacin or fenofibrate treatment for 24 weeks did not improve endot

271 Fenofibrate treatment further stimulates biliary phospha

272 In-vivo Fenofibrate treatment of an experimental rodent model of

273 Fenofibrate treatment opposed the development of obesity

274 urine model of hindlimb ischemia, daily oral fenofibrate treatment restored diabetes-impaired blood f

275 Fenofibrate treatment started within 1 week postburn and

276 , but not among carriers of other genotypes, fenofibrate treatment was associated with lower circulat

277 duction in nerve edema after 30 days of oral fenofibrate treatment, as evidenced by significant impro

278 ype 2 diabetes who would derive benefit from fenofibrate treatment, in addition to those with atherog

279 and mice, which were partially prevented by fenofibrate treatment.

280 e interindividual variability in response to fenofibrate treatment.

281 astatin treatment and 133 +/- 95 mg/dl after fenofibrate treatment.

282 at corneas, which were partially restored by fenofibrate treatment.

283 HDL-C (19%, P: < 0.01) increased with fenofibrate treatment; LDL-C and total LDL were unchange

284 further tested whether a PPARalpha agonist (fenofibrate) treatment improves the hepatic phenotype in

285 esent study, we investigated the efficacy of fenofibrate (Tricor), a pan-PPAR agonist that activates

286 Both gemfibrozil and fenofibrate up-regulated mRNA, protein, and enzymatic ac

287 The annual ratio of generic to brand-name fenofibrate use in the United States ranged from 0:1 to

288 In this study, fenofibrate use was associated with a decreased risk of

289 A total of 5835 fenofibrate users with NPDR at baseline (mean [SD] age,

290 among participants originally randomized to fenofibrate vs placebo (HR, 0.93; 95% CI, 0.83-1.05; P =

291 nofibrate, another animal group treated with fenofibrate was examined on post-discontinuation day 3 (

292 Fenofibrate was more efficacious than OM-3CA in signific

293 To assess the immunregulatory action of Fenofibrate, we conducted in-vitro treatment of anti-CD3

294 from mice treated with the PPARalpha agonist fenofibrate, we confirmed the specificity of the RNAi re

295 High concentrations of fenofibrate were able to increase the dissociation rate

296 studies investigating the mode of action of fenofibrate were reviewed.

297 t-hoc analysis, slight beneficial effects of fenofibrate were seen in patients with moderate hypertri

298 al epithelial lesion, which was prevented by fenofibrate while exacerbated by PPARalpha knockout.

299 , bile-acid sequestering agents, niacin, and fenofibrate with moderate dose statins appears to be rea

300 ession was observed in patients treated with fenofibrate, with no effect observed with intensive bloo