ライフサイエンスコーパス: fenofibrate

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

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

3 pharmaceutical drugs, such as pitofenone and fenofibrate.

4 6 weeks of oral administration of vehicle or fenofibrate.

5 Most patients (91%) were prescribed fenofibrate.

6 mal abrogated the potent antitumor effect of fenofibrate.

7 .5 mg/dL (34.9% to 41.7%) but was similar to fenofibrate.

8 wer than the marketed weak PPARalpha agonist fenofibrate.

9 therosclerosis drugs such as simvastatin and fenofibrate.

10 toma cells treated with the anticancer agent fenofibrate.

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

12 reduced inducibility of the MDR3 promoter by fenofibrate.

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

14 ole was predicted for the antilipidemic drug Fenofibrate.

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

16 compared to the effect of the standard drug fenofibrate.

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

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

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

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

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

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

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

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

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

26 Fenofibrate, a peroxisome proliferator-activated recepto

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

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

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

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

31 igated the cellular/molecular mechanisms for fenofibrate action.

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

33 Fenofibrate also ameliorated retinal NV in the oxygen-in

34 Fenofibrate also attenuated overexpression of intercellu

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

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

37 Fenofibrate also reduced electrically induced contractio

38 Fenofibrate also repressed the expression of the genes e

39 Fenofibrate also restored hepatic Sort1 protein levels i

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

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

42 Fenofibrate and bezafibrate are reasonable second-line t

43 Fenofibrate and bezafibrate are reasonable second-line t

44 Fenofibrate and gemfibrozil, previously reported to indu

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

46 Fenofibrate and LY518674 both raised safety concerns.

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

48 The PPARalpha agonist fenofibrate and overexpression of PPARalpha both attenua

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

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

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

52 Simvastatin, fenofibrate, and combination therapy each lowered hsCRP

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

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

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

56 Because gemfibrozil and fenofibrate are known to activate peroxisome proliferato

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

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

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

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

61 Fenofibrate but not cerivastatin reduces remnant lipopro

62 Fenofibrate, but not LY518674, increased creatine phosph

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 The benefits of fenofibrate for microvascular disease and its potential

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

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

89 Mice receiving fenofibrate had reduced suprarenal aortic diameter, redu

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

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

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

93 Further, fenofibrate improves retinal outcomes in rodent models o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 Fenofibrate inhibited Wnt signaling in the kidney of dia

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

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

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

117 In the Fenofibrate Intervention in Endpoint Lowering in Diabete

118 The Fenofibrate Intervention in Endpoint Lowering in Diabete

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

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

121 Fenofibrate is a peroxisome proliferator-activated recep

122 Fenofibrate is a peroxisome proliferator-activated recep

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

124 Fenofibrate is clinically successful in treating hypertr

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

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

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

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

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

130 Fenofibrate may be a potential new therapeutic option fo

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

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

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

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

135 Effects of fenofibrate on cytokine and chemokine gene expression we

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

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

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

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

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

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

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

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

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

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

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

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

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

149 among participants originally randomized to fenofibrate or placebo.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 In Canada, fenofibrate prescriptions increased from 321 prescriptio

165 Cerivastatin and fenofibrate reduce LDLIII concentration in nephrotic-ran

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

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

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

169 Fenofibrate reduced infarct size measured at 24 hours af

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

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

172 Fenofibrate regulates the expression of many different g

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

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

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

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

177 Fenofibrate's beneficial effects were blocked by a speci

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

179 Oral administration of fenofibrate significantly ameliorated retinal vascular l

180 Fenofibrate significantly reduced superoxide production

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

182 Fenofibrate significantly up-regulated MDR3 messenger RN

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

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

185 In addition, fenofibrate suppressed endothelial cell proliferation an

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

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

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

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

190 Fenofibrate therapy in 9795 patients comprising a mixed

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

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

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

194 In this study fenofibrate therapy was associated with reduced progress

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

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

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

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

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

200 Fenofibrate transactivates MDR3 gene transcription by wa

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

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

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

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

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

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

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

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

209 Fenofibrate treatment further stimulates biliary phospha

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

211 Fenofibrate treatment opposed the development of obesity

212 Fenofibrate treatment started within 1 week postburn and

213 e interindividual variability in response to fenofibrate treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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