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1 s was decreased in G6pc-/- mice treated with bezafibrate.
2 y ameliorated in the BACHD mice treated with bezafibrate.
3 P2C8 mRNA and protein levels were induced by bezafibrate.
4 as had previously been noted in a trial with bezafibrate.
5 ntly bound to the small molecule therapeutic bezafibrate.
6                 Patients received once-daily bezafibrate (400 mg) or placebo for 21 days.
7 atinine levels tended to mildly increase (3% bezafibrate, 5% placebo, P = .14).
8                         We hypothesized that bezafibrate, a broad peroxisome proliferator-activated r
9                               Preclinically, bezafibrate, a hyperlipidemia drug, upregulated CPT1A an
10 gulated in opposite manners by ritonavir and bezafibrate, a hypolipidemic agonist of the peroxisome p
11 DF rats were treated for 6 weeks with either bezafibrate, a lipid-lowering drug that does not affect
12                                              Bezafibrate, a pan-peroxisome proliferator-activated rec
13 cently, we showed that the administration of bezafibrate, a pan-PPAR agonist, increases the expressio
14 ntion of intracellular 4-HNE accumulation by bezafibrate, a peroxisome proliferator-activated recepto
15 l as activation of fatty acid oxidation with bezafibrate also protected Akt-expressing cells from glu
16                                              Bezafibrate also reduced serum alkaline phosphatase (-35
17                 We found that treatment with bezafibrate, an activator of mitochondrial biogenesis, a
18 proved for use in patients with PBC, whereas bezafibrate and fenofibrate are available as off-label t
19             A redeployed drug combination of bezafibrate and medroxyprogesterone acetate (BaP) has sh
20           The redeployed drug combination of bezafibrate and medroxyprogesterone acetate (designated
21 ranked highest for the primary outcome; both bezafibrate and seladelpar ranked highest for the second
22 nscription factor PPARalpha with the ligands bezafibrate and Wyeth-14,643.
23 n HepG2 cells, with a further increase after bezafibrate ( approximately 18-fold), 4-chloro-6-(2,3-xy
24                              Fenofibrate and bezafibrate are reasonable second-line therapies for dys
25                              Fenofibrate and bezafibrate are reasonable second-line therapies for dys
26                                              Bezafibrate (BEZ), a pan activator of peroxisome prolife
27                      For 5 of the chemicals (bezafibrate, climbazole, diclofenac, furosemide, and hyd
28 ternative, notably with the pan-PPAR agonist bezafibrate; clinical trial agents are also under develo
29 r concentrations than ionic PCs (metoprolol, bezafibrate, clofibric acid, diclofenac, gemfibrozil, ib
30 we demonstrate spatial mapping of the [FABP1+bezafibrate] complex across a thin section of liver by t
31                                              Bezafibrate decreased liver triglyceride and glycogen co
32 thology had developed, our data suggest that bezafibrate exerts a preventive effect on both tau patho
33  provide strong evidence that treatment with bezafibrate exerts neuroprotective effects which may be
34 ighlight the strong therapeutic potential of bezafibrate for treatment of HD.
35 mouse model of HD, we tested the efficacy of bezafibrate in a 'full-length' Htt mouse model, the BACH
36         Our data demonstrate the efficacy of bezafibrate in ameliorating both neuropathological featu
37              We found that administration of bezafibrate in the diet restored levels of PGC-1alpha, P
38                                  In summary, bezafibrate induced autophagy in the liver while increas
39 ed 15 355 patients who were screened for the Bezafibrate Infarction Prevention (BIP) trial.
40 analyses of the Helsinki Heart Study and the Bezafibrate Infarction Prevention Study.
41 n Trial, results of other studies, e.g., the Bezafibrate Intervention Program and the Diabetes Athero
42               Also, venlafaxine, acesulfame, bezafibrate, irbesartan, valsartan, ibuprofen and naprox
43                                 Moreover, as bezafibrate is a well-tolerated clinically approved drug
44                                              Bezafibrate is superior to placebo in improving moderate
45                                              Bezafibrate is therefore a promising agent for the treat
46 te that treatment with a PPAR-alpha agonist, bezafibrate, is able to reverse the miR-27b-induced lipi
47                 Hypolipidemic drugs, such as bezafibrate, known activators of the peroxisome prolifer
48                   For the primary end point, bezafibrate led in 45% (41% PSC, 55% PBC) and placebo in
49                   For the primary end point, bezafibrate led in 45% (41% PSC, 55% PBC) and placebo in
50 -lives (DT50) of diclofenac (<0.1-1.4 days), bezafibrate (&lt;0.1-4.8 days), sulfamethoxazole (2-33 days
51 r cholestatic ITCH) was to assess effects of bezafibrate on pruritus in patients with PSC, PBC, and S
52  studied the effects of the pan-PPAR agonist bezafibrate on tau pathology, inflammation, lipid metabo
53 human macrophages with the PPARalpha ligands bezafibrate or WY14643 inhibited OPN expression.
54 n the presence of inositol hexaphosphate and bezafibrate (or derivatives), liganded Hb at low pH (pH
55 roliferator-activated receptor-alpha agonist bezafibrate, or the nonsteroidal anti-inflammatory drug
56  activation of a PPARalpha-like receptor, as bezafibrate produced similar improvements in HS-fed flie
57                                              Bezafibrate ranked highest for the primary outcome; both
58                    For secondary end points, bezafibrate reduced morning (P = .01 vs placebo) and eve
59                                       L35, a bezafibrate-related compound, is one of the more potent
60                                     Finally, bezafibrate rescued lipid accumulation and apparent vacu
61 , treatment of type 2 diabetic patients with bezafibrate significantly decreased OPN plasma levels.
62 oglitazone), but not a PPAR-alpha activator (bezafibrate), strikingly diminished Egr-1 mRNA and prote
63 liferator-activated receptor (PPAR) agonists Bezafibrate, Tesaglitazar, and Pioglitazone on PCa tumor
64                                              Bezafibrate therefore exerts neuroprotective effects in
65 mal proliferator-activated receptor agonist, bezafibrate, to determine the drug's effect on liver met
66                                              Bezafibrate treatment also diminished microglial activat
67                                              Bezafibrate treatment lessened the rise in plasma TAG ob
68 pha to this PPARalpha response element after bezafibrate treatment of human hepatocytes.
69                                              Bezafibrate treatment prevented conversion of type I oxi
70                                              Bezafibrate treatment restored the impaired PPARgamma, P
71                                              Bezafibrate treatment significantly decreased tau hyperp
72 F1 gene augmentation and PGC1A induction via bezafibrate treatment supported the metabolic programmin
73                                        Since bezafibrate was given to the mice before tau pathology h
74                 Despite lowering plasma TAG, bezafibrate was not effective in preventing an increased
75 acologic treatment with the pan-PPAR agonist bezafibrate would correct a deficiency of PGC-1alpha and