ライフサイエンスコーパス: fluvastatin

1 tatin drugs (atorvastatin, rosuvastatin, and fluvastatin).

2 ed with an IC(50) within a range of 0.2-2muM fluvastatin.

3 d coronary atherosclerosis to treatment with fluvastatin.

4 Uptake in fluvastatin (0.056 +/- 0.011%, p < 0.0005) and diet with

5 arting dose was 32% for atorvastatin, 1% for fluvastatin, 10% for lovastatin and 22% for simvastatin.

6 Pravastatin (20 mg/kg per day) or fluvastatin (2 or 6 mg/kg per day) was added to the RAD

7 The pharmacokinetics and safety of fluvastatin, 20 mg/day, were evaluated in 20 hypercholes

8 carried forward were atorvastatin 20 mg/day, fluvastatin 40 mg/day + colestipol 20 g/day, lovastatin

9 ed in 12 stable RTR receiving everolimus and fluvastatin (80 mg/d).

10 rophilic statin, 50 mg. kg(-1). d(-1), n=9), fluvastatin (a cell-permeant lipophilic statin, 20 mg. k

11 We demonstrate that fluvastatin, an inhibitor of 3-hydroxy-3-methyl-glutaryl

12 e host mevalonate pathway with lovastatin or fluvastatin and fatty acid synthesis with 5-(tetradecylo

13 Pravastatin, fluvastatin and pitavastatin are considered to be the sa

14 Fluvastatin and simvastatin (5-10 mumol/L) treatment enh

15 Both fluvastatin and simvastatin increased iNOS mRNA and prot

16 Fluvastatin area under the curve, maximum plasma concent

17 Rats treated with fluvastatin, at either dose, had a significant (P< or =0

18 In vitro, fluvastatin, but not pravastatin, decreased numbers of r

19 Treatment with fluvastatin, but not pravastatin, decreased the degree o

20 y, we show that simvastatin, pravastatin and fluvastatin can induce PTEN expression in a dose-depende

21 atin (pravastatin) and four type II statins (fluvastatin, cerivastatin, atorvastatin, and rosuvastati

22 statin seems to be as safe as the everolimus/fluvastatin combination.

23 ous statins (eg, lovastatin, simvastatin, or fluvastatin) dramatically increased mitochondrial dysfun

24 Both simvastatin and fluvastatin enhanced nitric oxide ((.)NO) levels which w

25 In addition, fluvastatin exhibited growth-inhibitory properties on pr

26 itro and in vivo anti-fibrotic properties of fluvastatin (Flu).

27 Here, we studied fluvastatin (Fluva) and zoledronate (Zol), representativ

28 ed either normal saline solution or 15 mg/kg fluvastatin for 15 days.

29 ps of rabbits, in the fourth month, received fluvastatin (FS) (n = 6), low-dose MC (n = 7), high-dose

30 The fluvastatin group achieved a much higher peak plasma con

31 higher in the pravastatin group than in the fluvastatin group.

32 intima was lower in both the pravastatin and fluvastatin groups than in the placebo group, whereas th

33 n in vivo mouse model to investigate whether fluvastatin has an effect on decreasing both the adhesio

34 New lipophilic statins such as fluvastatin have antiinflammatory and antithrombogenic e

35 Fluvastatin impaired insulin signaling in lipopolysaccha

36 nical events, and response to treatment with fluvastatin in a well-characterized population.

37 benefits of the HMG-CoA reductase inhibitor fluvastatin in patients with low versus patients with hi

38 ring effect of rosuvastatin as compared with fluvastatin in RTR receiving everolimus.

39 tion study, a randomized controlled trial of fluvastatin in RTR.

40 a superior lipid-lowering effect compared to fluvastatin in stable RTR receiving everolimus.

41 ), as well as the response to treatment with fluvastatin in the Lipoprotein and Coronary Atherosclero

42 rfamily did not uniformly sensitize cells to fluvastatin, indicating that increased cellular demand f

43 Fluvastatin-induced activation of the NLRP3/caspase-1 pa

44 Resistance correlated with fluvastatin-induced upregulation of the statin target HM

45 Fluvastatin inhibited competitively with HMG-CoA, with a

46 These data demonstrate that fluvastatin is a potent suppressor of IgE-mediated MC ac

47 gh the predominant lipid-modifying effect of fluvastatin is to decrease LDL-C, patients with low HDL-

48 red the efficacy and safety of atorvastatin, fluvastatin, lovastatin, and simvastatin in patients wit

49 Similarly, higher doses of atorvasatin, fluvastatin, lovastatin, and simvastatin were associated

50 This suggests that metabolism of fluvastatin may be less affected by cyclosporine than th

51 FIB-4 score with atorvastatin (n = 944) and fluvastatin (n = 34) was -0.17 and -0.13, respectively (

52 tin) (CYP3A4-MET) or others (pravastatin and fluvastatin) (non-CYP3A4-MET).

53 The treatment effect of fluvastatin on minimum lumen diameter change was signifi

54 the starting dose than patients treated with fluvastatin or lovastatin, and significantly fewer (p <

55 at baseline and 12 weeks after therapy with fluvastatin or placebo in 320 subjects.

56 aseline and 2.5 years after randomization to fluvastatin or placebo.

57 aseline and 2.5 years after randomization to fluvastatin or placebo.

58 ine and 2.5 years following randomization to fluvastatin or placebo.

59 y was designed to investigate the effects of fluvastatin or pravastatin in a rodent model of GVD prod

60 a lesser response of apoA1 to treatment with fluvastatin (P=0.04).

61 patients (P=0.01); among low-HDL-C patients, fluvastatin patients had improved event-free survival co

62 e data lend further support for the study of fluvastatin, pravastatin, and other HMG-CoA reductase in

63 nant contribution to the binding affinity of fluvastatin, pravastatin, cerivastatin, and atorvastatin

64 us necessitating lipid-lowering therapy with fluvastatin, pravastatin, or atorvastatin.

65 Treatment with pravastatin, but not fluvastatin, preserved interstitial collagen content in

66 res from eight donors showed a wide range of fluvastatin responsiveness.

67 Fluvastatin selectively suppressed key FcepsilonRI signa

68 was sufficient to phenocopy the increase in fluvastatin sensitivity; knocking out ZEB1 reversed this

69 IgG-APS mice treated with fluvastatin showed significantly smaller thrombi, a redu

70 Fluvastatin showed the most significant inhibitory effec

71 Fluvastatin significantly decreased GVD in a rat model p

72 These findings indicate that fluvastatin significantly diminishes aPL-mediated thromb

73 pecific FXa inhibitor, hydroxychloroquine or fluvastatin significantly reduced FXa-induced and IgG-po

74 Fluvastatin significantly reduced progression among low-

75 In RTR already receiving fluvastatin, switching to rosuvastatin further decreased

76 Fluvastatin, the first entirely synthetic HMG-CoA reduct

77 nd its progression/regression in response to fluvastatin therapy in the Lipoprotein and Coronary Athe

78 In response to fluvastatin therapy, subjects with DD, compared with tho

79 e had less reduction in LDL cholesterol with fluvastatin, they had similar benefit in terms of CAD pr

80 the C57BL/6J mouse strain were responsive to fluvastatin, those from 129/SvImJ mice were completely r

81 in these patients support the broader use of fluvastatin to treat hypercholesterolemia in renal trans

82 ly reduced after diet withdrawal (n = 6) and fluvastatin treatment (n = 6); no uptake was observed in

83 Finally, fluvastatin treatment in vivo reduced engraftment of BaF

84 Long-term fluvastatin treatment of obese mice impaired insulin-sti

85 L-3 compensatory pathway were all negated by fluvastatin treatment.

86 nisms of resistance could be circumvented by fluvastatin treatment.

87 Fluvastatin was well tolerated, with no evidence of myop

88 Atorvastatin and fluvastatin were associated with the most significant an

89 Atorvastatin and fluvastatin were found to be potent inducers of cell dif

90 The effects of fluvastatin were reversed by mevalonic acid or geranylge