ライフサイエンスコーパス: fluvastatin

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

2 h was sustained by sequential treatment with fluvastatin.

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

4 and high concentrations (10 mg/kg; FS-H) of fluvastatin.

5 d coronary atherosclerosis to treatment with fluvastatin.

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

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

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

9 ravastatin 10-20 mg, lovastatin 10-20 mg, or fluvastatin 20-40 mg).

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

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

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

13 n [5 mg, 10 mg], simvastatin [20 mg, 40 mg], fluvastatin [80 mg], pravastatin [40 mg, 80 mg], lovasta

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

15 at inhibition of the mevalonate pathway with fluvastatin, a clinically approved drug, reduces both N-

16 wth factor 1 receptor (IGF1R) inhibitor, and fluvastatin, an HMG-CoA reductase inhibitor, as potentia

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

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

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

20 inus (Ct) mutated Ggamma in cells exposed to Fluvastatin and prenyl transferase inhibitors and monito

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

22 Both fluvastatin and simvastatin increased iNOS mRNA and prot

23 Animals were treated with fluvastatin and/or aspirin for 16 weeks and the experime

24 Simvastatin, fluvastatin, and pravastatin showed the most favorable t

25 Fluvastatin area under the curve, maximum plasma concent

26 se data support the immediate repurposing of fluvastatin as an adjuvant therapeutic to combat metasta

27 on, warranting immediate clinical testing of fluvastatin as an adjuvant therapy for breast cancer.

28 We identified fluvastatin as an inducer of galectin-7 expression by co

29 e rat model to investigate whether injecting fluvastatin at extraction sites prevents MRONJ-like lesi

30 extracting teeth, and immediately injecting fluvastatin at the extraction site.

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

32 fect in keratinocytes, and demonstrated that fluvastatin attenuated IL-6 and IL-8 production induced

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

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

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

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

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

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

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

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

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

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

43 in-specific manner, with stronger effects by fluvastatin, followed by simvastatin and atorvastatin, a

44 ngs suggest that a single local injection of fluvastatin following tooth extraction can potentially r

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

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

47 The fluvastatin group achieved a much higher peak plasma con

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

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

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

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

52 ffective, while statins like simvastatin and fluvastatin having lower effectiveness.

53 Fluvastatin impaired insulin signaling in lipopolysaccha

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

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

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

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

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

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

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

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

62 separated levels of protein N-glycosylation, fluvastatin-induced tumor cell death was enhanced by los

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

64 Fluvastatin inhibited competitively with HMG-CoA, with a

65 Fluvastatin inhibition of Rab5 has been shown to mediate

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

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

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

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

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

71 Fluvastatin-mediated cholesterol depletion (-27.8%) lowe

72 this study, we aimed to assess the effect of fluvastatin-mediated cholesterol management on primary r

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

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

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

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

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

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

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

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

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

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

83 in independent public datasets by confirming fluvastatin, paclitaxel, and rosiglitazone perturbation

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

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

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

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

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

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

90 Fluvastatin selectively suppressed key FcepsilonRI signa

91 metastatic breast cancer cells depend on the fluvastatin-sensitive mevalonate pathway to support prot

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

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

94 Fluvastatin showed the most significant inhibitory effec

95 Fluvastatin significantly decreased GVD in a rat model p

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

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

98 Fluvastatin significantly reduced progression among low-

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

100 Fluvastatin, the first entirely synthetic HMG-CoA reduct

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

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

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

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

105 completed on A375 cells after treatment with fluvastatin to describe changes in the melanoma transcri

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

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

108 Finally, fluvastatin treatment in vivo reduced engraftment of BaF

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

110 lycosylation in the endoplasmic reticulum by fluvastatin treatment promoted the recruitment of CD44 a

111 tsurgical metastatic breast cancer, adjuvant fluvastatin treatment reduced metastatic burden and impr

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

113 nisms of resistance could be circumvented by fluvastatin treatment.

114 Similarly, fluvastatin was more effective in inhibiting cell prolif

115 Fluvastatin was well tolerated, with no evidence of myop

116 Atorvastatin and fluvastatin were associated with the most significant an

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

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

119 in Renal Transplantation), a study comparing fluvastatin with placebo in stable renal transplant reci