ライフサイエンスコーパス: fasudil

1 an (fasudil and ripasudil) and one in China (fasudil).

2 ed by pharmacological ROCK1 inhibition using Fasudil.

3 neurons or treatment with the ROCK inhibitor fasudil.

4 ), and these impairments were abolished with fasudil.

5 nged with HDM extracts and then treated with fasudil.

6 pes by treatment with the ROCK/PKA inhibitor fasudil.

7 ogical intervention with the ROCK inhibitor, fasudil.

8 icial effects of ANG-(1-7) were prevented by fasudil.

9 y pretreatment with the rho kinase inhibitor fasudil.

10 udies revealed that the Rho-kinase inhibitor fasudil (1 micromol/L) significantly blunted artery cont

11 te experiments, diabetic db/db mice received fasudil (10 mg x kg(-) x day(-) i.p.) or simvastatin (40

12 als were randomly assigned to treatment with fasudil (136 or 213 mg x kg(-1) x d(-1) in drinking wate

13 ome mice also were given the ROCK1 inhibitor fasudil; 2 weeks later, serum EVs were isolated and char

14 tion-to-treat population comprised 35 in the fasudil 30 mg group, 39 in the fasudil 60 mg group, and

15 articipants in the placebo group, 108 in the fasudil 30 mg group, and 105 in the fasudil 60 mg group.

16 urred: two in the placebo group, four in the fasudil 30 mg group, and two in the fasudil 60 mg group.

17 was 0.00 (95% CI -0.11 to 0.10; p>0.99) for fasudil 30 mg versus placebo and 0.00 (-0.10 to 0.10; p>

18 was 0.07 (95% CI -0.05 to 0.20; p=0.25) for fasudil 30 mg versus placebo, and -0.03 (-0.18 to 0.10;

19 led and randomised; two individuals assigned fasudil 30 mg withdrew consent before the baseline visit

20 0.99) with placebo, 1.00 (0.90 to 1.00) with fasudil 30 mg, and 0.90 (0.76 to 0.97) with fasudil 60 m

21 1.00) with placebo, 1.00 (0.89 to 1.00) with fasudil 30 mg, and 1.00 (0.90 to 1.00) with fasudil 60 m

22 sed 35 in the fasudil 30 mg group, 39 in the fasudil 60 mg group, and 44 in the placebo group.

23 r in the fasudil 30 mg group, and two in the fasudil 60 mg group.

24 8 in the fasudil 30 mg group, and 105 in the fasudil 60 mg group.

25 placebo and 0.00 (-0.10 to 0.10; p>0.99) for fasudil 60 mg versus placebo.

26 acebo, and -0.03 (-0.18 to 0.10; p=0.70) for fasudil 60 mg versus placebo.

27 fasudil 30 mg, and 1.00 (0.90 to 1.00) with fasudil 60 mg; the difference in proportions was 0.00 (9

28 fasudil 30 mg, and 0.90 (0.76 to 0.97) with fasudil 60 mg; the difference in proportions was 0.07 (9

29 Fasudil, a clinically approved ROCK inhibitor, suppresse

30 nase (ROCK)/protein kinase A (PKA) inhibitor fasudil, a drug already tested on humans.

31 that was inhibited by treating animals with fasudil, a pharmacologic ROCK inhibitor, and that both R

32 The i.t. administration of fasudil, a Rho kinase inhibitor, reversed the hypertensi

33 inhibited by the clinically used vasodilator fasudil, a Rho-kinase inhibitor that blocks contractile

34 In this study, we tested the hypothesis that fasudil, a Rho-kinase inhibitor, could attenuate Ang II-

35 Similarly, fasudil, a ROCK inhibitor used clinically to treat cereb

36 creased vascular leak in vivo, reversible by fasudil, a ROCK inhibitor.

37 downstream from RhoA, we treated cells with fasudil, a selective Rho kinase inhibitor, and found tha

38 We examined whether fasudil, a selective Rho-A/Rho kinase inhibitor, affects

39 Fasudil, a selective Rho-A/Rho kinase inhibitor, has bee

40 Recent studies have shown that fasudil, a selective ROCK inhibitor, may play a pivotal

41 Compared to intravenous (IV) fasudil, a ~10 fold increase in the terminal plasma half

42 Fasudil administration significantly decreased the numbe

43 terestingly, blood glucose was unaffected by fasudil administration.

44 Fasudil also blocks habitual responding for cocaine, an

45 Fasudil also decreased the expression and phosphorylatio

46 Despite more occlusive vascular lesions, fasudil also markedly reduced right ventricular systolic

47 Fasudil also reduced mucous secretion and MUC5AC express

48 The ROCK inhibitor, fasudil, also reduced airway responsiveness in OVA-chall

49 ought to evaluate the efficacy and safety of fasudil, an orally available rho kinase inhibitor, in pa

50 t not systemic, effects of the vasodilators, fasudil and imatinib, in PAH rats.

51 e functionalization of the medicinal agents, fasudil and milrinone.

52 ave been approved for clinical use in Japan (fasudil and ripasudil) and one in China (fasudil).

53 enous catheter was used to administer saline/fasudil and sample venous plasma ATP ([ATP](V) ).

54 ctural fragments of the Rho kinase inhibitor fasudil and the NRF2 inducers caffeic and ferulic acids

55 e presence of Rho-effector kinase inhibitors Fasudil and Y-27632, but ATP-induced IL-1 beta release w

56 oactive and drug molecules such as caffeine, Fasudil, and Metyrapone.

57 Inhaled fasudil, another Rho kinase inhibitor, caused selective

58 However, fasudil as a monotherapy did not affect behavioral funct

59 mm ST-segment depression was increased with fasudil at both peak and trough compared with placebo (1

60 demonstrate that inhibition of Rho-kinase by fasudil attenuated Ang II-induced AAA through inhibition

61 Inhibition of Rho-kinase (ROCK) with fasudil blocked HG-induced podocyte MP formation.

62 human CCM endothelium, and they suggest that fasudil could ameliorate both CCM disease and vascular l

63 At the higher dose, fasudil decreased AAA by 45% while significantly inhibit

64 FSD-C10, a Fasudil derivative, was shown to reduce severity of expe

65 Fasudil did not affect heart rate or blood pressure, and

66 Further investigation of fasudil doses >80 mg three times daily is indicated.

67 Fasudil down-regulated the levels of IL-17, IL-4 and IL-

68 Treatment with fasudil during the postinflammatory fibrotic phase of lu

69 Co-administration of BI-2536 and fasudil either in the LSL-KRAS(G12D) mouse model or in a

70 We find that the inhibitor fasudil enhances action-outcome memory, resulting in goa

71 entrapment efficiency of optimized liposomal fasudil formulations was between 68.1+/-0.8% and 73.6+/-

72 tion of an investigational anti-PAH molecule fasudil (HA-1077), a Rho-kinase inhibitor, into liposoma

73 While acute administration of fasudil had no impact on seizure activity, seven weeks o

74 As fasudil has been safely used in humans, our results sugg

75 In preclinical studies, fasudil has been shown to attenuate neurodegeneration, m

76 petitive small molecule inhibitors (Y-27632, fasudil, hydroxyfasudil, and H-1152P).

77 s systemically with the Rho-kinase inhibitor fasudil improved blood flow and circulating ATP response

78 Fasudil improved Seattle Angina Questionnaire scores.

79 independent vasodilation was not affected by fasudil in either CAD or healthy subjects.

80 75%; P < 0.05), which tended to improve with fasudil in OA (P = 0.082).

81 te the safety, tolerability, and efficacy of fasudil in patients with amyotrophic lateral sclerosis.

82 In particular, the presence of fasudil in the solvent either modulates pre-existing sta

83 n's disease) binding the small-molecule drug fasudil in which the observed protein-ligand interaction

84 e hypothesis that Rho-kinase inhibition (via fasudil) in vivo would improve local haemodynamic and AT

85 Fasudil increased endothelium-dependent vasodilation in

86 transduction pathway with the ROCK inhibitor fasudil induced myofibroblast apoptosis through a mechan

87 bition of the spatial rescue of alpha2C-ARs, fasudil inhibited alpha2-AR-mediated mobilization of cal

88 Fasudil inhibited HDM extract-induced MUC5AC expression,

89 eased in lungs from both groups of rats, and fasudil (intravenous) reversed the increased phosphoryla

90 roof-of-principle that aerosolized liposomal fasudil is a feasible option for a non-invasive, control

91 Fasudil is a small molecule inhibitor of Rho-associated

92 Hydroxyfasudil, a metabolite of fasudil, may be selective for ROCK over PKA through a re

93 fter intratracheal instillation of liposomal fasudil, mean pulmonary arterial pressure (MPAP) was red

94 The effect of fasudil on efficacy outcomes should be explored in large

95 mg twice daily) or 60 mg (30 mg twice daily) fasudil or matched placebo intravenously for 20 days ove

96 Fasudil or matching placebo was force-titrated from 20 m

97 ucible exercise times were randomized 1:1 to fasudil or placebo.

98 prevented by inhibition of Rho kinase, using fasudil or RNA interference.

99 lockade of the RhoA/ROCK pathway with either fasudil or simvastatin would ameliorate progression of d

100 n A receptor blocker BQ123 and completely by fasudil or Y-27632.

101 ssigned to receive the Rho kinase inhibitor, fasudil, or placebo for 1 month each in a double-blind c

102 VC were lower in OA vs. YA and improved with fasudil (P < 0.05).

103 Pharmacological inhibition of MSK1 (H89, fasudil, PHA767491) was evaluated in the murine model an

104 ndicate that the Rho-A/Rho kinase inhibitor, fasudil, plays a negative regulatory role in allergen-in

105 ation of the Rho-associated kinase inhibitor fasudil prevented renal fibrosis and restored expression

106 activity, using the clinically approved drug fasudil, prevented dendritic network disorganization, me

107 its selective nature, our hypoxia-activated fasudil prodrug could be used to treat diseases where ti

108 Under normoxia the fasudil prodrug displayed significantly reduced activity

109 luding the FDA-approved drug belumosudil and fasudil, reactivate FXN expression in cultured FA iPSCs,

110 Fasudil reduced Rho kinase activity by 59+/-18% in CAD s

111 , non-placebo-controlled trials suggest that fasudil reduces myocardial ischemia in patients with sta

112 thelium-dependent vasodilation achieved with fasudil relative to placebo was inversely proportional t

113 , treatment with the approved ROCK inhibitor fasudil resulted in increased apoptosis and decreased vi

114 By masking fasudil's active site with a bioreductive 4-nitrobenzyl

115 f alphaS in neat water from those in aqueous fasudil (small molecule of interest) solution.

116 trobenzyl group, we synthesized a prodrug of fasudil that is inactive in normoxia.

117 a bioreductive prodrug of a ROCK inhibitor, fasudil, that functions selectively under hypoxic condit

118 Administration of the ROCK1 inhibitor fasudil to mice with NASH reduced serum levels of EVs; t

119 Fasudil transiently reduces prelimbic cortical dendritic

120 n systemic blood pressure when compared with fasudil-treated controls.

121 The fasudil-treated mice exhibited a significant reduction i

122 Fasudil treatment resulted in a dose-dependent reduction

123 hallenged with ovalbumin (OVA) followed with fasudil treatment.

124 Fasudil up to 80 mg three times daily significantly incr

125 ic FA mice of both sexes with belumosudil or fasudil upregulates FXN expression, ameliorates the mito

126 as numerically greater in patients receiving fasudil versus those receiving placebo.

127 The t1/2 of IV fasudil was 0.39+/-0.12 h.

128 When fasudil was administered 30 minutes before simvastatin (

129 plasma half-life was observed when liposomal fasudil was administered as aerosols.

130 Improved blood flow regulation with fasudil was also associated with increased skeletal musc

131 In 1995 fasudil was approved for the treatment of cerebral vasos

132 epared by hydration and extrusion method and fasudil was loaded by ammonium sulfate-induced transmemb

133 In the early group, intravenous fasudil was more effective than intravenous bradykinin,

134 Fasudil was well tolerated and safe in people with amyot

135 randomized trial, the efficacy and safety of fasudil were evaluated in stable angina patients.

136 In our simulations, fasudil, when bound, favored certain charge-charge and p

137 ffect of RhoA/ROCK inhibitors (C3-exoenzmye, fasudil, Y-27632, ibuprofen, siRhoA, and p21) in experim

138 Inhibition of Rho kinase (fasudil, Y27632 or H-1152) did not affect constriction o