ライフサイエンスコーパス: clotrimazole

1 s, including the antifungal voriconazole and clotrimazole.

2 ose dependent and recovered after washout of clotrimazole.

3 tments but was up-regulated by reserpine and clotrimazole.

4 ed pharmacokinetic properties compared to 1, Clotrimazole.

5 activities that are relatively resistant to clotrimazole.

6 t test) in arginine-supplemented mice versus clotrimazole.

7 terconazole, 66% for miconazole, and 53% for clotrimazole.

8 were not affected by 17-ODYA (10 microM) or clotrimazole (10 microM), inhibitors of the cytochrome P

9 fungal voriconazole (2.35 A), and antifungal clotrimazole (2.50 A).

10 dazole promoted iNOSox dimerization, whereas clotrimazole (30 microM) and miconazole (15 microM) did

11 When added to cells expressing iNOS, clotrimazole (50 microM) had no effect on iNOS protein e

12 of apamin 1 microM, iberiotoxin 200 nM, and clotrimazole 500 nM; 3) blocking remaining K(+) current

13 the synthesis of 7alpha,25-OHC in vivo with clotrimazole, a CYP7B1 inhibitor, reduced the content of

14 specific inhibitor of EET biosynthesis, and clotrimazole, a cytochrome P450 inhibitor, significantly

15 Clotrimazole, a membrane-permeant triarylmethane, blocke

16 We report that clotrimazole, a potent antiproliferative agent both in v

17 The antimycotic clotrimazole, a potent inhibitor of the intermediate-con

18 bjects who have sickle cell anemia with oral clotrimazole, a specific Gardos channel inhibitor.

19 Clotrimazole also bound to iNOSox dimers in the absence

20 It is noteworthy that clotrimazole also functions as a ligand activator of CAR

21 The effect was prevented by clotrimazole, an inhibitor of the Ca2+-sensitive K+ (KCa

22 used a rational design strategy to develop a clotrimazole analog that selectively inhibits IKCa1 with

23 iously to mediate sensitivity of K(Ca)3.1 to clotrimazole and 1-[(2-chlorophenyl)diphenylmethyl]-1H-p

24 It was sensitive to block by clotrimazole and could be potently and reversibly potent

25 ers able to activate both receptors, such as clotrimazole and dieldrin.

26 ween methods was observed for miconazole and clotrimazole and for C. krusei isolates tested against t

27 (K(Ca)) with components sensitive to apamin, clotrimazole and iberiotoxin.

28 (Kd ~107 and ~12 muM), whereas ketoconazole, clotrimazole and itraconazole bound strongest to CYP5218

29 y the same binding affinity as econazole and clotrimazole and ketoconazole with somewhat lower affini

30 ol (DTT) and by cytochrome P-450 inhibitors (clotrimazole and miconazole), we measured the carotid si

31 mpletely reversed the suppressant effects of clotrimazole and NaCN on ICa.

32 s with the exceptions only of miconazole and clotrimazole and of terconazole against C. krusei isolat

33 ing point the biological activity spectra of clotrimazole and tioconazole because their putative targ

34 The IK channel blockers clotrimazole and TRAM-34 inhibited whole cell swelling-a

35 magnitudes of inhibition were observed with clotrimazole and TRAM-34.

36 posaconazole) and topically (miconazole and clotrimazole) and by a tetrazole-based drug candidate, V

37 of CYP46A1 in complex with voriconazole and clotrimazole, and in the present work we cocrystallized

38 Imidazole, 1-phenylimidazole, clotrimazole, and miconazole all bound to the iNOSox mon

39 -normalized doses of tacrolimus, prednisone, clotrimazole, and statins.

40 istent with channel blockade, charybdotoxin, clotrimazole, and the highly selective IKCa1 inhibitors,

41 The EDC selected was clotrimazole (at 2 mug/L and 10 mug/L), a widely used an

42 ne pharmacophore of chloroquine with that of clotrimazole-based antimalarials.

43 g the heme iron via their nitrogen atoms and clotrimazole being at a 4 A distance from the heme iron.

44 hibition at concentrations below 100 microM: clotrimazole, benzyl benzoate, nicardipine, and delavird

45 Bulky imidazoles like clotrimazole block NO synthesis by inhibiting assembly o

46 tions showed that bulky heme ligands such as clotrimazole bound strongly to TXAS (Kd approximately 0.

47 re reversed by the CYP inhibitors SKF525A or clotrimazole, but not by the K(Ca) channel blocker, char

48 These results demonstrate that clotrimazole can inhibit the MRP1 which is present in hu

49 In particular, clotrimazole causes a sustained depletion of intracellul

50 s sensitive to low nM concentrations of both clotrimazole (CLT) and its des-imidazolyl metabolite, 2-

51 The antifungal antibiotic clotrimazole (CLT) blocks directly and with high potency

52 Clotrimazole (CLT) has been shown to inhibit proliferati

53 Clotrimazole (CLT) prevents dehydration of the human HbS

54 ion of the UPR by the drugs thapsigargin and clotrimazole (CLT), which disrupt ER calcium homeostasis

55 Clotrimazole concentrations ranged from 0.03 to 16 micro

56 Curiously, Pdr5p-mediated transport of clotrimazole continues at intracellular concentrations o

57 ression upon binding to rifampicin (Rif) and clotrimazole (CTZ) by recruiting transcriptional coactiv

58 Eight new ruthenium complexes of clotrimazole (CTZ) with high antiparasitic activity have

59 ytes to the pharmaceuticals ibuprofen (IBU), clotrimazole (CTZ), clofibric acid (CFA) and propranolol

60 The antifungal drug, clotrimazole, demonstrated ability to inhibit secretory

61 We conclude that resistance to clotrimazole develops in isolates of C. albicans from HI

62 NO2(-) generation, whereas the CP inhibitor clotrimazole did not.

63 dministration of the imidazole antimycotics, clotrimazole, econazole and miconazole, which are potent

64 Clotrimazole, econazole, miconazole and CN- also signifi

65 Binding of econazole and clotrimazole exhibits positive cooperativity that may re

66 sex ratio skews also occurred for the lower clotrimazole exposure concentration at the higher water

67 Elevated water temperature and clotrimazole exposure independently induced male-skewed

68 Clotrimazole, fluconazole, itraconazole, ketoconazole, v

69 000 screened), all pharmacologically active: clotrimazole, flunarizine, and chlorhexidine.

70 If the MIC of clotrimazole for an isolate of C. albicans was > or =0.5

71 However, clotrimazole greatly inhibited NO2(-)-dependent NO gener

72 Clotrimazole has been shown to have potent anti-malarial

73 ted the potential emergence of resistance to clotrimazole in a prospectively monitored HIV-infected p

74 Gardos channel inhibitors, charybdotoxin and clotrimazole, independently blocked the PGE2-stimulated

75 tagonist nifedipine blocked ICa within 30 s, clotrimazole-induced suppression of ICa required 5.1 +/-

76 d II reduced ICa by 85 +/- 3 % and abolished clotrimazole-induced suppression of ICa.

77 ly, inhibitors of K(Ca2+), charybdotoxin and clotrimazole, inhibited HD cell formation.

78 Similarly, the PXR activator clotrimazole is a potent deactivator of hCAR.

79 We show here that clotrimazole is also a substrate for CYP46A1.

80 sphatidylinositol-4,5-bisphosphate (PIP2) or clotrimazole is necessary for channel opening by PS.

81 7 mM), charybdotoxin (Kd = 10 +/- 1 nM), and clotrimazole (Kd = 387 +/- 34 nM), but is resistant to a

82 Azole antibiotics (clotrimazole, ketoconazole, and itraconazole) widely use

83 Patients were started on a dose of 10 mg clotrimazole/kg/d for one week.

84 At dosages of 20 mg clotrimazole/kg/d, all subjects showed Gardos channel in

85 se levels in two subjects treated with 30 mg clotrimazole/kg/d.

86 y blocked by charybdotoxin (Ki = 2.5 nM) and clotrimazole (Ki = 24.8 nM) but were minimally affected

87 er, inhibition of cytochrome P450 enzymes by clotrimazole limits its therapeutic value.

88 al laboratory's ability to determine MICs of clotrimazole may help to distinguish microbiologic resis

89 Six (40%) of 15 patients for whom the clotrimazole MIC was > or =0.5 microg/ml required amphot

90 The four imidazoles (econazole, clotrimazole, miconazole, and ketoconazole) were active:

91 ne, fluconazole, ketoconazole, itraconazole, clotrimazole, miconazole, and terconazole) and compared

92 der to assess the effect of inoculum size on clotrimazole MICs.

93 resistant to agents (SKF 96365, miconazole, clotrimazole, nitrendipine, and trifluoperazine) that in

94 f) of 0.112 s(-1); and 3) both imidazole and clotrimazole (nitrogen-based ligands) bind TXAS in a two

95 TPgammaS prevented the suppressant effect of clotrimazole on ICa.

96 din-2-yl)piperazine-1-carboxamide (BCTC) and clotrimazole or by elevated temperature.

97 isolated ventricular myocytes incubated with clotrimazole or CN-.

98 Inhibition of TRPM2-L by pretreatment with clotrimazole or expression of TRPM2-S significantly incr

99 Selectively blocking IKCa1 channels with clotrimazole or TRAM-34 suppressed mitogenesis of preact

100 wn translation initiation inhibitors such as clotrimazole or troglitazone.

101 th high doses (50 mg/kg/day) of nicardipine, clotrimazole, or pregnenolone 16alpha-carbonitrile, but

102 ys confirmed three (ebastine, astemizole and clotrimazole) out of seven tested candidates ( 40% true

103 s, MRP1-associated transport is inhibited by clotrimazole over the range 2-20 microm, and the inhibit

104 ere significantly more efficacious than were clotrimazole, oxiconazole nitrate, and sertaconazole nit

105 Consequently, clotrimazole preferentially decreases the expression of

106 drugs, including rifampicin, phenobarbital, clotrimazole, reserpine, and isosafrole.

107 t of 0.5 microg/ml may be useful in defining clotrimazole resistance in C. albicans.

108 is known about the potential contribution of clotrimazole resistance to the development of refractory

109 nd 1.5 x 10(5) M(-1) s(-1) for imidazole and clotrimazole, respectively, followed by a slow conformat

110 , mediated by both Cl(-) and HCO(3) (-), and clotrimazole sensitive.

111 ed by axotomy, but iberiotoxin-sensitive and clotrimazole-sensitive current densities are increased i

112 K+ influx) and the Gardos channel (taken as clotrimazole-sensitive K+ influx, 5 microM) in human red

113 In contrast, inhibition by BCTC and that by clotrimazole share a different set of common features.

114 therapy with 2 KCa3.1 blockers, TRAM-34 and clotrimazole, significantly reduced the development of a

115 idolate to inhibit K-Cl cotransport and oral clotrimazole to inhibit the Gardos channel.

116 Clotrimazole troches are widely used in the treatment of

117 Resistance to clotrimazole was highly associated with clinically overt

118 e inhibited basal and stimulated J(lyz), but clotrimazole was without effect.

119 tifungal susceptibility testing of yeasts to clotrimazole, we compared MICs in macrodilution and micr

120 d male-skewed sex ratios, and the effects of clotrimazole were greater at the higher temperature.

121 When the data for miconazole and clotrimazole were removed from the analysis, agreement w

122 uous drugs, five analogues of the antifungal clotrimazole were studied.

123 Finally, the transport substrate clotrimazole, which is a noncompetitive inhibitor of Pdr

124 plete, concentration-dependent inhibition by clotrimazole, which is also known to be a potent transpo

125 ted by the P450 inhibitors, ketoconazole and clotrimazole with IC(50) values of 1 and 0.4 microM, res

126 competitive and caused by the interaction of clotrimazole with the transporter at a site that is dist