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1 ose dependent and recovered after washout of clotrimazole.
2 tments but was up-regulated by reserpine and clotrimazole.
3 s, including the antifungal voriconazole and clotrimazole.
4 ed pharmacokinetic properties compared to 1, Clotrimazole.
5  activities that are relatively resistant to clotrimazole.
6 e cation channel blockers, 9-phenanthrol and clotrimazole.
7 t test) in arginine-supplemented mice versus clotrimazole.
8 terconazole, 66% for miconazole, and 53% for clotrimazole.
9  were not affected by 17-ODYA (10 microM) or clotrimazole (10 microM), inhibitors of the cytochrome P
10 fungal voriconazole (2.35 A), and antifungal clotrimazole (2.50 A).
11 dazole promoted iNOSox dimerization, whereas clotrimazole (30 microM) and miconazole (15 microM) did
12         When added to cells expressing iNOS, clotrimazole (50 microM) had no effect on iNOS protein e
13  of apamin 1 microM, iberiotoxin 200 nM, and clotrimazole 500 nM; 3) blocking remaining K(+) current
14  the synthesis of 7alpha,25-OHC in vivo with clotrimazole, a CYP7B1 inhibitor, reduced the content of
15  specific inhibitor of EET biosynthesis, and clotrimazole, a cytochrome P450 inhibitor, significantly
16                                              Clotrimazole, a membrane-permeant triarylmethane, blocke
17                               We report that clotrimazole, a potent antiproliferative agent both in v
18                              The antimycotic clotrimazole, a potent inhibitor of the intermediate-con
19 bjects who have sickle cell anemia with oral clotrimazole, a specific Gardos channel inhibitor.
20                                              Clotrimazole also bound to iNOSox dimers in the absence
21                        It is noteworthy that clotrimazole also functions as a ligand activator of CAR
22                  The effect was prevented by clotrimazole, an inhibitor of the Ca2+-sensitive K+ (KCa
23 used a rational design strategy to develop a clotrimazole analog that selectively inhibits IKCa1 with
24 iously to mediate sensitivity of K(Ca)3.1 to clotrimazole and 1-[(2-chlorophenyl)diphenylmethyl]-1H-p
25                 It was sensitive to block by clotrimazole and could be potently and reversibly potent
26 ers able to activate both receptors, such as clotrimazole and dieldrin.
27 ween methods was observed for miconazole and clotrimazole and for C. krusei isolates tested against t
28 (K(Ca)) with components sensitive to apamin, clotrimazole and iberiotoxin.
29                 In the presence of the drugs clotrimazole and isavuconazole, the AcCYP51 drug complex
30 (Kd ~107 and ~12 muM), whereas ketoconazole, clotrimazole and itraconazole bound strongest to CYP5218
31 y the same binding affinity as econazole and clotrimazole and ketoconazole with somewhat lower affini
32 ol (DTT) and by cytochrome P-450 inhibitors (clotrimazole and miconazole), we measured the carotid si
33 mpletely reversed the suppressant effects of clotrimazole and NaCN on ICa.
34 s with the exceptions only of miconazole and clotrimazole and of terconazole against C. krusei isolat
35 ing point the biological activity spectra of clotrimazole and tioconazole because their putative targ
36  DM heme domain bound to the imidazole drugs clotrimazole and tioconazole, and to the triazole drugs
37                      The IK channel blockers clotrimazole and TRAM-34 inhibited whole cell swelling-a
38  magnitudes of inhibition were observed with clotrimazole and TRAM-34.
39 d to the validation of additional compounds, clotrimazole and vemurafenib.
40  posaconazole) and topically (miconazole and clotrimazole) and by a tetrazole-based drug candidate, V
41  of CYP46A1 in complex with voriconazole and clotrimazole, and in the present work we cocrystallized
42                Imidazole, 1-phenylimidazole, clotrimazole, and miconazole all bound to the iNOSox mon
43 -normalized doses of tacrolimus, prednisone, clotrimazole, and statins.
44 istent with channel blockade, charybdotoxin, clotrimazole, and the highly selective IKCa1 inhibitors,
45                         The EDC selected was clotrimazole (at 2 mug/L and 10 mug/L), a widely used an
46 ne pharmacophore of chloroquine with that of clotrimazole-based antimalarials.
47 g the heme iron via their nitrogen atoms and clotrimazole being at a 4 A distance from the heme iron.
48 hibition at concentrations below 100 microM: clotrimazole, benzyl benzoate, nicardipine, and delavird
49                        Bulky imidazoles like clotrimazole block NO synthesis by inhibiting assembly o
50 tions showed that bulky heme ligands such as clotrimazole bound strongly to TXAS (Kd approximately 0.
51                                     Although clotrimazole-bound AcCYP51 adopted a typical CYP monomer
52 re reversed by the CYP inhibitors SKF525A or clotrimazole, but not by the K(Ca) channel blocker, char
53               These results demonstrate that clotrimazole can inhibit the MRP1 which is present in hu
54                               In particular, clotrimazole causes a sustained depletion of intracellul
55 s sensitive to low nM concentrations of both clotrimazole (CLT) and its des-imidazolyl metabolite, 2-
56                    The antifungal antibiotic clotrimazole (CLT) blocks directly and with high potency
57                                              Clotrimazole (CLT) has been shown to inhibit proliferati
58                                              Clotrimazole (CLT) prevents dehydration of the human HbS
59 ion of the UPR by the drugs thapsigargin and clotrimazole (CLT), which disrupt ER calcium homeostasis
60                                              Clotrimazole concentrations ranged from 0.03 to 16 micro
61       Curiously, Pdr5p-mediated transport of clotrimazole continues at intracellular concentrations o
62 ression upon binding to rifampicin (Rif) and clotrimazole (CTZ) by recruiting transcriptional coactiv
63             Eight new ruthenium complexes of clotrimazole (CTZ) with high antiparasitic activity have
64 ytes to the pharmaceuticals ibuprofen (IBU), clotrimazole (CTZ), clofibric acid (CFA) and propranolol
65                         The antifungal drug, clotrimazole, demonstrated ability to inhibit secretory
66               We conclude that resistance to clotrimazole develops in isolates of C. albicans from HI
67  NO2(-) generation, whereas the CP inhibitor clotrimazole did not.
68 dministration of the imidazole antimycotics, clotrimazole, econazole and miconazole, which are potent
69                                              Clotrimazole, econazole, miconazole and CN- also signifi
70                     Binding of econazole and clotrimazole exhibits positive cooperativity that may re
71  sex ratio skews also occurred for the lower clotrimazole exposure concentration at the higher water
72               Elevated water temperature and clotrimazole exposure independently induced male-skewed
73                                              Clotrimazole, fluconazole, itraconazole, ketoconazole, v
74 000 screened), all pharmacologically active: clotrimazole, flunarizine, and chlorhexidine.
75                                If the MIC of clotrimazole for an isolate of C. albicans was > or =0.5
76                                     However, clotrimazole greatly inhibited NO2(-)-dependent NO gener
77                                              Clotrimazole has been shown to have potent anti-malarial
78 ted the potential emergence of resistance to clotrimazole in a prospectively monitored HIV-infected p
79 Gardos channel inhibitors, charybdotoxin and clotrimazole, independently blocked the PGE2-stimulated
80 tagonist nifedipine blocked ICa within 30 s, clotrimazole-induced suppression of ICa required 5.1 +/-
81 d II reduced ICa by 85 +/- 3 % and abolished clotrimazole-induced suppression of ICa.
82 ly, inhibitors of K(Ca2+), charybdotoxin and clotrimazole, inhibited HD cell formation.
83                 Similarly, the PXR activator clotrimazole is a potent deactivator of hCAR.
84                            We show here that clotrimazole is also a substrate for CYP46A1.
85 sphatidylinositol-4,5-bisphosphate (PIP2) or clotrimazole is necessary for channel opening by PS.
86 7 mM), charybdotoxin (Kd = 10 +/- 1 nM), and clotrimazole (Kd = 387 +/- 34 nM), but is resistant to a
87                           Azole antibiotics (clotrimazole, ketoconazole, and itraconazole) widely use
88     Patients were started on a dose of 10 mg clotrimazole/kg/d for one week.
89                          At dosages of 20 mg clotrimazole/kg/d, all subjects showed Gardos channel in
90 se levels in two subjects treated with 30 mg clotrimazole/kg/d.
91 y blocked by charybdotoxin (Ki = 2.5 nM) and clotrimazole (Ki = 24.8 nM) but were minimally affected
92 used for prostate cancer therapy, as well as clotrimazole, known to inhibit P450 17A1.
93 er, inhibition of cytochrome P450 enzymes by clotrimazole limits its therapeutic value.
94 al laboratory's ability to determine MICs of clotrimazole may help to distinguish microbiologic resis
95        Six (40%) of 15 patients for whom the clotrimazole MIC was > or =0.5 microg/ml required amphot
96              The four imidazoles (econazole, clotrimazole, miconazole, and ketoconazole) were active:
97 ne, fluconazole, ketoconazole, itraconazole, clotrimazole, miconazole, and terconazole) and compared
98 der to assess the effect of inoculum size on clotrimazole MICs.
99  resistant to agents (SKF 96365, miconazole, clotrimazole, nitrendipine, and trifluoperazine) that in
100 f) of 0.112 s(-1); and 3) both imidazole and clotrimazole (nitrogen-based ligands) bind TXAS in a two
101 TPgammaS prevented the suppressant effect of clotrimazole on ICa.
102 din-2-yl)piperazine-1-carboxamide (BCTC) and clotrimazole or by elevated temperature.
103 isolated ventricular myocytes incubated with clotrimazole or CN-.
104   Inhibition of TRPM2-L by pretreatment with clotrimazole or expression of TRPM2-S significantly incr
105     Selectively blocking IKCa1 channels with clotrimazole or TRAM-34 suppressed mitogenesis of preact
106 wn translation initiation inhibitors such as clotrimazole or troglitazone.
107 th high doses (50 mg/kg/day) of nicardipine, clotrimazole, or pregnenolone 16alpha-carbonitrile, but
108 ys confirmed three (ebastine, astemizole and clotrimazole) out of seven tested candidates ( 40% true
109 s, MRP1-associated transport is inhibited by clotrimazole over the range 2-20 microm, and the inhibit
110 ere significantly more efficacious than were clotrimazole, oxiconazole nitrate, and sertaconazole nit
111                                Consequently, clotrimazole preferentially decreases the expression of
112  drugs, including rifampicin, phenobarbital, clotrimazole, reserpine, and isosafrole.
113 t of 0.5 microg/ml may be useful in defining clotrimazole resistance in C. albicans.
114 is known about the potential contribution of clotrimazole resistance to the development of refractory
115 nd 1.5 x 10(5) M(-1) s(-1) for imidazole and clotrimazole, respectively, followed by a slow conformat
116                                Ketoconazole, clotrimazole, ritonavir, indinavir, and itraconazole are
117 , mediated by both Cl(-) and HCO(3) (-), and clotrimazole sensitive.
118 ed by axotomy, but iberiotoxin-sensitive and clotrimazole-sensitive current densities are increased i
119  K+ influx) and the Gardos channel (taken as clotrimazole-sensitive K+ influx, 5 microM) in human red
120  In contrast, inhibition by BCTC and that by clotrimazole share a different set of common features.
121  therapy with 2 KCa3.1 blockers, TRAM-34 and clotrimazole, significantly reduced the development of a
122 idolate to inhibit K-Cl cotransport and oral clotrimazole to inhibit the Gardos channel.
123                                              Clotrimazole troches are widely used in the treatment of
124 bition is not observed with ketoconazole and clotrimazole until the changes are completed.
125                                Resistance to clotrimazole was highly associated with clinically overt
126 e inhibited basal and stimulated J(lyz), but clotrimazole was without effect.
127 tifungal susceptibility testing of yeasts to clotrimazole, we compared MICs in macrodilution and micr
128 d male-skewed sex ratios, and the effects of clotrimazole were greater at the higher temperature.
129             When the data for miconazole and clotrimazole were removed from the analysis, agreement w
130 uous drugs, five analogues of the antifungal clotrimazole were studied.
131             Finally, the transport substrate clotrimazole, which is a noncompetitive inhibitor of Pdr
132 plete, concentration-dependent inhibition by clotrimazole, which is also known to be a potent transpo
133 ted by the P450 inhibitors, ketoconazole and clotrimazole with IC(50) values of 1 and 0.4 microM, res
134 competitive and caused by the interaction of clotrimazole with the transporter at a site that is dist

 
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