ライフサイエンスコーパス: quinidine

1 chona alkaloid derivative (TMS-quinine or Me-quinidine).

2 o resistance to quinine and its diastereomer quinidine.

3 may have some ability to act on quinine and quinidine.

4 de, dofetilide, propafenone, amiodarone, and quinidine.

5 afe and clinically beneficial alternative to quinidine.

6 sed by KCNT1 mutations who were treated with quinidine.

7 ompletely protected HDAC1 from the action of quinidine.

8 e before undergoing apoptosis in response to quinidine.

9 ponents that are differentially sensitive to quinidine.

10 howing increased current that was reduced by quinidine.

11 showed strong differences in sensitivity to quinidine.

12 the presence of the K+ channel-blocking drug quinidine.

13 d outward current (Isus), was insensitive to quinidine.

14 intravenous treatment, and an impediment to quinidine.

15 malities in CHF and in subjects treated with quinidine.

16 ter-defibrillator alone but did not recur on quinidine.

17 inhibitory doses of [3H]chloroquine and [3H] quinidine.

18 an activating mutation in KCNT1 treated with quinidine.

19 hmic events resulting from unavailability of quinidine.

20 splay a reduced sensitivity to blockage with quinidine.

21 ssibly attributable to the unavailability of quinidine.

22 ffectively prevented by the CYP2D6 inhibitor quinidine.

23 ed information regarding the availability of quinidine.

24 t this pocket is large enough to accommodate quinidine.

25 ents received medical treatment, mainly with quinidine.

26 ricular action potentials in the presence of quinidine.

27 which is inhibited by low pH and blocked by quinidine.

28 rized versions of the substrates quinine and quinidine.

29 a new agent containing dextromethorphan and quinidine.

30 ensitive K+ channel) blockers anandamide and quinidine.

31 the stereospecific responses to quinine and quinidine.

32 Quinidine (10 microM) prevented VT in six out of six fle

33 nic Scn5a+/- hearts (at 1.0 microM), whereas quinidine (10 microM) reduced EGD ratios and prolonged V

34 Quinidine (10 muM) and the phosphodiesterase-3 inhibitor

35 The effects of quinidine (100 and 300 muM) are also tested.

36 microM bupivacaine (55% inhibition) and 1 mM quinidine (105 % inhibition).

37 nsitivity to the IKr blockers dofetilide and quinidine 2- to 5-fold.

38 techniques were used to study the effects of quinidine 2.5 to 20 micromol/L on APD in ventricular epi

39 TRESK-2 was inhibited by 10 microm quinidine, 20 microm arachidonate and acid (pH 6.3) at 4

40 epithelial cells, and were inhibited by 1 mM quinidine, 20 mM TEA or 5 mM Ba2+ ions.

41 ilarly, potassium decreased QTUc dispersion (quinidine, 210+/-62 to 130+/-75 ms(1/2), P<.01; CHF, 132

42 TASK-3 was blocked by barium (57%, 3 mM), quinidine (37%, 100 microM), and lidocaine (62%, 1 mM).

43 lock with 4-aminopyridine (1 to 2 mmol/L) or quinidine (5 micromol/L) restored the dome, normalized t

44 of the transient outward current antagonist quinidine (5 mumol/L) or the phosphodiesterase III inhib

45 ngation, especially in the precordial leads (quinidine, 590+/-79 to 479+/-35 [+/-SD] ms(1/2), P<.001;

46 e blockade of I(K) by high concentrations of quinidine, a selective I(K) blocker, raises a question a

47 ith human liver microsomes, the inclusion of quinidine, a specific 2D6 inhibitor, resulted in approxi

48 hance our understanding of the mechanisms of quinidine action, we studied its effect on APD in canine

49 er effect has no consistent correlation with quinidine actions on action potential duration (APD) in

50 Mechanistic analysis has suggested that quinidine acts as a cationic open-channel blocker at a s

51 One patient became allergic to quinidine after 7 days.

52 changes in QT interval after the infusion of quinidine, after which E2-treated animals responded simi

53 inidine (GBa)1, the other being sensitive to quinidine alone (Gquin).

54 Addition of Ba2+ alone, quinidine alone, or both inhibitors together revealed tw

55 sensitivity to TEA (5 mM) and sensitivity to quinidine, an analogue of quinine.

56 Treatment with quinidine, an open-channel blocker used to treat the hum

57 sign, 152 patients received dextromethorphan-quinidine and 127 received placebo during the study.

58 pe equations, the conformational behavior of quinidine and 9-epi-quinidine has also been investigated

59 n of flecainide but was superior to those of quinidine and amiodarone.

60 [K+]o) on IKr block by the nonspecific agent quinidine and by the specific IKr blocker dofetilide.

61 was additionally blocked by NPPB, verapamil, quinidine and dideoxyforskolin.

62 Quinidine and digoxin are both substrates for P-glycopro

63 For quinidine and flecainide, which bind preferentially to t

64 by the class Ia and Ic antiarrhythmic drugs quinidine and flecainide.

65 educed from 5.8 to 3.8 with dextromethorphan-quinidine and from 6.7 to 5.8 with placebo.

66 educed from 7.1 to 3.8 with dextromethorphan-quinidine and from 7.0 to 5.3 with placebo.

67 Quinidine and GF120918 inhibit the transport of P-gp sub

68 synthesis, whereas K(ATP) channel blockers (quinidine and glibenclamide) attenuated DNA synthesis.

69 also demonstrate that the cinchona alkaloids quinidine and quinine give rise to products (some in as

70 tion reduces the channel's affinity for both quinidine and the N-terminal domain.

71 se proarrhythmia may be idiosyncratic (e.g., quinidine), and for patients who are to begin an antiarr

72 neurons was attenuated by CYP2D6 inhibitor, quinidine, and also partly by monoamine oxidase B inhibi

73 noline derivatives quinine, its stereoisomer quinidine, and chloroquine may worsen or provoke disorde

74 At 5 x 10(-5) M, quinine, quinidine, and chloroquine reduced the quantal content o

75 rst-generation modulators such as verapamil, quinidine, and cyclosporin required high doses of drugs

76 Quinine, quinidine, and primaquine were much less powerful.

77 n the presence and absence of flecainide and quinidine, and the extent to which Scn5a+/- hearts model

78 w that mutant PfCRT also transports quinine, quinidine, and verapamil, indicating that the protein be

79 m channel-blocking drug quinidine: following quinidine application, push mutants, but not wild-type,

80 Previously we showed quinidine arrested MCF-7 cells in G(1) phase of the cell

81 ethyl substituent has been incorporated into quinidine as a conformational stabilizer and a probe to

82 on can be treated with ethanol and catalytic quinidine as a sulfinyl transfer catalyst to provide a c

83 data point to I(to) block (4-aminopyridine, quinidine) as an effective pharmacological treatment.

84 n the presence of free heme, chloroquine and quinidine associate with the heme polymer.

85 to extracellular acidosis and intracellular quinidine binding remained, suggesting that transmembran

86 Quinidine block also revealed that mutant receptors gene

87 from 2.7 +/- 0.9 to 79 +/- 32 nmol/L and for quinidine block from 0.4 +/- 0.1 to 3.8 +/- 1.2 mumol/L.

88 IC50 for quinidine block of basal IKs was 5.8+/-1.2 micromol/L, v

89 We studied quinidine block of Kv1.4DeltaN, a K(+) channel lacking N

90 f recovery from the time-dependent aspect of quinidine block was similar to recovery from normal C-ty

91 are age-related changes in both the IC50 for quinidine blockade of Ito, as well as the mechanism of q

92 The antiarrhythmic agent quinidine blocks the human cardiac hKv1.5 channel expres

93 than Asp strongly attenuated the binding of quinidine, bufuralol, and several other P450 2D6 ligands

94 ractory periods prolonged on procainamide or quinidine, but no tachyarrhythmias could be induced with

95 was inhibited by verapamil, desipramine, and quinidine, but not by MPP+ (1-methyl-4-phenylpyridinium)

96 We conducted a survey of the availability of quinidine by contacting professional medical societies a

97 roduction of the CF3 group on the C9 atom in quinidine can significantly increase the conformational

98 A quinidine-catalyzed diastereoselective addition of alpha

99 l pacing, before and following flecainide or quinidine challenge.

100 Quinidine, cilostazol, and milrinone suppress the hypoth

101 R syndrome and examines the effectiveness of quinidine, cilostazol, and milrinone to prevent hypother

102 plasma digoxin concentration occurring with quinidine coadministration in wild-type mice and thus su

103 With an increase of quinidine concentration, this effect subsided and disapp

104 ms, ARIs were significantly prolonged at low quinidine concentrations.

105 at control conditions and in the presence of quinidine consistently led to vortex-like reentry whose

106 stage 2, patients receiving dextromethorphan-quinidine continued; those receiving placebo were strati

107 P-glycoprotein-mediated digoxin transport by quinidine contributes to the digoxin-quinidine interacti

108 Flecainide or quinidine decreased the pacing rates at which this occur

109 heimer disease, combination dextromethorphan-quinidine demonstrated clinically relevant efficacy for

110 of racemic 1-aryl-2-tetralones with a chiral quinidine-derived ammonium salt under basic conditions i

111 e and cinchona alkaloid thioureas (such as a quinidine-derived thiourea) produces the corresponding g

112 (P=0.05) in wild-type animals; by contrast, quinidine did not increase digoxin brain concentrations

113 Quinidine did not show evidence for direct inhibition of

114 al ABC transporter substrate inhibitors like quinidine, diltiazem, and ritonavir also enhanced transd

115 nitrosobenzene catalyzed by a newly designed quinidine dimer to afford the desired products in good y

116 explained by differences in solubility, but quinidine displays a much larger Kads than expected on t

117 lassic proarrhythmic HERG blockers (sotalol, quinidine, dofetilide) in both cardiac and noncardiac ce

118 nidine itself is a P-glycoprotein substrate, quinidine doses were reduced in mdr1a(-/-) mice to produ

119 ntrations of doxorubicin were not altered by quinidine; doxorubicinol liver concentrations were incre

120 target for antibodies induced by quinine and quinidine, drugs structurally unrelated to ranitidine.

121 vitro, there is a significant difference of quinidine effects in M cells versus epicardial and endoc

122 d by the previous study: (1) Are the complex quinidine effects in vitro reflected in its actions on t

123 (2) What are the cellular determinants of quinidine effects on QT interval in ECG?

124 ticle, we report a significant difference in quinidine effects on the action potential duration betwe

125 pen channel block, there were time-dependent quinidine effects: the rate of inactivation during a sin

126 the electrophysiological mechanism by which quinidine elicits its antiarrhythmic effect in the pedia

127 ocker nifedipine, the sodium channel blocker quinidine, etc.

128 a higher Kads than cinchonidine, quinine, or quinidine even though, according to previous work, it ca

129 nitrogen atom instead, and both quinine and quinidine exhibit additional bonding via the methoxy oxy

130 ation of the potassium channel-blocking drug quinidine: following quinidine application, push mutants

131 A female patient on quinidine for atrial fibrillation who develops ventricul

132 s, one of which was blocked by both Ba2+ and quinidine (GBa)1, the other being sensitive to quinidine

133 Hospitals must maintain intravenous quinidine gluconate on formulary because it is the only

134 re found to follow the sequence cinchonine > quinidine > cinchonidine > quinine > 6-methoxyquinoline

135 nformational behavior of quinidine and 9-epi-quinidine has also been investigated.

136 ibited by the K+ channel inhibitors Ba2+ and quinidine in a dose-dependent manner.

137 transcellular transport of both digoxin and quinidine in cultured cell lines that express P-glycopro

138 In contrast, the effects of quinidine in M cells varied from prolongation to shorten

139 The ability of quinidine in therapeutic concentrations to prolong repol

140 ibility related (12 cases) to the absence of quinidine, including 2 fatalities possibly attributable

141 Moreover, quinidine increased digoxin brain concentrations by 73.2

142 Quinidine increased plasma digoxin concentrations by 73.

143 and V512A) reduced the dissociation rate for quinidine, increased the affinity (0.7, 1.5, 3.4, and 1.

144 In endocardium and epicardium, quinidine induced monotonic and concentration-dependent

145 ith E4031 and TTX suggested that in M cells, quinidine-induced APD lengthening was attributable to bl

146 HERG, and IsK mRNA levels, QT duration, and quinidine-induced changes in QT interval in isolated rab

147 This quinidine-induced channel internalization was confirmed

148 Surprisingly, quinidine-induced endocytosis was calcium-dependent and

149 ce of the rapid block and the time-dependent quinidine-induced inactivation were similar, but the tim

150 vented the development of the time-dependent quinidine-induced inactivation.

151 Importantly, whereas acute quinidine-induced internalization was reversible, chroni

152 In situ, quinidine-induced prolongation of repolarization is unif

153 cross the ventricular wall before and during quinidine infusion.

154 at the P-GP inhibitors trans-flupentixol and quinidine inhibit VMAT2.

155 In addition, 5 micromol/L quinidine inhibited P-glycoprotein-mediated digoxin tran

156 Quinidine inhibited the hydroxylation of imipramine comp

157 ous virus production by >100-fold, with one (quinidine) inhibiting infectious virus production by 450

158 Quinidine inhibits proliferation and promotes cellular d

159 port by quinidine contributes to the digoxin-quinidine interaction.

160 sitively charged lipophilic compound such as quinidine interacts with the hydrophobic moieties on S6

161 Initially, quinidine intracellularly blocked the open channel so ra

162 We conclude that quinidine is a breast tumor cell differentiating agent t

163 The antiarrhythmic drug quinidine is a partial antagonist of KCNT1 and hence may

164 are both substrates for P-glycoprotein, and quinidine is a potent inhibitor of digoxin transport in

165 The lack of accessibility of quinidine is a serious medical hazard at the global leve

166 The antiarrhythmic action of quinidine is associated with a slowing of conduction and

167 Quinidine is currently the recommended treatment for sev

168 Glu-216, whereas the protonated nitrogen of quinidine is equidistant from Asp-301 and Glu-216 with p

169 Although quinidine is known to elevate plasma digoxin concentrati

170 Clinical studies have suggested that quinidine is less effective when used for the treatment

171 Quinidine is the only oral medication that is effective

172 Because the in vitro data showed that quinidine itself is a P-glycoprotein substrate, quinidin

173 low potassium chloride Tyrode solution plus quinidine led to prolongation of the action potential an

174 chloroquine (log K(ads) = 5.55 +/- 0.03) and quinidine (log K(ads) = 4.92 +/- 0.01) suggest that the

175 rene N-oxygenation, human P450 3A4-catalyzed quinidine N-oxygenation, rat P450 2B1-catalyzed oxidatio

176 nistration of either procainamide (n = 3) or quinidine (n = 3).

177 andomized in a 1:1 ratio to dextromethorphan-quinidine (n = 59) or placebo (n = 60).

178 d in a 3:4 ratio to receive dextromethorphan-quinidine (n = 93) or placebo (n = 127).

179 on underwent electrophysiological testing on quinidine (n=54), disopyramide (n=2), or both (n=4).

180 Quinidine normalized the QT interval and prevented stimu

181 ge-related changes in the cardiac actions of quinidine on action potential duration and interaction w

182 Second, the effect of quinidine on digoxin disposition was studied in wild-typ

183 The differences may influence the actions of quinidine on repolarization of the heart in situ and det

184 The effective block by quinidine on synaptic currents as well as nonliganded op

185 er investigate the effect of chloroquine and quinidine on the formation of beta-hematin.

186 treatment with the P-glycoprotein inhibitors quinidine or verapamil) or warfarin (dose adjusted to ma

187 16.8-480 microg of GF120918 or 0.3-3.0 mg of quinidine) or vehicle (buffer or DMSO, respectively) was

188 Volume regulation was blocked by Ba2+, quinidine, or 5-nitro-2-(3-phenylpropylamino) benzoic ac

189 anthrones with cyclic allylic bromides using quinidine- or quinine-derived catalysts is described.

190 naires requesting information concerning the quinidine preparation available at their hospital.

191 sadogenic hERG blockers, such as sotalol and quinidine, produced statistically and physiologically si

192 CL of 300 ms, therapeutic concentrations of quinidine prolonged ARIs and QT intervals.

193 is that, following rapid open channel block, quinidine promotes development of the C-type inactivated

194 We propose that quinidine promotes the entry of the channel into a C-typ

195 N) but reduced sensitivity to its enantiomer quinidine (QD), indicative of a unique stereospecific re

196 al drugs chloroquine (CQ), quinine (QN), and quinidine (QD).

197 Ketoconazole (KET) and quinidine (QIN), substrates specific to cyt P450 3A enzy

198 ct from TWIK-1 channels in their response to quinidine, quinine, and barium.

199 mplex with alternative ligands, prinomastat, quinidine, quinine, or ajmalicine, displaced both thiori

200 uding cimetidine, and type II cations (e.g., quinidine, quinine, verapamil, and rhodamine123) are als

201 rval, 0.09-0.81; P=0.02), 23% in response to quinidine (r=0.48; 95% confidence interval, -0.03 to 0.7

202 ubjects received single doses of dofetilide, quinidine, ranolazine, and placebo.

203 Quinidine reduced maximum theta' in WT and caused earlie

204 or 4-methoxyphenethylamine or the inhibitor quinidine; reduction is not the most rate-limiting step.

205 Although quinidine represents an encouraging opportunity for ther

206 mutant muscles were similar to those of the quinidine-resistant fraction of I(K).

207 of embryoid bodies treated with sotalol and quinidine, respectively, compared with negligible early

208 However, binding of the N-terminal or quinidine restores normal recovery from inactivation.

209 .5-GFP with the class I antiarrhythmic agent quinidine resulted in a dose- and temperature-dependent

210 of bradycardic stimulation, hypokalemia, and quinidine resulted in early afterdepolarizations.

211 ated the effects of postnatal development on quinidine's interaction with major repolarizing currents

212 5 min despite the high retentitivity of the quinidine selector.

213 to lack the C-terminal alpha-helix generated quinidine-sensitive currents (43-51% block by 10 microM

214 hab(3) mutation were similar to those of the quinidine-sensitive fraction of I(K).

215 at depolarized voltages and was Ba(2+)- and quinidine-sensitive.

216 Finally, exposure to quinidine significantly reduces this gain of function fo

217 luding lidocaine, phenytoin, flecainide, and quinidine, suggesting that these drugs interact with a c

218 ed into (1) 12 healthy subjects treated with quinidine sulfate (5 doses of 300 mg/5 h) or placebo and

219 Because levels of quinidine sulfate attainable in clinical practice shorte

220 We treated 6 SCCMS patients with quinidine sulfate in an open-label trial, using objectiv

221 The Na+/Mg2+ exchange inhibitor quinidine suppressed both the gramicidin- and muscarinic

222 efloquine, a close derivative of quinine and quinidine that exhibits antimalarial and antiarrhythmic

223 These data point to the importance that quinidine, that in several countries has been removed fr

224 In the presence of quinidine, the biliary excretion of doxorubicin was redu

225 sion alone, cardioversion plus amiodarone or quinidine therapy, and rate control with antithrombotic

226 early, this cannot reflect the permeation of quinidine through the electric field, but must be the re

227 s study was to determine the availability of quinidine throughout the world.

228 nesis and its modification by flecainide and quinidine to alterations in DeltaAPD90 in Scn5a+/Delta h

229 able in MCF-7 cells 30 min after addition of quinidine to the growth medium.

230 ne H4 appeared within 2 h of the addition of quinidine to the medium, and levels were maximal by 24 h

231 mice treated with MPTP and a P-GP inhibitor (quinidine, trans-flupentixol or cyclosporine A), the eli

232 Quinidine-treated MCF-7 cells showed elevated p21(WAF1),

233 epi- and endocardia of untreated hearts, and quinidine-treated WT hearts.

234 ially arrhythmogenic QT abnormalities during quinidine treatment and in CHF can be nearly normalized

235 the lower arrhythmogenicity associated with quinidine treatment.

236 0 3A4-catalyzed oxidations of nifedipine and quinidine, two prototypic substrates, in liver microsome

237 blockade of Ito, as well as the mechanism of quinidine unblocking.

238 It was inhibited by both Ba2+ and quinidine, underwent run-down in excised patches in the

239 ts included falls (8.6% for dextromethorphan-quinidine vs 3.9% for placebo), diarrhea (5.9% vs 3.1% r

240 vents occurred in 7.9% with dextromethorphan-quinidine vs 4.7% with placebo.

241 ation/Aggression scores for dextromethorphan-quinidine vs placebo (ordinary least squares z statistic

242 Quinidine was associated with a decrease in doxorubicin

243 Treatment with quinidine was correlated with a marked reduction in seiz

244 In contrast, quinidine was found to inhibit both adult and pediatric

245 Quinidine was infused continuously; its plasma level inc

246 ver, the cycle length of the arrhythmia with quinidine was longer than that for control ([mean +/- SE

247 ong the 98 drugs described in these reports, quinidine was mentioned in 38 case reports, gold in 11,

248 Dextromethorphan-quinidine was not associated with cognitive impairment,

249 Quinidine was readily available in 19 countries (14%), n

250 P-gp substrates (amprenavir, loperamide, and quinidine), we have successfully fitted the elementary r

251 ectrophysiological effects of flecainide and quinidine were compared in Langendorff-perfused wild-typ

252 genic Scn5a+/Delta hearts in the presence of quinidine, which increased EGD ratio but left DeltaAPD90

253 ensitive currents (43-51% block by 10 microM quinidine), while the currents generated by those constr

254 Six of the hits (guanfacine, quinidine, xylometazoline, oxymetazoline, fenoldopam, an