ライフサイエンスコーパス: quinidine

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

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

3 rized versions of the substrates quinine and quinidine.

4 a new agent containing dextromethorphan and quinidine.

5 ensitive K+ channel) blockers anandamide and quinidine.

6 the stereospecific responses to quinine and quinidine.

7 o resistance to quinine and its diastereomer quinidine.

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

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

10 ompletely protected HDAC1 from the action of quinidine.

11 e before undergoing apoptosis in response to quinidine.

12 ponents that are differentially sensitive to quinidine.

13 showed strong differences in sensitivity to quinidine.

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

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

16 malities in CHF and in subjects treated with quinidine.

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

18 afe and clinically beneficial alternative to quinidine.

19 sed by KCNT1 mutations who were treated with quinidine.

20 howing increased current that was reduced by quinidine.

21 intravenous treatment, and an impediment to quinidine.

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

23 an activating mutation in KCNT1 treated with quinidine.

24 hmic events resulting from unavailability of quinidine.

25 e(2) and one equivalent of either quinine or quinidine.

26 splay a reduced sensitivity to blockage with quinidine.

27 ssibly attributable to the unavailability of quinidine.

28 ffectively prevented by the CYP2D6 inhibitor quinidine.

29 ed information regarding the availability of quinidine.

30 t this pocket is large enough to accommodate quinidine.

31 ents received medical treatment, mainly with quinidine.

32 ricular action potentials in the presence of quinidine.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 ocking hyperexcitable K(Na)1.1 channels with quinidine, a class I antiarrhythmic drug, has shown vari

48 ture of full-length human Na(v) 1.5 bound to quinidine, a class Ia antiarrhythmic drug, at 3.3 A reso

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

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

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

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

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

54 current ventricular fibrillation resulted in quinidine administration in 12/24 SCVF (50%) with excell

55 One patient became allergic to quinidine after 7 days.

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

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

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

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

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

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

62 function of P-gp (log IC(50) of 4.20 nM for quinidine and 4.61 nM for the mPEG-glycine-quinidine con

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

64 ed in the presence of two CYP2D6 inhibitors, quinidine and ajmalicine.

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

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

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

68 Quinidine and digoxin are both substrates for P-glycopro

69 d increased rotor complexity. Application of quinidine and disopyramide, but not sotalol, normalized

70 Furthermore, treatment with quinidine and flecainide abolished LBLPS-induced ventric

71 For quinidine and flecainide, which bind preferentially to t

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

73 Quinidine and fluoxetine blocked all GoF variants, where

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

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

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

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

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

79 ard the clinically used antiarrhythmic drugs quinidine and ranolazine, but not flecainide.

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

81 pothesis (2.28 x 10(-)(3) mumol/g tissue for quinidine and ~4.10 x 10(-)(4) mumol/g tissue for the co

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

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

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

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

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

87 Amiodarone, quinidine, and dofetilide are AADs with numerous and cli

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

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

90 potency of these compounds when compared to quinidine, and their selectivity for KCNT1 over hERG and

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

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

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

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

95 Here, we explore the FDA-approved drug quinidine as a P-gp inhibitor.

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

97 Quinidine as the catalyst initiates a peroxyhemiacetaliz

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

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

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

101 Quinidine block also revealed that mutant receptors gene

102 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.

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

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

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

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

107 ative sodium-activated potassium currents to quinidine blockade.

108 )1.6 binds to and highly sensitizes Slack to quinidine blockade.

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

110 of quinine and the (R)-ligand in the case of quinidine, both with >99% ee.

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

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

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

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

115 alaria, arrhythmia, and pseudobulbar effect, quinidine can induce acquired long QT syndrome and torsa

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

117 e, crown ether, and zwitterionic quinine and quinidine carbamate-based chiral stationary phases).

118 A quinidine-catalyzed diastereoselective addition of alpha

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

120 Quinidine, cilostazol, and milrinone suppress the hypoth

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

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

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

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

125 The mPEG-glycine-quinidine conjugate retained its ability to inhibit the

126 r quinidine and 4.61 nM for the mPEG-glycine-quinidine conjugate).

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

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

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

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

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

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

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

134 ars), 3 (16%) of patients discharged without quinidine developed recurrent polymorphic VT.

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

136 Quinidine did not show evidence for direct inhibition of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 Quinidine has been used as an anticonvulsant to treat pa

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

161 REK-1 autoantibodies that are antagonized by quinidine in both HEK293 cells and human induced pluripo

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

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

164 The ability of quinidine in therapeutic concentrations to prolong repol

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

166 Moreover, quinidine increased digoxin brain concentrations by 73.2

167 Quinidine increased plasma digoxin concentrations by 73.

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

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

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

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

172 This quinidine-induced channel internalization was confirmed

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

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

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

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

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

178 cross the ventricular wall before and during quinidine infusion.

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

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

181 Quinidine inhibited the hydroxylation of imipramine comp

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

183 Quinidine inhibits proliferation and promotes cellular d

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

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

186 Additionally, the distribution of quinidine into perfused mouse myocardium was decreased b

187 Initially, quinidine intracellularly blocked the open channel so ra

188 Patients treated with quinidine invariably survived to hospital discharge.

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

190 Quinidine is a known KCNT1 blocker, but its clinical use

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

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

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

194 Pore blockade by quinidine is achieved through both direct obstruction of

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

196 Quinidine is currently the recommended treatment for sev

197 Quinidine is effective in SCVF and should be considered

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

199 Although quinidine is known to elevate plasma digoxin concentrati

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

201 Quinidine is positioned right beneath the selectivity fi

202 Quinidine is the only oral medication that is effective

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

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

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

206 -anhydride 17 was enabled by a high yielding quinidine-mediated opening with benzyl alcohol to genera

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

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

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

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

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

212 he effects of the drug compounds flecainide, quinidine, nifedipine, verapamil, blebbistatin and omeca

213 Quinidine normalized the QT interval and prevented stimu

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

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

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

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

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

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

220 16.8-480 microg of GF120918 or 0.3-3.0 mg of quinidine) or vehicle (buffer or DMSO, respectively) was

221 transient outward current blockers (such as quinidine), or surgical interventions, including left ca

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

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

224 hrough a glycine linker, making a monovalent quinidine-polymer conjugate, which was then evaluated fo

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

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

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

228 volves a resolution, through the quinine- or quinidine-promoted methanolysis of the cyclic anhydride

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

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

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

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

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

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

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

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

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

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

239 Quinidine reduced maximum theta' in WT and caused earlie

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

241 Although quinidine represents an encouraging opportunity for ther

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

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

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

245 .5-GFP with the class I antiarrhythmic agent quinidine resulted in a dose- and temperature-dependent

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

247 However, the detailed mechanism underlying quinidine's blockade against KCNT1 (Slack) remains elusi

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

249 5 min despite the high retentitivity of the quinidine selector.

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

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

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

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

254 the fragment-sized natural products quinine, quinidine, sinomenine, and griseofulvin with chromanone

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

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

257 Because levels of quinidine sulfate attainable in clinical practice shorte

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

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

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

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

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

263 Lilly announced it would stop manufacturing quinidine, the only Food and Drug Administration-approve

264 There were no recurrent arrhythmias during quinidine therapy Conclusions: Arrhythmic storm with rec

265 n patients with coronary disease responds to quinidine therapy when other antiarrhythmic drugs (inclu

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

267 nous amiodarone, but invariably responded to quinidine therapy.

268 polyethylene glycol (mPEG) was conjugated to quinidine through a glycine linker, making a monovalent

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

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

271 We hypothesize that the conjugation of quinidine to a polymer will permit its use as a P-gp inh

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

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

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

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

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

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

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

279 the lower arrhythmogenicity associated with quinidine treatment.

280 0 3A4-catalyzed oxidations of nifedipine and quinidine, two prototypic substrates, in liver microsome

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

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

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

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

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

286 Quinidine was associated with a decrease in doxorubicin

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

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

289 Quinidine was infused continuously; its plasma level inc

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

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

292 Dextromethorphan-quinidine was not associated with cognitive impairment,

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

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

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

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

297 antiarrhythmic drugs, such as flecainide and quinidine, which may reduce ventricular arrhythmias and

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

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