ライフサイエンスコーパス: chloroquine

1 amodiaquine and the former first-line agent chloroquine.

2 sensitivity of the mutant parasite lines to chloroquine.

3 oroquine-resistant strains more sensitive to chloroquine.

4 illing profile that is comparable to that of chloroquine.

5 hen cardiac autophagy in vivo was blocked by chloroquine.

6 y inhibited by raising Golgi luminal pH with chloroquine.

7 r cheek injection of capsaicin, formalin, or chloroquine.

8 ared to 17% when treated in combination with chloroquine.

9 1040, 1494, and 1585 nmol/L for double-dose chloroquine.

10 wing alkalinization of the phagolysosomes by chloroquine.

11 te's accumulation of, and susceptibility to, chloroquine.

12 0% versus 16% when given in combination with chloroquine.

13 en artesunate-mefloquine than in those given chloroquine (18.0 h [range 6.0-48.0] vs 24.0 h [6.0-60.0

14 ainst BT-474 breast cancer cells compared to chloroquine, a clinically relevant autophagy inhibitor.

15 of hematin crystallization and inhibition by chloroquine, a common quinoline antimalarial drug.

16 l or genetic means by using 3-methyladenine, chloroquine, a dominant negative form of ATG4B or silenc

17 Treatment with chloroquine, a drug known to inhibit the secretion of ma

18 SO solution containing the antimalarial drug chloroquine, a known inhibitor of beta-hematin formation

19 sensitive to the antiproliferative effect of chloroquine, a lysosomotropic agent often used as a phar

20 ce of impaired autophagosome clearance after chloroquine administration in these mice indicative of i

21 Chloroquine affects neither sporozoites nor liver-stages

22 ssfully treated with the autophagy inhibitor chloroquine after failure of the BRAF(V600E) inhibitor v

23 e 300 mg and 600 mg had better efficacy than chloroquine alone (treatment differences 51.7% [95% CI 3

24 or to chloroquine plus primaquine [n=50]; or chloroquine alone [n=54]).

25 relapse prevention was more efficacious than chloroquine alone, with a similar safety profile.

26 quine, and two (4%) of 54 patients receiving chloroquine alone, with no evidence of an additional eff

27 or 600 mg, primaquine 15 mg for 14 days, or chloroquine alone.

28 nal-tract infections than those treated with chloroquine alone.

29 -87) with primaquine, and 37.5% (23-52) with chloroquine alone.

30 ne plus primaquine, compared with receipt of chloroquine alone.

31 LMP-inducing agent chloroquine also displayed a synergistic anticancer effe

32 stemic mouse infection model, treatment with chloroquine also reduced SCVs.

33 or inhibiting autophagy pharmacologically by chloroquine, also induced the expression of CCL5 in mela

34 Further, they are resistant to chloroquine, an antimalarial drug that interferes with H

35 In vitro and in vivo administration of chloroquine, an endo/lysosomal inhibitor, mimicked Pepst

36 Chloroquine, an inhibitor of lysosomal degradation, did

37 s of bioactive quinoline derivatives such as chloroquine analogues.

38 id (FA) oxidation that was inhibited by both chloroquine and 3-methyl adenine, consistent with traffi

39 mpacted H2O2 levels in mitochondria, whereas chloroquine and a glucose-6-phosphate dehydrogenase (G6P

40 Resistance to chloroquine and antifolate drugs has evolved independent

41 ro assay to elucidate the modes of action of chloroquine and artemisinin.

42 hat is superior to established antimalarials chloroquine and atovaquone.

43 e-chase experiments, together with lysosome (chloroquine and bafilomycin A1) and autophagic (3-methyl

44 came increasingly colocalized in response to chloroquine and bafilomycin treatments.

45 they displayed synergistic interactions with chloroquine and dihydroartemisinin against parasite.

46 Chloroquine and hydroxychloroquine exert beneficial effe

47 n signals of the important antimalaria drugs chloroquine and mefloquine were strongly enhanced utiliz

48 sites comparable to the known antimalarials, chloroquine and mefloquine.

49 ertaken to further investigate the effect of chloroquine and quinidine on the formation of beta-hemat

50 ver, our analyses suggest that PfCRT accepts chloroquine and quinine at distinct but antagonistically

51 Detailed kinetic analyses revealed that chloroquine and quinine compete for transport via PfCRT

52 parasites also have increased sensitivity to chloroquine and some other quinoline antimalarials, but

53 in coendemic areas where Pv is resistant to chloroquine and specific treatment for Pv hypnozoites no

54 d through use of inhibitors of the lysosome (chloroquine) and heparanase (PG545), both alone and in c

55 ous heat, capsaicin, and itch (histamine and chloroquine) and impaired thermoregulation but did not i

56 Histamine, chloroquine, and capsaicin intradermally elicited simila

57 s-positive neurons elicited by id histamine, chloroquine, and capsaicin, respectively, 3.7%, 4.3%, an

58 ositive following id injection of histamine, chloroquine, and capsaicin, respectively.

59 ine (SP), SP+amodiaquine, SP+piperaquine, SP+chloroquine, and co-trimoxazole.

60 s, chlorpromazine, methyl-beta-cyclodextrin, chloroquine, and concanamycin A dramatically reduced SHF

61 , including artemisinin combination therapy, chloroquine, and sulfadoxine-pyrimethamine.

62 ts the intraerythrocytic development of both chloroquine- and pyrimethamine-resistant P. falciparum s

63 esting that the antiproliferative effects of chloroquine are independent of its suppressive actions o

64 chloroquine-azithromycin arm compared to the chloroquine arm (P = .04 and P = .02, respectively).

65 The novel use of chloroquine as a macrophage-preconditioning agent presen

66 of cell surface BMPR-II with agents such as chloroquine as a potential therapeutic approach for heri

67 umors from mice treated with penfluridol and chloroquine as compared to penfluridol alone.

68 Several compounds were equipotent to chloroquine as inhibitors of the 3D7 strain of P. falcip

69 utant PfCRT transports the antimalarial drug chloroquine away from its target, whereas the wild-type

70 infections were significantly longer in the chloroquine-azithromycin arm compared to the chloroquine

71 Children treated routinely with chloroquine-azithromycin had fewer respiratory and gastr

72 Chloroquine-azithromycin is being evaluated as combinati

73 the effect of treating clinical malaria with chloroquine-azithromycin on the incidence of respiratory

74 nfections among children assigned to receive chloroquine-azithromycin or chloroquine for all symptoma

75 gastrointestinal-tract infections comparing chloroquine-azithromycin to chloroquine monotherapy were

76 Inhibiting autophagy by chloroquine, bafilomycin, 3-methyladenine or LC3BsiRNA,

77 We reasoned that chloroquine, based on its ability to inhibit autophagy a

78 tration of the autophagy-lysosomal inhibitor chloroquine, before EAE onset, delayed disease progressi

79 Cotreatment with the autophagy inhibitor chloroquine blocked the decrease in human ataxin-3 level

80 In cultured rat PASMCs we confirmed that chloroquine both inhibited autophagy pathways and increa

81 While the chloroquine-bridged ferrocenyl derivatives were less act

82 5-50 times lower than an equitoxic amount of chloroquine but did not affect the viability of normal m

83 ced the ability of this protein to transport chloroquine by approximately 93 and 82%, respectively, w

84 ntradermal (id) microinjection of histamine, chloroquine, capsaicin, or vehicle into the left cheek.

85 modium falciparum-infected mosquitoes during chloroquine chemoprophylaxis (hereafter, chemoprophylaxi

86 Volunteers immunized under chloroquine chemoprophylaxis with Plasmodium falciparum

87 larial drug and autophagy/lysosome inhibitor chloroquine (CHQ) is considered as potential trigger of

88 etrial cells, a phenotypical bitter tastant (chloroquine, ChQ) reverses the rise in intracellular Ca(

89 e, but not alpha-methyl-5-hydroxytryptamine, chloroquine, compound 48/80, or bile acid, was markedly

90 to determine the in vivo efficacy of higher chloroquine concentrations against P. falciparum with re

91 laria recurrence rates by day 28 whole-blood chloroquine concentrations at the time of recurrence and

92 In parallel, median chloroquine concentrations were 471, 688, and 809 nmol/L

93 ce-conferring genotype (pfcrt 76T) and day 7 chloroquine concentrations were determined.

94 mal inhibitor and potential chemotherapeutic chloroquine consistently decreased catabolism for all su

95 h Plasmodium chabaudi by mosquito bite under chloroquine cover does not generate pre-erythrocytic imm

96 ABSTRACT: Chloroquine (CQ) and histamine are pruritogens commonly

97 Chloroquine (CQ) and hydroxychloroquine (HCQ) are used t

98 hthalmology recommendations on screening for chloroquine (CQ) and hydroxychloroquine (HCQ) retinopath

99 g the treatment effects of the antimalarials chloroquine (CQ) and quinacrine (Q) on KRAS mutant lung

100 h high malaria endemicity, the withdrawal of chloroquine (CQ) as first-line treatment of Plasmodium f

101 ptosis, while the inhibition of autophagy by chloroquine (CQ) enhanced palmitic acid-induced apoptosi

102 emonstrate that the common anti-malaria drug chloroquine (CQ) extends the lifespan of ZIKV-infected i

103 Chloroquine (CQ) has been evaluated as an autophagy bloc

104 Chloroquine (CQ) has been used as first line malaria the

105 Chloroquine (CQ) is a widely used antimalarial drug with

106 with HDACis and autophagy inhibitors such as chloroquine (CQ) led to a massive accumulation of ubiqui

107 effect of the acidotropic, antimalarial drug chloroquine (CQ) on the antifungal capacity of polymorph

108 lled and randomly assigned to receive either chloroquine (CQ) or artemether-lumefantrine (AL), alone

109 c events (e.g., autophagosome maturation) by chloroquine (CQ) or Lamp2 shRNA, it was substantially di

110 show that a lysosome-independent activity of chloroquine (CQ) prevents degradation of PUMA protein, p

111 cently, several studies have emphasized that chloroquine (CQ) resistance (CQR) can be quantified in t

112 orter (PfCRT) are the primary determinant of chloroquine (CQ) resistance in the malaria parasite Plas

113 dence of the development of Plasmodium vivax chloroquine (CQ) resistance, there have been no trials c

114 KEY POINTS: Chloroquine (CQ) stimulates itch nerves and causes inten

115 lycogen autophagy in skeletal muscles, using chloroquine (CQ) to simulate a vacuolar myopathy that is

116 In Ethiopia, chloroquine (CQ) without primaquine is the first-line tr

117 higher potency of autophagy inhibition than chloroquine (CQ), a well-known autophagy inhibitor that

118 skin-nerve preparation was used to evaluate chloroquine (CQ)- and histamine-induced activation of af

119 target of rapamycin) pathway inhibitors and chloroquine (CQ)-an anti-malarial drug used as a cancer

120 induction of PfCRT, we quantified PfCRT and chloroquine (CQ)-dependent yeast growth inhibition and [

121 valuated for their in vitro activity against chloroquine (CQ)-resistant and sensitive strains of Plas

122 Chloroquine (CQ)-resistant Plasmodium vivax is increasin

123 oline-derived antimalarial family, including chloroquine (CQ).

124 pharmacologic inhibition of autophagy using chloroquine (CQ).

125 two antimalarial drugs, primaquine (PQ) and chloroquine (CQ).

126 lled trial of blood- plus liver-stage drugs (chloroquine [CQ], 3 d; artemether-lumefantrine [AL], 3 d

127 Eligible patients received chloroquine (days 1-3) and were randomly assigned (1:1:1

128 utophagy inhibitors bafilomycin A1 (Baf) and chloroquine demonstrate that autophagy is required for A

129 s, pharmacological autophagy inhibition with chloroquine derivatives depletes cells with high CD44 ex

130 We found that chloroquine diphosphate (CLQ), an antimalarial drug, inh

131 nonhemolytic antimalarial drugs: mefloquine, chloroquine, doxycycline, and pyrimethamine.

132 ingly, classical lysosome inhibitors such as chloroquine, E64D, and pepstatin A were also able to inh

133 Chloroquine enhanced PAEC expression of BMPR-II followin

134 Chloroquine exerted a direct pH-dependent antifungal eff

135 igned to receive chloroquine-azithromycin or chloroquine for all symptomatic malaria episodes over th

136 laria-naive, healthy adult volunteers taking chloroquine for antimalarial chemoprophylaxis (vaccine a

137 on, raising the possibility of reintroducing chloroquine for malaria prevention and treatment.

138 bility of single-dose tafenoquine plus 3-day chloroquine for P vivax malaria radical cure.

139 -dose tafenoquine 300 mg coadministered with chloroquine for P vivax malaria relapse prevention was m

140 A 2-muM concentration of chloroquine fully arrests layer generation and step adva

141 (mean 11.5 h [95% CI 8.3-14.6]) than in the chloroquine group (14.8 h [11.7-17.8]; p=0.034).

142 62%; 95% CI 52.2-70.6]) than in those in the chloroquine group (83 [75%; 65.6-82.5]; p=0.035).

143 rsus 61 (55% [45-64]) of 111 patients in the chloroquine group (difference in proportion 29% [95% CI

144 up versus 2828 days per 1000 patients in the chloroquine group (incidence rate ratio 0.858 [95% CI 0.

145 ine group and 41 (84%) of 49 patients in the chloroquine group at baseline, and in three (6%) of 49 p

146 Although chloroquine had no effect on basal bone resorption, it i

147 he involvement of TLR3 in this process using chloroquine (IC50 11.9 mum) and a dominant negative TLR3

148 dose and 66%, 84%, and 91% after double-dose chloroquine in children aged <5, 5-9, and 10-14 years, r

149 d AO affect the accumulation and activity of chloroquine in these parasites.

150 pe that was mimicked by the fusion inhibitor chloroquine in wild-type cells and rescued by expression

151 sosomal degradation, such as bafilomycin and chloroquine, increased HIF-1alpha levels and HIF-1 activ

152 i and cytosolic vesicles upon treatment with chloroquine, indicating that HS was degraded in lysosome

153 Chloroquine inhibited proliferation and increased apopto

154 Further studies reveal that chloroquine inhibits hematin crystallization by binding

155 ecause concentrations increase with age when chloroquine is prescribed according to body weight.

156 Chloroquine is the first-line treatment for Plasmodium v

157 imatinib was reduced more than tenfold when chloroquine is used simultaneously, which suggests that

158 e (FQ), an antimalarial ferrocenic analog of chloroquine, is a novel inhibitor of HCV.

159 lkalinization of the acidic environment with chloroquine led to a rapid increase in the number of S.

160 The values for chloroquine (log K(ads) = 5.55 +/- 0.03) and quinidine (

161 Here, we show that the antimalarial drug, chloroquine, markedly increased cell surface expression

162 G-protein-coupled receptor C11 agonist), and chloroquine (mas-related G-protein-coupled receptor A3 a

163 is used simultaneously, which suggests that chloroquine may increase the efficacy of TKIs through ly

164 on of its degradation with compounds such as chloroquine, may limit bone destruction in common bone d

165 offers significant advantages compared with chloroquine monotherapy and supports a unified treatment

166 ctions comparing chloroquine-azithromycin to chloroquine monotherapy were 0.67 (95% confidence interv

167 -tract infections compared to treatment with chloroquine monotherapy.

168 eive either artesunate-mefloquine (n=127) or chloroquine (n=125); 226 (90%) patients comprised the mo

169 PK inhibitor compound C, lysosomal inhibitor chloroquine or autophagy inhibitor 3MA enhanced gemcitab

170 activity) were randomised to receive 3 d of chloroquine or dihydroartemisinin-piperaquine in combina

171 gnaling through the endosome is inhibited by chloroquine or dynasore.

172 gy in the tumor cells as well as whether the chloroquine or hydroxychloroquine actually inhibit the a

173 k for maculopathy associated with the use of chloroquine or hydroxychloroquine are not undergoing rou

174 oxychloroquine use, and 1409 (7.8%) had used chloroquine or hydroxychloroquine for at least 4 years.

175 , expert recommendations, long-term users of chloroquine or hydroxychloroquine sulfate should undergo

176 Patients' amount of chloroquine or hydroxychloroquine use in the 5 years sin

177 high-risk patients, each additional month of chloroquine or hydroxychloroquine use was associated wit

178 r SLE, 6339 (35.1%) had at least 1 record of chloroquine or hydroxychloroquine use, and 1409 (7.8%) h

179 Among chloroquine or hydroxychloroquine users and those at hig

180 its (annual visits in >/=3 of 5 years) among chloroquine or hydroxychloroquine users, including those

181 ation of apoptosis, whereas cotreatment with chloroquine or knockdown of Atg7, but not Beclin-1 or Am

182 noculated by mosquitoes to volunteers taking chloroquine or mefloquine (chemoprophylaxis with sporozo

183 nhibiting autophagy with clomipramine (CMI), chloroquine or metformin increased apoptosis and signifi

184 t mite or aerosol ova-albumin challenge, and chloroquine or quinine were tested in both prophylactic

185 The lysosomal inhibitor chloroquine or siRNA knockdown of Atg7 inhibited ORMDL1

186 amine itch did not affect the itch evoked by chloroquine or SLIGRL-NH2, and vice versa.

187 torial activity between a Chk1 inhibitor and chloroquine or the LDHA/LDHB inhibitor GSK 2837808A.

188 nd was inhibited by Unc93b1(3d) mutation and chloroquine or TLR9 deficiency, indicating continued dep

189 nce of an endosomal acidification inhibitor (chloroquine) or a lysosomal degradation inhibitor (Z-FL-

190 h lysosomal inhibitors (ammonium chloride or chloroquine) or inhibitors of cathepsins (Z-FF-FMK or Z-

191 tophagy by pharmacological (3-methyladenine, chloroquine, or bafilomycin A1) or genetic approaches (s

192 2% were Fos-positive following id histamine, chloroquine, or capsaicin.

193 injection of various pruritogens (histamine, chloroquine, or endothelin-1) and recorded spontaneous s

194 ated using lysosomotropic weak bases (NH4Cl, chloroquine, or methylamine) that increased lysosomal pH

195 mal stress inducers, including palmitate and chloroquine, or Torin1, an inhibitor of mammalian target

196 ine (DHA + PIP) was 6.92% vs 29.1% following chloroquine (P < .001).

197 Blockade of autophagic flux by chloroquine partially diminished the protective effect o

198 c countrywide sampling demonstrates that the chloroquine pfcrt genotype has reached near-fixation, ra

199 ax infection recurrence following receipt of chloroquine plus one of 4 doses of tafenoquine (50, 100,

200 [n=57], 300 mg [n=57], 600 mg [n=56]; or to chloroquine plus primaquine [n=50]; or chloroquine alone

201 of tafenoquine (50, 100, 300, or 600 mg) or chloroquine plus primaquine, compared with receipt of ch

202 were randomly assigned to a treatment group (chloroquine plus tafenoquine 50 mg [n=55], 100 mg [n=57]

203 no evidence of an additional effect on QT of chloroquine plus tafenoquine coadministration.

204 ergistic growth inhibition when treated with chloroquine plus the tyrosine kinase inhibitors erlotini

205 lls, inhibition of lysosome degradation with chloroquine prevented CTLA4 loss.

206 cytokines, and inhibition of autophagy with chloroquine prevents the ability of IL-6 to protect from

207 c signatures were also found for atovaquone, chloroquine, proguanil, cycloguanil and methylene blue.

208 live Pf sporozoites (PfSPZ Challenge) under chloroquine prophylaxis (PfSPZ-CVac), and were protected

209 48/80, endothelin-1), not non-histaminergic (chloroquine) pruritogens in Trpv4 keratinocyte-specific

210 ffective quinoline antimalarial drugs (e.g., chloroquine, quinine, amodiaquine) function by preventin

211 , and was blocked by the lysosomal inhibitor chloroquine, rather than proteasome inhibitor MG-132.

212 The autophagy/lysosome inhibitor chloroquine reduced RANKL-induced OC formation and funct

213 ide, bafilomycin A1, or the antimalaria drug chloroquine reduced SCVs in infected host cells.

214 -Bissau, routinely used triple standard-dose chloroquine remained effective for decades despite the e

215 cted with P. falciparum genotypes conferring chloroquine resistance (n = 195, P < .001).

216 We determined rates of chloroquine resistance according to P. vivax malaria rec

217 mutation) both conferred a moderate gain of chloroquine resistance and a reduction in growth rates i

218 le from Cambodia (Cam734) conferred moderate chloroquine resistance and enhanced growth rates, when t

219 micin protection assay in combination with a chloroquine resistance assay to quantify total and cytos

220 sporter, PfCRT, are the major determinant of chloroquine resistance in this lethal human malaria para

221 Chloroquine resistance is dose dependent and can be over

222 pe PfCRT and a PfCRT variant associated with chloroquine resistance transport both ferrous and ferric

223 rtain mutations in the Plasmodium falciparum chloroquine resistance transporter (PfCRT) alter the par

224 n drug resistance determinants P. falciparum chloroquine resistance transporter (PfCRT) and multidrug

225 Mutations in the chloroquine resistance transporter (PfCRT) are the prima

226 sion of the wild-type (WT) allele K76 of the chloroquine resistance transporter gene (pfcrt) at the e

227 The chloroquine resistance transporter of the human malaria

228 s expressing an Asian/African variant of the chloroquine resistance transporter PfCRT.

229 Mutations in the "chloroquine resistance transporter" (PfCRT) are a major

230 r2 (multidrug resistance protein 2) and crt (chloroquine resistance transporter) also showed strong a

231 Mutations in the Plasmodium falciparum chloroquine resistance transporter, PfCRT, are the major

232 n within the gene encoding the P. falciparum chloroquine resistance transporter, PfCRT.

233 Chloroquine resistance was present in 58 (53%) of 113 as

234 om very low frequencies, peaking in 2000 for chloroquine resistance-associated crt and mdr1 genes and

235 Chloroquine resistance-conferring isoforms of PfCRT redu

236 s protein was saturable and inhibited by the chloroquine resistance-reverser verapamil.

237 cy studies to establish the global extent of chloroquine resistance.

238 stance haplotypes, and all clusters shared a chloroquine-resistance genotype matching the pfcrt haplo

239 unds provided better IC90 activities against chloroquine resistant (CQR) malaria than CQ, and seven c

240 In chloroquine-resistant (but not chloroquine-sensitive) pa

241 ed this hypothesis with a clinically derived chloroquine-resistant (CQ(r)) malaria parasite and with

242 smodial activities of QC, MB, and AO against chloroquine-resistant and chloroquine-sensitive P. falci

243 iplasmodial activity in the nM range against chloroquine-resistant as well as chloroquine-sensitive s

244 m and maintained potent activity against the chloroquine-resistant Dd2 parasite.

245 encing was performed in 685, of whom 1 had a chloroquine-resistant genotype.

246 quinoline show improved activity against the chloroquine-resistant K1 strain.

247 considerations about optimal agents to treat chloroquine-resistant malaria.

248 alysis has confounded global surveillance of chloroquine-resistant P. vivax, which is now present acr

249 hinol B shows similarly high potency against chloroquine-resistant Plasmodium falciparum.

250 A high prevalence of chloroquine-resistant Plasmodium vivax in Indonesia has

251 ses enlarged digestive vacuoles, and renders chloroquine-resistant strains more sensitive to chloroqu

252 We show that a MO conjugate that targets the chloroquine-resistant transporter PfCRT is effective aga

253 uction of the C101F or L272F mutation into a chloroquine-resistant variant of PfCRT reduced the abili

254 ective for decades despite the existence of "chloroquine-resistant" P. falciparum.

255 acquired by the PfCRT variant as a result of chloroquine selection.

256 a TLR7/8 dependent mechanism; this leads to chloroquine sensitive production of pro-inflammatory cyt

257 reased lipophilicity and were potent against chloroquine-sensitive (NF54) and -resistant (Dd2 and 7G8

258 erentially improves the activity against the chloroquine-sensitive 3D7 strain.

259 34c was found to be equipotent on chloroquine-sensitive and -resistant cell lines and on b

260 stant transporter PfCRT is effective against chloroquine-sensitive and -resistant parasites, causes e

261 y active against intraerythrocytic stages of chloroquine-sensitive and resistant Plasmodium falciparu

262 MB, and AO against chloroquine-resistant and chloroquine-sensitive P. falciparum and determined wheth

263 The return of chloroquine-sensitive Plasmodium falciparum to the limit

264 nge against chloroquine-resistant as well as chloroquine-sensitive strains of Plasmodium falciparum h

265 In chloroquine-resistant (but not chloroquine-sensitive) parasites, AO and QC increased th

266 2F variant of PfCRT confirmed this increased chloroquine sensitivity and enlarged food vacuole phenot

267 ll patients by day 3, was 100% predictive of chloroquine sensitivity.

268 th mAbs to HLA-DR (but not HLA-A, -B, -C) or chloroquine significantly reduced this nickel-specific I

269 find that the heme-binding antimalarial drug chloroquine specifically increases labile cytosolic heme

270 t of mice with a clinically relevant dose of chloroquine substantially decreased the accumulation of

271 To characterize chloroquine susceptibility over a wide geographic area,

272 contrast to the rapid and complete return of chloroquine-susceptible falciparum malaria after chloroq

273 mg/kg artesunate and 25 mg/kg mefloquine) or chloroquine (target dose 25 mg/kg).

274 Chloroquine targets both limbs of fungal pathogenesis an

275 aimed to compare artesunate-mefloquine with chloroquine to define the optimum treatment for uncompli

276 epatotoxicity, effects that were reversed by chloroquine to disrupt autophagy.

277 displaying an unprecedented binding mode of chloroquine to ferrocene through the bridging of the cyc

278 The widespread use of chloroquine to treat Plasmodium falciparum infections ha

279 We further show that iron and chloroquine transport via PfCRT is electrogenic.

280 amil to be a partial mixed-type inhibitor of chloroquine transport via PfCRT, further supporting the

281 f several genes of P. falciparum involved in chloroquine transport, apicoplast biogenesis, and phosph

282 infected mosquito bites during prophylactic chloroquine treatment (chemoprophylaxis and sporozoites

283 igher elevations in intracellular Abeta than chloroquine treatment alone.

284 ria-inducing Plasmodium yoelii revealed that chloroquine treatment could lead to significant alterati

285 Chloroquine treatment increased whole lung and PASMC p62

286 se in plasma levels of FABP4 is inhibited by chloroquine treatment of mice.

287 ase in DR and fibrosis were attenuated after chloroquine treatment, suggesting that the autophagy-lys

288 sed autophagy, effects that were reversed by chloroquine treatment.

289 m as a function of cellular localization and chloroquine treatment.

290 cell surface BMPR-II, which was inhibited by chloroquine treatment.

291 stance had favorable clinical responses when chloroquine was added to vemurafenib.

292 er impaired or hyperactive in motor neurons, chloroquine was administered to 3-mo-old G85R SOD1YFP mi

293 Standard or double-dose chloroquine was given to 892 children aged <15 years wit

294 This effect of chloroquine was not seen in the absence of intact Tet38

295 , the clinically approved antimalarial agent chloroquine was shown to reduce nanoparticle uptake in m

296 Chloroquine was used for malaria treatment until resista

297 roquine-susceptible falciparum malaria after chloroquine was withdrawn from Malawi, a reemergence of

298 Resistance markers for antifolates and chloroquine were also highly prevalent.

299 noteworthy antiviral compound identified was chloroquine, which disrupted entry and replication of tw

300 ivity profiles comparable to artemisinin and chloroquine while acting through two distinct mechanisms