ライフサイエンスコーパス: quinacrine

1 atment with the phospholipase A(2) inhibitor quinacrine.

2 anscription factor and a probable target for Quinacrine.

3 responsible for FER-dependent resistance to quinacrine.

4 cell lines; this activation is inhibited by quinacrine.

5 ose with persistent giardiasis were provided quinacrine.

6 ediate quinacrine, and 51 of 68 who chose no quinacrine.

7 ATP vesicles were visualized with quinacrine.

8 ffected more likely to choose not to receive quinacrine.

9 e agent, the result previously observed with quinacrine.

10 ications for the well known antimalaria drug quinacrine.

11 onic noncompetitive inhibitors, procaine and quinacrine.

12 nown spectrum of activity of chloroquine and quinacrine.

13 YA or the phospholipase A2 (PLA2) inhibitor, quinacrine.

14 s also stained intensely when incubated with quinacrine.

15 Quinacrine (10-50 microM), an inhibitor of phospholipase

16 ral system and were offered a choice between quinacrine (300 mg daily), no quinacrine, or randomisati

17 The phospholipase A2 (PLA2) inhibitor, quinacrine (5 mg/kg) or saline (of equal volume), was ad

18 lphostin C, 1 micromol/L), phospholipase A2 (quinacrine, 5 micromol/L), and cyclooxygenase (indometha

19 Quinacrine, a drug with antimalarial and anticancer acti

20 ent resulted in a dramatic redistribution of quinacrine, a fluorescent congener of CQ, from cytoplasm

21 However, quinacrine, a fluorescent open-channel blocker, has been

22 Quinacrine, a phospholipase A2 inhibitor, inhibited ET-1

23 ty using the pharmacological agonist of p53, quinacrine, accelerates venous thrombus resolution in a

24 Quinacrine achieved clinical and parasitological cure in

25 ine treatment and opted for retreatment with quinacrine achieved clinical cure.

26 erivative QX-314 and the acridine derivative quinacrine act directly as open channel blockers, but ca

27 This unexpected outcome is consistent with quinacrine affecting the intrinsic properties of the CWD

28 To determine whether or not quinacrine also binds near the lipid bilayer when the re

29 For example, quinacrine, an acidotropic fluorescent base, does not ac

30 hospholipase A2 inhibitors (BPB, ONO-RS-082, quinacrine and AACOCF3) and the lipoxygenase inhibitor A

31 rted by 45% and 30% of patients treated with quinacrine and albendazole plus chloroquine, respectivel

32 In contrast, the inhibitors quinacrine and chloroquine bind exclusively to the reduc

33 are discussed in the light of the ability of quinacrine and chloroquine to induce remission of rheuma

34 y of the quinacrine, but the effects of both quinacrine and chloroquine were enhanced by inhibition o

35 Because quinacrine and chlorpromazine have been used in humans f

36 rred treatment, 26 of 38 who chose immediate quinacrine, and 51 of 68 who chose no quinacrine.

37 he binding of the fluorescent NCIs ethidium, quinacrine, and crystal violet as well as [(3)H]thienylc

38 ed by the PLA2 inhibitors aristolochic acid, quinacrine, and PTK.

39 Quinacrine at a dose of 300 mg per day was reasonably to

40 men of the ion channel but probably near the quinacrine binding locus at a nonluminal domain in the A

41 The data support a model for high-affinity quinacrine binding to the same, single locus of the acet

42 ounded by five alpha-helical M2s, imply that quinacrine binds midway down M2 in the same site previou

43 Together, the results indicate that quinacrine binds to a site on the open receptor that is

44 e patient received experimental therapy with quinacrine, but deteriorated and died after a clinical c

45 fication) did not reduce the efficacy of the quinacrine, but the effects of both quinacrine and chlor

46 agents that target IkappaB kinase 2, 9AA and quinacrine can effectively suppress both basal and induc

47 It is further shown that quinacrine can inhibit the binding of [3H]phencyclidine

48 We report that quinacrine, chloroquine, and structurally related compou

49 ng an oral dose of 40 mg/kg/day for 30 days, quinacrine concentration in the brain of wild-type mice

50 One patient treated with quinacrine developed severe neuropsychiatric side effect

51 Extended exposure for 24 h to quinacrine did not further sensitize these cells to TRAI

52 2, including imatinib, mycophenolic acid and quinacrine dihydrochloride.

53 ly two patients chose randomisation; 40 took quinacrine during follow-up (37 who chose it at enrollme

54 In vitro, the off-patent antibiotic Quinacrine efficiently suppressed PRMT5 transcription, c

55 itude of the rapid agonist-induced change in quinacrine emission to 44% +/- 12% of the control value,

56 ast to this reported inhibitory effect, that quinacrine enhances deer and elk PrP(Sc) accumulation an

57 uired to monitor a portion of the changes in quinacrine fluorescence associated with its binding to t

58 dence exists on efficacy and tolerability of quinacrine for nitroimidazole-refractory giardiasis.

59 but not in the outer half, were protected by quinacrine from reaction with 2-aminoethyl methanethiosu

60 e mean ranks were significantly lower in the quinacrine group (14.68) compared to the saline controls

61 Four of 40 patients who took quinacrine had a transient response on neurological rati

62 Quinacrine had an effectiveness rate of 100% in refracto

63 The lipophilic cationic compound quinacrine has been used as an antimalarial drug for ove

64 AA) and its derivative, the antimalaria drug quinacrine, have selective toxicity for tumor cells and

65 misation to immediate quinacrine or deferred quinacrine in an open-label, patient-preference trial.

66 report on the pharmacokinetic properties of quinacrine in mice.

67 in a 6-fold increase in the accumulation of quinacrine in the brain.

68 prove the poor pharmacokinetic properties of quinacrine in the CNS.

69 nalyses indicate that only the inhibition of quinacrine in the desensitized state seems to be mediate

70 The binding site for quinacrine in the open channel of mouse-muscle ACh recep

71 of vma mutants and are unable to accumulate quinacrine in the vacuole, indicating loss of vacuolar a

72 examined the distribution and metabolism of quinacrine in the wild-type and Mdr1(0/0) brains.

73 mutants to accumulate the lysosomotropic dye quinacrine in their vacuoles, five new vma complementati

74 genotype, and evaluates the efficacy rate of quinacrine in those with persistent giardiasis.

75 notypes and show no vacuolar accumulation of quinacrine, indicating loss of vacuolar acidification in

76 Quinacrine induced apoptosis in colon carcinomas and pot

77 in these control cells, neither 17-ODYA nor quinacrine inhibited EGF-induced ERK tyrosine phosphoryl

78 Quinacrine is a noncompetitive antagonist of the nicotin

79 he P-glycoprotein (P-gp) efflux transporter, quinacrine is actively exported from the brain, preventi

80 Quinacrine is an effective treatment for nitroimidazole-

81 We show that quinacrine kills cancer cells primarily by inhibiting th

82 d real-time confocal fluorescence imaging of quinacrine-labeled renin granules, we detected significa

83 rmed by simultaneous fluorescence imaging of quinacrine-loaded zymogen granules.

84 gesting that the activity of chloroquine and quinacrine may in part be due to disruption of pH-depend

85 The antimalarial drug quinacrine (mepacrine) prevents this conversion in vitro

86 dy assessed the efficacy and tolerability of quinacrine monotherapy (100 mg 3 times per day for 5 day

87 In addition, an alkylating derivative, quinacrine mustard, affinity labeled a subset of the sub

88 Half-maximal inhibition required 10 nM quinacrine or 100 nM chloroquine.

89 no quinacrine, or randomisation to immediate quinacrine or deferred quinacrine in an open-label, pati

90 reacted faster in the additional presence of quinacrine or QX-314.

91 choice between quinacrine (300 mg daily), no quinacrine, or randomisation to immediate quinacrine or

92 Moreover, this effect of quinacrine persisted for up to 7 days when the quinacrin

93 Quinacrine phenocopied PRMT5 RNA interference and small

94 Importantly, 2 h of quinacrine pretreatment resulted in decreased expression

95 ts of the antimalarials chloroquine (CQ) and quinacrine (Q) on KRAS mutant lung cancer cells, we demo

96 duction of PrP(Sc) levels in brain, we added quinacrine (Qa) to the treatment regimen.

97 all molecule screen, here we have identified Quinacrine (QC) as a sensitizer for Cytarabine (AraC) in

98 ss, and whether hydroxychloroquine (HCQ) and quinacrine (QC) differentially suppress inflammatory cyt

99 The 9-aminoacridine (9AA) derivative quinacrine (QC) has a long history of safe human use as

100 Quinacrine (QC), a CQ analogue with a fused acridinyl st

101 pounds that have been used to treat malaria (quinacrine [QC] and methylene blue [MB]) or to study P.

102 panel of antimalarial agents and found that quinacrine (QN) had 60-fold higher potency of autophagy

103 s of P-gp-deficient Mdr1(0/0) mice, we found quinacrine reached concentrations of approximately 80 mi

104 Ro 31-8220, but not quinacrine, reduced the sensitization to arachidonic aci

105 reported serious adverse events were judged quinacrine-related.

106 Overexpression of FER from a cDNA confers quinacrine resistance to several different types of canc

107 n-based insertional mutagenesis to isolate a quinacrine-resistant cell line in which an inserted CMV

108 Quinacrine's ability to reduce levels of pathogenic prio

109 We found that the fluorescent ATP marker quinacrine stained rabbit and bovine ciliary epithelia b

110 , fluid phase endocytosis of Lucifer Yellow, quinacrine staining of acidic intracellular compartments

111 Combination antimalarials that include quinacrine, thalidomide analogs, and Mycophenalate Mofet

112 rtality was lower in those who chose to take quinacrine than in those who did not, this was due to co

113 to assess the proximity of the nAcChR-bound quinacrine to the lipid bilayer while the receptor was t

114 th cortical and striatal damage were summed, quinacrine treated animals also exhibited a significantl

115 However, after 24 h of reperfusion the quinacrine treated rats (n = 18) showed significantly lo

116 inacrine persisted for up to 7 days when the quinacrine treated rats continued to receive a median sc

117 Quinacrine treated rats showed significantly reduced inf

118 prisingly, despite increased prion titers in quinacrine-treated cells, transmission of the resulting

119 Accordingly, quinacrine-treated CWD prions were comprised of an alter

120 stool samples with persisting symptoms after quinacrine treatment (94% parasitological efficacy) and

121 nistration of the phospholipase A2 inhibitor quinacrine virtually eliminated adenosine-induced vasodi

122 50) for chlorpromazine was 3 microM, whereas quinacrine was 10 times more potent.

123 Quinacrine was 50-fold more active than chloroquine, and

124 Quinacrine was a highly effective treatment in nitroimid

125 2% of the control value, indicating that the quinacrine was binding to a site proximal to the membran

126 Quinacrine was concentrated within a vacuolar system wit

127 Quinacrine was effective even when added after the CpG-O

128 Short course of quinacrine was effective in treating refractory cases.

129 Quinacrine was used in 54 (62%); 51 received monotherapy

130 f 9-substituted, acridine-based analogues of quinacrine were synthesized, which demonstrated variable

131 subapical granules, labelled with FM 1-43 or quinacrine, were competent for Ca(2+)-regulated exocytos

132 t alternative to the acridine-based compound quinacrine, which is currently under clinical evaluation

133 Quinacrine, which predominantly blocks the activity of P

134 ridine (9AA), including the antimalaria drug quinacrine, which strongly induced p53 function in RCC a