ライフサイエンスコーパス: quinacrine

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

2 ose with persistent giardiasis were provided quinacrine.

3 responsible for FER-dependent resistance to quinacrine.

4 cell lines; this activation is inhibited by quinacrine.

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

6 ATP vesicles were visualized with quinacrine.

7 ffected more likely to choose not to receive quinacrine.

8 e agent, the result previously observed with quinacrine.

9 ications for the well known antimalaria drug quinacrine.

10 onic noncompetitive inhibitors, procaine and quinacrine.

11 nown spectrum of activity of chloroquine and quinacrine.

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

13 s also stained intensely when incubated with quinacrine.

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

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

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

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

18 Quinacrine, a drug with antimalarial and anticancer acti

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

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

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

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

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

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

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

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

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

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

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

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

31 Because quinacrine and chlorpromazine have been used in humans f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 Quinacrine had an effectiveness rate of 100% in refracto

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

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

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

58 report on the pharmacokinetic properties of quinacrine in mice.

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

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

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

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

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

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

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

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

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

68 Quinacrine induced apoptosis in colon carcinomas and pot

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

70 Quinacrine is a noncompetitive antagonist of the nicotin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 reported serious adverse events were judged quinacrine-related.

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

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

95 Quinacrine's ability to reduce levels of pathogenic prio

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

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

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

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

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

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

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

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

104 Quinacrine treated rats showed significantly reduced inf

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

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

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

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

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

110 2% of the control value, indicating that the quinacrine was binding to a site proximal to the membran

111 Quinacrine was concentrated within a vacuolar system wit

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

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

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

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

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

117 Quinacrine, which predominantly blocks the activity of P

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