ライフサイエンスコーパス: disulfiram

1 presence of the copper exchanger/ionophore, disulfiram.

2 that proposed for the classic ALDH inhibitor disulfiram.

3 ed after oral tariquidar, and injected after disulfiram.

4 role for increasing cocaine free urines with disulfiram.

5 hiocarbamate (DDC), a metabolite of the drug disulfiram.

6 ing cultures with the RA synthesis inhibitor disulfiram.

7 oxidative decomposition of small amounts of disulfiram.

8 Patients received either disulfiram (250 mg/d) or placebo in identical capsules.

9 for 2 weeks and subsequently randomized into disulfiram (250 mg/day, n = 34) and placebo groups (n =

10 0 elective surgical patients received either disulfiram (500 mg orally, n = 10) or nothing (controls,

11 A recent study suggested that disulfiram, a drug used to treat alcoholism, might act a

12 We previously reported that disulfiram, a drug used to treat chronic alcoholism, inh

13 hibitors (tariquidar, a known inhibitor, and disulfiram, a putative inhibitor) and 2 routes of admini

14 overexpression as shown by its reversion by disulfiram, a specific ALDH1 inhibitor.

15 In vitro, disulfiram activated HIV transcription in a primary T-ce

16 rm pilot study to evaluate whether 500 mg of disulfiram administered daily for 14 days to HIV-1-infec

17 During disulfiram administration, residual viremia did not chan

18 or the proximal inhibitors of ALDH following disulfiram administration.

19 re disulfiram to timepoints during and after disulfiram administration.

20 Disulfiram affects relevant signaling pathways and can b

21 uation of trifluoroacetic acid production by disulfiram after halothane anaesthesia suggests that P45

22 The inhibitory action of disulfiram against V-ATPase pumps revealed a novel effec

23 e we highlight the potential for repurposing disulfiram (also known by the trade name Antabuse), an o

24 r protein 18 kDa (TSPO) via a combination of disulfiram, an FDA approved drug for alcoholism, and (64

25 ent of novel antigiardial therapies and that disulfiram, an FDA-approved drug, is a promising candida

26 Specifically, disulfiram, an inactive (64)Cu ligand, was first injecte

27 Inhibition of Candida ADH enzyme using disulfiram and 4-methylpyrazole resulted in thicker biof

28 otently and reversibly inhibited by the drug disulfiram and by hydrogen peroxide.

29 Disulfiram and CBT are effective therapies for general p

30 m of action of the alcohol deterrent agents, disulfiram and cyanamide.

31 In contrast, the reduced forms of disulfiram and cystamine, diethyl dithiocarbamate and cy

32 ctural basis for G. lamblia CK inhibition of disulfiram and its analog, thiram, their activities agai

33 ed completely by nonspecific CYP inhibitors (disulfiram and liarozole).

34 The synergistic interaction between disulfiram and radiotherapy was evaluated by combination

35 the presence of the ALDH inhibitor cyanamide/disulfiram and subjected to oxidative stress displayed a

36 Disulfiram and valproic acid are known to inhibit ALDH5A

37 equired for the radiosensitizing activity of disulfiram, and copper-complexed disulfiram enhanced the

38 ssion in liver, sensitivity to the inhibitor disulfiram, and high activity for the oxidation of retin

39 ve compounds such as N-ethylmaleimide (NEM), disulfiram, and organic disulfides [e.g., 2,2'-dithiobis

40 osatetraynoic acid), and two marketed drugs: disulfiram (Antabuse; a compound used in the treatment o

41 stigated the molecular and chemical basis of disulfiram as a multidrug resistance modulator.

42 dentified cystamine, thiamine disulfide, and disulfiram as compounds that have been shown to inhibit

43 We demonstrate that disulfiram, but not N-ethylmaleimide, inhibits in a conc

44 d unexpectedly decreased about 40%-60% after disulfiram, but the accuracy of the radiometabolite corr

45 e exploited MRP4 (ABCC4) to demonstrate that disulfiram can inhibit ATP binding by forming disulfide

46 Disulfiram changed the shape of the brain time-activity

47 Clonogenic cell kill after treatment with disulfiram concentrations less than 4 muM was copper-dep

48 Disulfiram, converted in vivo to an effective inhibitor

49 ein and showed that the antialcoholism drug, disulfiram, could inhibit HCV replication to a similar e

50 (500 mg, 1000 mg, and 2000 mg) and received disulfiram daily for 3 days.

51 Disulfiram decreased plasma-free (18)F-fluoride ion (fro

52 Escalating the disulfiram dosage caused a biphasic reduction in the sur

53 on of P450 2E1 by a single preoperative oral disulfiram dose greatly diminished production of the hal

54 The alcohol-abuse deterrent disulfiram (DSF) is shown to have a highly selective tox

55 showed that in the presence of copper (Cu), disulfiram (DSF), a clinically used antialcoholism drug,

56 Disulfiram (DSF), a member of the dithiocarbamate family

57 One of the dithiocarbamates identified, disulfiram (DSF), is an FDA-approved drug that has previ

58 se with the low DBH level genotype showed no disulfiram effect.

59 urines from 80% to 62% (p = .0001), and this disulfiram efficacy differed by DBH genotype group.

60 activity of disulfiram, and copper-complexed disulfiram enhanced the efficacy not only of external-be

61 One compound, disulfiram, enhanced BCECF fluorescence intensity (altho

62 Furthermore, some of the physiology of the disulfiram-ethanol reaction, that could not be accounted

63 ospective dose-escalation study, to optimise disulfiram exposure we included adults with HIV on suppr

64 Controlled studies of disulfiram (grade B) reveal a mixed outcome pattern--som

65 Disulfiram has been an effective cocaine addiction pharm

66 primary cell model, the antialcoholism drug disulfiram has been shown to induce HIV-1 transcription

67 Disulfiram has been used for several decades in the trea

68 Of all the medications tested to date, disulfiram has demonstrated the most consistent effect t

69 Disulfiram has emerged as a promising treatment for coca

70 Taken together, our results suggest that disulfiram has unique molecular interactions with both t

71 reveals that patients who continuously used disulfiram have a lower risk of death from cancer compar

72 C-loperamide, suggesting that the effects of disulfiram in humans were mediated entirely by inhibitio

73 y of a novel viral target and a new role for disulfiram in inhibiting HCV replication will enhance th

74 and p-nitrophenyl esters, and inhibition by disulfiram in relation to oxidation and hydrolysis catal

75 microM), we verified V-ATPase inhibition by disulfiram in secondary assays that measured ATP hydroly

76 1 (1.5-2.9; p<0.0001) to the timepoint after disulfiram in the 500 mg group; 1.9 (1.6-2.4; p<0.0001)

77 Neither oral tariquidar nor oral disulfiram increased brain uptake of (11)C-dLop.

78 The role of copper in disulfiram-induced toxicity was investigated by clonogen

79 A single oral dose of disulfiram inhibited about 70% of the defluorination of

80 Blockade of RA synthesis with disulfiram inhibited RA-induced transcription and produc

81 o human ALDH-1 is 10 times less sensitive to disulfiram inhibition than are the hamster and rat cytos

82 , and benzaldehyde and was more sensitive to disulfiram inhibition.

83 Disulfiram inhibits ATP hydrolysis and the binding of [a

84 Disulfiram is a safe and well-tolerated drug that may be

85 Since disulfiram is rapidly metabolized in vivo, it is believe

86 dly metabolized in vivo, it is believed that disulfiram is too short-lived to inhibit ALDH directly.

87 Use of disulfiram is widespread but less clearly supported by t

88 foxide (DETC-MeSO), a metabolite of the drug disulfiram, is a selective carbamoylating agent for sulf

89 ne the nature of inhibition of human ALDH by disulfiram, its confirmed metabolite S-methyl N,N-diethy

90 of subject-to-subject variability in plasma disulfiram levels.

91 Disulfiram may be suited for future studies of combinati

92 eted studies on supervised administration of disulfiram may be warranted.

93 Therefore, disulfiram may have anticancer potential in combination

94 ion to modifying cysteines at the ATP sites, disulfiram may interact with the drug-substrate binding

95 Single-dose disulfiram may provide effective prophylaxis against hal

96 elative to copper resulted in attenuation of disulfiram-mediated cytotoxicity, copper was required fo

97 Disulfiram, MeDTC sulfoxide, and MeDTC sulfone, respecti

98 ads to reduced DbetaH activity, and as such, disulfiram might not be an effective treatment of cocain

99 before and after administration of 500 mg of disulfiram (n = 6) or 2,000 mg of cimetidine (n = 2).

100 We assessed the effect of disulfiram on HIV transcription in a dose-escalation stu

101 al or viral proteins that can be targeted by disulfiram or other clinically safe Zn-ejectors.

102 aH level genotype dropped from 84% to 56% on disulfiram (p = .0001), whereas those with the low DBH l

103 ariance, corrected for population structure, disulfiram pharmacotherapy reduced cocaine-positive urin

104 Likewise, disulfiram radiosensitization of tumor cells was copper-

105 The extent to which disulfiram reactivates latent HIV-1 in patient cells is

106 4(+) T cell model that the FDA-approved drug disulfiram reactivates latent HIV-1 without global T cel

107 ly small and variable effects on 2 subjects, disulfiram reduced skull radioactivity by about 70% and

108 Participants assigned to disulfiram reduced their cocaine use significantly more

109 am was copper-dependent, the molar excess of disulfiram relative to copper resulted in attenuation of

110 Short-term administration of disulfiram resulted in increases in cell-associated unsp

111 ystal structure of G. lamblia CK soaked with disulfiram revealed that the compound thiocarbamoylated

112 We demonstrate that in intact cells, disulfiram reverses either MDR1- or MRP1-mediated efflux

113 yde dehydrogenase alone, may be explained by disulfiram's effect on glutamate receptors.

114 ical analyses reveal the molecular target of disulfiram's tumour-suppressing effects as NPL4, an adap

115 Disulfiram seems to exert a direct effect on cocaine use

116 However, disulfiram showed no in vivo efficacy in monkeys to enha

117 the ATP sites are protected with excess ATP, disulfiram stimulates ATP hydrolysis by both transporter

118 previously reported neurological effects of disulfiram, such as its ability to prevent O2-induced se

119 Dexamethasone and disulfiram (tetraethylthiuram disulfide; Antabuse) were

120 itiocarb-copper complex as the metabolite of disulfiram that is responsible for its anti-cancer effec

121 ur purpose was to determine the potential of disulfiram to enhance the antitumor efficacy of external

122 to test the ability of the less toxic agent disulfiram to inhibit defluorination in humans.

123 Moreover, the administration of disulfiram to neonatal mice decreased in vivo cell proli

124 Administration of disulfiram to patients on antiretroviral therapy does no

125 these models to estimate changes from before disulfiram to timepoints during and after disulfiram adm

126 In control and disulfiram-treated patients cumulative 96 h postoperativ

127 spectively, were significantly diminished in disulfiram-treated patients.

128 I 1.3-2.2; p<0.0001) to the timepoint during disulfiram treatment and 2.1 (1.5-2.9; p<0.0001) to the

129 Furthermore, disulfiram treatment enhanced the toxicity of (131)I-MIB

130 ur findings show that both dexamethasone and disulfiram treatment increase the activity of PHM in atr

131 o identify a subset of individuals for which disulfiram treatment might be an effective pharmacothera

132 In contrast, disulfiram treatment, which depletes stores of alpha-ami

133 Benefits of disulfiram use and CBT were most pronounced for particip

134 results demonstrate that the cytotoxicity of disulfiram was copper-dependent, the molar excess of dis

135 The cytotoxic effect of disulfiram was maximal when administered with equimolar

136 tep-wise injection protocol of (64)CuCl2 and disulfiram was used to accomplish the purpose of synthes

137 Disulfiram was well tolerated at all doses.

138 cts experienced by participants who received disulfiram were mild and were not considerably different

139 This suggests that the interaction of disulfiram with the drug-binding site is independent of