ライフサイエンスコーパス: disulfiram

1 ing cultures with the RA synthesis inhibitor disulfiram.

2 oxidative decomposition of small amounts of disulfiram.

3 ng activity of bi-TPB-PPB in the presence of disulfiram.

4 presence of the copper exchanger/ionophore, disulfiram.

5 that proposed for the classic ALDH inhibitor disulfiram.

6 ed after oral tariquidar, and injected after disulfiram.

7 role for increasing cocaine free urines with disulfiram.

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

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

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

11 motherapy alone, or SOC with the addition of disulfiram (400 mg daily) and copper (2.5 mg daily).

12 0 elective surgical patients received either disulfiram (500 mg orally, n = 10) or nothing (controls,

13 e, we show that inhibiting RA synthesis with disulfiram, a deterrent of human alcohol abuse, improves

14 Here we identify disulfiram, a drug for treating alcohol addiction, as an

15 Disulfiram, a drug prescribed for the treatment of alcoh

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

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

18 Disulfiram, a potent ALDH2 inhibitor, is an approved dru

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

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

21 ifetime receipt of FDA-approved medications (disulfiram, acamprosate, and naltrexone), psychotherapy

22 therapy was defined as the documented use of disulfiram, acamprosate, naltrexone, gabapentin, topiram

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

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

25 During disulfiram administration, residual viremia did not chan

26 or the proximal inhibitors of ALDH following disulfiram administration.

27 re disulfiram to timepoints during and after disulfiram administration.

28 Disulfiram affects relevant signaling pathways and can b

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

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

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

32 Treatment with disulfiram, an ALDH2 inhibitor, exacerbated 4HNE-mediate

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

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

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

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

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

38 Disulfiram and CBT are effective therapies for general p

39 andomized to either SOC (n = 45) or SOC plus disulfiram and copper (n = 43), 63 (72%) were male; the

40 More patients in the SOC plus disulfiram and copper group had adverse events grade 3 o

41 These findings suggest that disulfiram and copper is without benefit in patients wit

42 Treating TNBC cells with a disulfiram and copper mixture (DSF/Cu) specifically decr

43 with recurrent glioblastoma, the addition of disulfiram and copper to chemotherapy, compared with che

44 ce between the study groups (SOC vs SOC plus disulfiram and copper) in 6 months survival (62% [26 of

45 onths (95% CI, 3.9-9.3 months) with SOC plus disulfiram and copper, and median progression-free survi

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

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

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

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

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

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

52 findings uncover a novel therapeutic use for disulfiram and suggest that GSDMD is a therapeutic targe

53 Disulfiram and valproic acid are known to inhibit ALDH5A

54 d injectable naltrexone, 152 (63.0%) covered disulfiram, and 103 (42.7%) covered all 4 medications.

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

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

57 uantity limit requirements) for acamprosate, disulfiram, and oral and injectable naltrexone together

58 istration (FDA)-approved MAUDs (acamprosate, disulfiram, and oral and injectable naltrexone) and non-

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

60 amifostine, sodium diethyldithiocarbamate or disulfiram, and sodium thiosulfate.

61 Disulfiram (Antabuse((R))) is a prescription alcohol sob

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

63 Conversely, disulfiram appeared to up-regulate arginine catabolism f

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

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

66 Disulfiram blocks pyroptosis and cytokine release in cel

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

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

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

70 We concluded that disulfiram can serve as a booster and adjuvant for antic

71 Disulfiram changed the shape of the brain time-activity

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

73 Disulfiram, converted in vivo to an effective inhibitor

74 nanoparticles coloaded with regorafenib and disulfiram/copper ion chelate repolarized the tumor-prom

75 nanoparticles coloaded with regorafenib and disulfiram/copper ion chelate repolarized the tumor-prom

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

77 At nanomolar concentration, disulfiram covalently modifies human/mouse Cys191/Cys192

78 ing a metabolite of the clinically used drug disulfiram (CuET), prolonged PARP1 trapping and enhanced

79 (500 mg, 1000 mg, and 2000 mg) and received disulfiram daily for 3 days.

80 GSDMD inhibitor disulfiram decreased eCIRP release in vitro.

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

82 The metabolomic analysis indicated that disulfiram depletes coenzyme A and attenuates the catabo

83 vitro and cell-based assays showed that the disulfiram derivative bis-(diethyldithiocarbamate)-coppe

84 ifostine, sodium diethyldithiocarbamate, and disulfiram did not show hearing preservation.

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

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

87 bi-TPB-PPB may be associated with the use of disulfiram (DSF) a known aldehyde dehydrogenase 2 (ALDH2

88 have been exposed to the cell stress inducer disulfiram (DSF) and copper (Cu)(DSF/Cu) plus ionizing i

89 1 was knocked out and ALDH1A1 inhibited with disulfiram (DSF) either alone or together with PD-L1 ant

90 In this study, we demonstrated that Disulfiram (DSF) induces ferroptosis to synergize with T

91 Disulfiram (DSF) is an FDA-approved drug that has been r

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

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

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

95 dies suggest that the alcohol aversion drug, disulfiram (DSF), inhibited MGMT and improved the effica

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

97 ding z-VAD, necrostatin-1, ferrostatin-1, or disulfiram (DSF), to block the different forms of PCD.

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

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

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

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

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

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

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

105 Disulfiram has been an effective cocaine addiction pharm

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

107 Disulfiram has been used for several decades in the trea

108 Disulfiram has demonstrated broad antitumoral effect in

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

110 Disulfiram has emerged as a promising treatment for coca

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

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

113 macotherapy with naltrexone, acamprosate, or disulfiram; however, these medications are rarely used.

114 ther revealed that the primary metabolite of disulfiram (i.e., diethyldithiocarbamate) is likely invo

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

116 The role of disulfiram in inhibiting GSDMD provides new therapeutic

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

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

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

120 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)

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

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

123 RNA-seq transcriptome analysis revealed that disulfiram induces oxidative stress, redox imbalance, me

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

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

126 GSDMD inhibitor disulfiram inhibited serum levels of eCIRP in endotoxemi

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

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

129 Disulfiram inhibits ATP hydrolysis and the binding of [a

130 In the final analysis, disulfiram inhibits the growth of S. aureus by inducing

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

132 We found that disulfiram is capable of killing breast cancer cells wit

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

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

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

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

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

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

139 Disulfiram may be suited for future studies of combinati

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

141 Therefore, disulfiram may have anticancer potential in combination

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

143 Single-dose disulfiram may provide effective prophylaxis against hal

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

145 Disulfiram, MeDTC sulfoxide, and MeDTC sulfone, respecti

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

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

148 s approved in the United States to treat AUD-disulfiram, naltrexone (oral and long-acting injectable

149 acid, progesterone, estradiol, epinephrine, disulfiram, nitazoxanide and some drug combinations incl

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

151 ught to define the principal mechanisms that disulfiram operates as a growth inhibitor of Staphylococ

152 Inhibition of GSDMD with disulfiram or genic deletion abrogated NET formation, re

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

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

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

156 defined as oral naltrexone, acamprosate, or disulfiram pharmacy fills within 2 days of discharge.

157 Likewise, disulfiram radiosensitization of tumor cells was copper-

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

159 4(+) T cell model that the FDA-approved drug disulfiram reactivates latent HIV-1 without global T cel

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

161 Participants assigned to disulfiram reduced their cocaine use significantly more

162 mprosate have central nervous system action, disulfiram reduces alcohol intake through peripheral mec

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

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

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

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

167 New work in The EMBO Journal now describes a disulfiram role in immunotherapy of cancer, involving di

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

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

170 Disulfiram seems to exert a direct effect on cocaine use

171 In vivo Ca(2+) imaging shows that disulfiram sharpens orientation tuning of visual cortica

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

173 Disulfiram still allows IL-1beta and GSDMD processing, b

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

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

176 amifostine, sodium diethyldithiocarbamate or disulfiram, systemic sodium thiosulfate, intratympanic t

177 Dexamethasone and disulfiram (tetraethylthiuram disulfide; Antabuse) were

178 bited by small molecule compounds, including disulfiram that directly targets the PHD finger of PHF23

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

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

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

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

183 Administration of disulfiram to patients on antiretroviral therapy does no

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

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

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

187 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

188 P = .02), and 10 patients (24%) discontinued disulfiram treatment because of adverse effects.

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

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

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

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

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

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

195 Recently, the anti-alcohol abuse drug disulfiram was found to target cancer through Npl4, a co

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

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

198 Disulfiram was well tolerated at all doses.

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

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