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1 anced by the thioredoxin-reductase inhibitor auranofin.
2 classical cytotoxic Au(I)-phosphine compound auranofin.
3                         Trx depletion (using auranofin, 2-5 muM) reduced Cav3.2 currents and their CO
4 brucei brucei cells were highly sensitive to auranofin, a compound that specifically targets selenopr
5       Such an effort led to the discovery of auranofin, a drug initially approved as an anti-rheumati
6                                              Auranofin, a known inhibitor of selenoprotein synthesis
7  TXNRD1 antioxidant pathways with MK2206 and auranofin, a U.S. Food and Drug Administration-approved
8                       This screen identified auranofin, a US Food and Drug Administration (FDA)-appro
9                                 Tungstate or auranofin addition also blocked this enhanced biofilm de
10 e thioredoxin reductase 1 inhibitor (TXNRD1) auranofin (AF) to NSCLC cells treated with combination o
11 al action of stannous salts and a gold drug, auranofin, against Treponema denticola is mediated throu
12                           The TrxR inhibitor auranofin also increased PDGF-beta receptor phosphorylat
13  betalac translocation, and was sensitive to auranofin, an inhibitor of thioredoxin reductase.
14 utrient-deprivation conditions we identified auranofin, an orally bioavailable FDA-approved antirheum
15 hibitors of thioredoxin reductase, including auranofin and 1-chloro-2,4-dinitrobenzene, attenuated H(
16 al therapy and two experimental drugs, i.e., auranofin and buthionine sulfoximine, was able to reduce
17                The protection was blocked by auranofin and required an intact selenocysteine residue
18 antireservoir treatment, i.e., the gold salt auranofin and the investigational chemotherapeutic agent
19 o novel gold complexes, which we compared to auranofin and to their phosphonium analogue.
20 bitors, either lanthanum chloride (LaCl3) or auranofin (AUR), also increase survival rates of mice un
21 bolism with buthionine sulfoximine (BSO) and auranofin (AUR), respectively, induced significant decre
22 and behaved differently from phosphonium and auranofin, both in vitro and in vivo.
23 r better biological effects as compared with Auranofin, but contrary to Auranofin they were found to
24                                              Auranofin decreases the reducing capacity of target bact
25                                 In addition, auranofin displayed synergistic lethality with heme oxyg
26  a rationale to reposition the approved drug auranofin for clinical evaluation in the therapy of CLL.
27 , this study provides valuable evidence that auranofin has significant promise to be repurposed as a
28            Gold phosphine complexes, such as auranofin, have been recognized for decades as antirheum
29 crosulfonamide (NSA) synergizes with BSO and auranofin in killing TSC-deficient cells.
30 ntracellular reactive oxygen species levels, auranofin induced a lethal endoplasmic reticulum stress
31          Treatment with the H-TrxR inhibitor auranofin inhibited HOSCN metabolism in 16HBE lysates an
32          Our biochemical studies showed that auranofin inhibits the bacterial thioredoxin reductase,
33  1 DMARD (hydroxychloroquine, sulfasalazine, auranofin, intramuscular gold, D-penicillamine, methotre
34                           We also found that auranofin is active against other Gram-positive bacteria
35                                Additionally, auranofin is capable of eradicating intracellular MRSA p
36                                 Furthermore, auranofin is efficacious in a mouse model of MRSA system
37                                 In contrast, auranofin killed cells and oxidized Trx1, also targeting
38  hamster model of amebic liver abscess, oral auranofin markedly decreased the number of parasites, th
39  drugs, and that the existing clinical agent auranofin may be repurposed to aid in the treatment of s
40  also confirmed that the lack of activity of auranofin observed against Gram-negative bacteria is due
41                                              Auranofin overcame apoptosis resistance mediated by prot
42                              This new use of auranofin represents a promising therapy for amebiasis,
43 ibition of TrxR2 in isolated mitochondria by auranofin resulted in increased H(2)O(2) emission, an ef
44                                              Auranofin (Ridaura) is approved for use in treating rheu
45                                              Auranofin's ability to suppress bacterial protein synthe
46               The present study demonstrates auranofin's antibacterial activity is a complex process
47 idant enzymes, with siRNAs or its inhibitor, auranofin, sensitized NSCLC cells to MK2206 treatment in
48 ric disulfide DJ-1 complex was stabilized by auranofin, suggesting that thioredoxin recycles it in ce
49  thioredoxin reductase assays suggested that auranofin targets the E. histolytica thioredoxin reducta
50 ized, and along with the antiarthritic drug, auranofin, tested as inhibitors of the cysteine-dependen
51                                 Analogous to auranofin, the N-heterocyclic carbenes (NHCs) were also
52  as compared with Auranofin, but contrary to Auranofin they were found to be less cytotoxic in vitro.
53 e (BSO, glutathione synthesis inhibitor) and auranofin (thioredoxin reductase inhibitor) induces oxid
54 -1 transgenic mice, an in vivo model of CLL, auranofin treatment markedly reduced tumor cell burden a
55                                     Finally, auranofin was efficacious in a murine model of methicill
56                                              Auranofin was ten times more potent against E. histolyti
57 holoronitrosourea) or thioredoxin reductase (auranofin) was effective in causing EOMA death as well.
58                               The effects of auranofin were reproduced in cardiomyocytes; superoxide
59                          This contrasts with auranofin, where the absence of Sec more strongly pertur

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