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1 anced by the thioredoxin-reductase inhibitor auranofin.
2 classical cytotoxic Au(I)-phosphine compound auranofin.
4 brucei brucei cells were highly sensitive to auranofin, a compound that specifically targets selenopr
7 TXNRD1 antioxidant pathways with MK2206 and auranofin, a U.S. Food and Drug Administration-approved
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
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
18 antireservoir treatment, i.e., the gold salt auranofin and the investigational chemotherapeutic agent
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
23 r better biological effects as compared with Auranofin, but contrary to Auranofin they were found to
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
30 ntracellular reactive oxygen species levels, auranofin induced a lethal endoplasmic reticulum stress
33 1 DMARD (hydroxychloroquine, sulfasalazine, auranofin, intramuscular gold, D-penicillamine, methotre
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
43 ibition of TrxR2 in isolated mitochondria by auranofin resulted in increased H(2)O(2) emission, an ef
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
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
57 holoronitrosourea) or thioredoxin reductase (auranofin) was effective in causing EOMA death as well.
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