ライフサイエンスコーパス: auranofin

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