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1 hrough the activity of the FDA-approved drug auranofin.
2 c and exclusive interaction between TrxB and auranofin.
3 ibit thioredoxin reductase (TrxR) similar to auranofin.
4 ent on porcine skin sites exposed to topical auranofin.
5 que mechanistic insights differentiated from auranofin.
6 rediction we validate in vitro with the drug auranofin.
7 ties either similar to or lower than that of auranofin.
8 ared to other standards such as Cisplatin or Auranofin.
9 anced by the thioredoxin-reductase inhibitor auranofin.
10 classical cytotoxic Au(I)-phosphine compound auranofin.
11 city was observed in pigs exposed to topical auranofin.
12                            Most importantly, auranofin (0.125 mg/kg and 0.25 mg/kg) significantly pre
13 andrace cross pigs were exposed topically to auranofin (1%, 2%, and 3%) for 4-14 days and evaluated f
14 LYHO/JngJ mice and then treated with topical auranofin (2%), topical mupirocin (2%), or oral clindamy
15                         Trx depletion (using auranofin, 2-5 muM) reduced Cav3.2 currents and their CO
16                                 Furthermore, auranofin (5 mg/kg) generated a 3.15-log(10) reduction (
17                    All hamsters treated with auranofin (5 mg/kg) survived a lethal challenge with C.
18                                 Furthermore, auranofin (5 mg/kg) was as effective as vancomycin, the
19              We explored this mechanism with Auranofin, a clinical candidate for reducing HIV reservo
20 brucei brucei cells were highly sensitive to auranofin, a compound that specifically targets selenopr
21                          Here we report that auranofin, a drug approved for the treatment of rheumato
22       Such an effort led to the discovery of auranofin, a drug initially approved as an anti-rheumati
23                                              Auranofin, a known inhibitor of selenoprotein synthesis
24                               Interestingly, auranofin, a thioredoxin reductase inhibitor, sensitized
25  TXNRD1 antioxidant pathways with MK2206 and auranofin, a U.S. Food and Drug Administration-approved
26                       This screen identified auranofin, a US Food and Drug Administration (FDA)-appro
27                                      SAS and auranofin activity was largely mitigated by the ferropto
28                                 Tungstate or auranofin addition also blocked this enhanced biofilm de
29 e thioredoxin reductase 1 inhibitor (TXNRD1) auranofin (AF) to NSCLC cells treated with combination o
30 lly, S. aureus did not develop resistance to auranofin after repeated exposure for two weeks via a mu
31 nite supplementation dampens the activity of auranofin against C. difficile regardless of the presenc
32 al action of stannous salts and a gold drug, auranofin, against Treponema denticola is mediated throu
33 ral mechanism and support the repurposing of auranofin-alone or in combination with ribavirin-as a th
34                           The TrxR inhibitor auranofin also increased PDGF-beta receptor phosphorylat
35 to the nontranscriptional apoptotic pathway, auranofin also inhibited the transcriptional activity of
36 trategies that included ART intensification, auranofin (an apoptotic-inducer antirheumatic drug), nic
37                                              Auranofin, an anti-rheumatic drug, was identified to hav
38                  Further, the TrxR inhibitor auranofin, an approved anti-rheumatoid arthritis drug, s
39                                              Auranofin, an FDA-approved arthritis drug, has recently
40 ncer showed that the selenoprotein inhibitor auranofin, an FDA-approved gold salt, chemically induced
41 x potential and Ca(2+) levels in response to auranofin, an inhibitor of antioxidative enzymes, via du
42  betalac translocation, and was sensitive to auranofin, an inhibitor of thioredoxin reductase.
43 utrient-deprivation conditions we identified auranofin, an orally bioavailable FDA-approved antirheum
44                             In this work, 40 auranofin analogues were synthesized by varying the stru
45 hibitors of thioredoxin reductase, including auranofin and 1-chloro-2,4-dinitrobenzene, attenuated H(
46 al therapy and two experimental drugs, i.e., auranofin and buthionine sulfoximine, was able to reduce
47  promotion mediated by the FDA-approved drug auranofin and D-amino acid oxidase as an effective antiv
48                The protection was blocked by auranofin and required an intact selenocysteine residue
49 we demonstrated that combined treatment with auranofin and ribavirin exhibits synergistic antiviral a
50 ty in vitro for combined treatment with both auranofin and ribavirin suggests a potential clinically
51 antireservoir treatment, i.e., the gold salt auranofin and the investigational chemotherapeutic agent
52 o novel gold complexes, which we compared to auranofin and to their phosphonium analogue.
53                                              Auranofin appears to be a potent and safe topical agent
54 lactide (PLA) (PEG-PLA) NPs were loaded with auranofin (ARN), an antirheumatic drug, to induce mitoge
55 d a high-throughput screen, which identified auranofin as a small-molecule inhibitor of the proapopto
56 elenoproteins are still just as sensitive to auranofin as their respective wild-type strains.
57           Upon testing in a CDI mouse model, auranofin at low clinically achievable doses (0.125 mg/k
58 tion of the pharmacological TXNRD1 inhibitor auranofin (AUR) effectively suppressed the growth of HCC
59 bitors, either lanthanum chloride (LaCl3) or auranofin (AUR), also increase survival rates of mice un
60 bolism with buthionine sulfoximine (BSO) and auranofin (AUR), respectively, induced significant decre
61                                              Auranofin binds to the UBA1's ubiquitin fold domain and
62 and behaved differently from phosphonium and auranofin, both in vitro and in vivo.
63 r better biological effects as compared with Auranofin, but contrary to Auranofin they were found to
64                  These findings suggest that auranofin can serve as a much-needed tool for UBA1 resea
65                          Remarkably, topical auranofin completely eradicated MRSA (8-log(10) reductio
66 atenin protein was not changed regardless of auranofin concentration.
67    Collectively, these results indicate that auranofin could potentially provide an effective, safe a
68                                              Auranofin decreases the reducing capacity of target bact
69                                              Auranofin did not affect Caspase 3/7 activity compared t
70                   Instead, it suggested that auranofin directly interacts with the cysteine thiols in
71                                 In addition, auranofin displayed synergistic lethality with heme oxyg
72 rescent redox protein roGFP2, we showed that auranofin does indeed directly interact with cysteine pa
73       We also revealed that ROS promotion by auranofin drives activation of antioxidant, ER stress, a
74                                              Auranofin effectively inhibited the development of tumor
75                                              Auranofin eradicated MRSA in PUs within four days (7.92-
76                                    Moreover, auranofin exhibited a long postantibiotic effect (PAE) i
77                                 Furthermore, auranofin exhibited a prolonged post-antibiotic effect o
78              A time-kill assay revealed that auranofin exhibited rapid bactericidal activity against
79                        We revealed here that auranofin exhibits robust, dose-dependent antiviral acti
80  to determine the mechanism of inhibition of auranofin for bacterial TrxB in the presence of thioredo
81  a rationale to reposition the approved drug auranofin for clinical evaluation in the therapy of CLL.
82 that repurposing gold-containing drugs, like auranofin, for treatment of gonorrhea warrants further i
83                                        Since auranofin has been used for many years as an FDA-approve
84 , this study provides valuable evidence that auranofin has significant promise to be repurposed as a
85            Gold phosphine complexes, such as auranofin, have been recognized for decades as antirheum
86 t study investigated the in vivo efficacy of auranofin in a CDI hamster model.
87                               Repurposing of auranofin in different disease indications such as cance
88 strains, suggesting the possibility of using auranofin in dual therapy.
89 crosulfonamide (NSA) synergizes with BSO and auranofin in killing TSC-deficient cells.
90 7) was found to be higher than cisplatin and auranofin in OvCa cells sensitive and resistant to cispl
91 e antitumor activity of FDA-approved SAS and auranofin in patient-derived xenograft models of MYCN-am
92                                              Auranofin, in combination with azithromycin, ceftriaxone
93 we uncovered a novel mechanism of action for auranofin, in which it induces cellular autophagy to deg
94 toid arthritis drugs sulfasalazine (SAS) and auranofin: in MYCN-amplified, patient-derived xenograft
95 but has GR activity that can be inhibited by auranofin indicates a mechanism for the reduction of glu
96 ntracellular reactive oxygen species levels, auranofin induced a lethal endoplasmic reticulum stress
97 ncentrations and buthionine sulfoximine- and auranofin-induced inhibition of glutathione- and thiored
98                                  DFO reduced auranofin-induced ROS, further linking increased iron ca
99 elevant in vitro model, we demonstrated that auranofin inhibited fatty-acid-induced apoptotic cell de
100          Treatment with the H-TrxR inhibitor auranofin inhibited HOSCN metabolism in 16HBE lysates an
101                        The PKCiota inhibitor auranofin inhibited KP tumor growth and sensitized these
102          Our biochemical studies showed that auranofin inhibits the bacterial thioredoxin reductase,
103  1 DMARD (hydroxychloroquine, sulfasalazine, auranofin, intramuscular gold, D-penicillamine, methotre
104                                              Auranofin is a gold-containing anti-rheumatic drug with
105                                  In summary, auranofin is a novel inhibitor of IRF3 functions and may
106                           We also found that auranofin is active against other Gram-positive bacteria
107                                              Auranofin is an inhibitor of human thioredoxin reductase
108                                Additionally, auranofin is capable of eradicating intracellular MRSA p
109                                 Furthermore, auranofin is efficacious in a mouse model of MRSA system
110 suggesting that selenite's neutralization of auranofin is not because of compensation for a chemicall
111                         The gold(I) complex, auranofin, is active against T. vaginalis and other prot
112                                 In contrast, auranofin killed cells and oxidized Trx1, also targeting
113 otein phosphatase (Dusp)-1 mRNA induction by Auranofin-loaded nanoparticles (ARN-NPs) and viability o
114 ctivities up to 65 folds higher than that of auranofin, making them effective against Gram-negative p
115  hamster model of amebic liver abscess, oral auranofin markedly decreased the number of parasites, th
116  drugs, and that the existing clinical agent auranofin may be repurposed to aid in the treatment of s
117                      ROS inhibition reversed auranofin-mediated ROS promotion and antiviral activity,
118 gistic activity of these drugs resulted from auranofin-mediated upregulation of NOXA pro-apoptotic pr
119  also confirmed that the lack of activity of auranofin observed against Gram-negative bacteria is due
120 ay (thioredoxin/thioredoxin reductase) using auranofin or inhibiting DNA repair using the poly (ADP-r
121                        ROS promotion through auranofin or other means represents an underexplored ant
122          More specifically, we observed that auranofin orchestrates upregulation of the NOXA-encoding
123                                              Auranofin overcame apoptosis resistance mediated by prot
124                                              Auranofin promotes ubiquitination and degradation of mis
125                                    Moreover, auranofin reduced the burden of intracellular N. gonorrh
126                              This new use of auranofin represents a promising therapy for amebiasis,
127 ibition of TrxR2 in isolated mitochondria by auranofin resulted in increased H(2)O(2) emission, an ef
128 dy is to investigate the in vivo efficacy of auranofin (rheumatoid arthritis FDA-approved drug) in a
129                                              Auranofin (Ridaura) is approved for use in treating rheu
130 cose (Solganal), and the orally administered auranofin (Ridaura), are utilized in modern medicine for
131                                              Auranofin's ability to suppress bacterial protein synthe
132               The present study demonstrates auranofin's antibacterial activity is a complex process
133 e is often suggested to be a major factor in auranofin's antibacterial mode of action.
134 at a rate that indicates their pertinence in auranofin's antibacterial mode of action.
135                                              Auranofin's in vitro activity against strains of S. aure
136                                              Auranofin's in vitro antibacterial activity was stable i
137                 The present study highlights auranofin's potential to be investigated further as a tr
138 inhibition of selenoprotein biosynthesis was auranofin's primary mechanism of action against C. diffi
139 idant enzymes, with siRNAs or its inhibitor, auranofin, sensitized NSCLC cells to MK2206 treatment in
140                                              Auranofin, sodium aurothiomalate and aurothioglucose inh
141 ric disulfide DJ-1 complex was stabilized by auranofin, suggesting that thioredoxin recycles it in ce
142  thioredoxin reductase assays suggested that auranofin targets the E. histolytica thioredoxin reducta
143 ized, and along with the antiarthritic drug, auranofin, tested as inhibitors of the cysteine-dependen
144                                 Analogous to auranofin, the N-heterocyclic carbenes (NHCs) were also
145  as compared with Auranofin, but contrary to Auranofin they were found to be less cytotoxic in vitro.
146 e (BSO, glutathione synthesis inhibitor) and auranofin (thioredoxin reductase inhibitor) induces oxid
147 evaluated the safety profile and efficacy of auranofin to treat diabetic PUs infected with methicilli
148 we investigated the potential of repurposing auranofin to treat pressure ulcers infected with MRSA.
149            The Au:protein stoichiometries of auranofin-treated roGFP2 and thioredoxin strongly sugges
150 -1 transgenic mice, an in vivo model of CLL, auranofin treatment markedly reduced tumor cell burden a
151                                Additionally, auranofin treatment resulted in decreased expression of
152 cient cells were unable to degrade IRF3 upon auranofin treatment, suggesting that the autophagic degr
153                                 Furthermore, auranofin treatment, which induces the cyclin D-CDK4 dis
154 ukemia cells with and without hydroxyurea or auranofin treatment.
155                  These results indicate that auranofin warrants further investigation as a new agent
156                                     Finally, auranofin was efficacious in a murine model of methicill
157                                              Auranofin was found superior to ceftriaxone in reducing
158                                              Auranofin was identified as a drug that effectively inhi
159                                              Auranofin was ten times more potent against E. histolyti
160 holoronitrosourea) or thioredoxin reductase (auranofin) was effective in causing EOMA death as well.
161 luid (SIF), on the antibacterial activity of auranofin were investigated.
162                               The effects of auranofin were reproduced in cardiomyocytes; superoxide
163                           Both cisplatin and auranofin were used for comparative purposes.
164                          This contrasts with auranofin, where the absence of Sec more strongly pertur
165                                              Auranofin, which is known to elevate intracellular ROS,
166 O with the thioredoxin reductase 1 inhibitor auranofin, which may prove useful in the management of N

 
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