AuranofinAuranofin
MedChemExpress (MCE)
HY-B1123
34031-32-8
SKF-39162
98.0%
4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months
-20°C, 1 month (sealed storage, away from moisture)
Room temperature in continental US
may vary elsewhere.
Auranofin (SKF-39162) is a thioredoxin reductase (TrxR) inhibitor with an IC50 of 0.2 μM. Auranofin exhibits antiviral activity against SARS-CoV21, with a CC50 of 4.2 μM for monkey kidney Vero E6 cells.
Auranofin is a drug that is approved for the treatment of rheumatoid arthritis but is being investigated for potential therapeutic application in a number of other diseases including cancer, neurodegenerative disorders. Auranofin induces apoptosis in cells through a Bax/Bak-dependent mechanism associated with selective disruption of mitochondrial redox homeostasis in conjunction with oxidation of Prx3[1].Auranofin inhibits proliferation and survival of SKOV3 cells in a dose- and time-dependent manner. Auranofin treatment activates the pro-apoptotic caspase-3, increases protein levels of apoptosis-inducing proteins Bax and Bim and reduces the expression of the anti-apoptotic mediator Bcl-2 in SKOV3 cells[2].Auranofin is a lipophilic gold compound with anti-inflammatory and immunosuppressive properties. Auranofin inhibits the cell growth and induction of mitochondrial apoptosis in PC3 human prostate cancer cells. Treatment with auranofin significantly inhibits cell viability with an IC50 value of 2.5 μM after 24 h[3].
Prophylactic treatment of adjuvant-induced arthritis rats with auranofin results in a slight reduction in paw edema, a complete normalization of the depressed IL-2 production, and a reduction of the elevated IL-1 production, but has no effect on the depressed IL-3 production[4].
Rats: Prophylactically, auranofin (6.7 to 15 mg of gold/kg), indomethacin (2 mg/kg) or tragacanth vehicle control were administered orally at daily intervals beginning on the day of adjuvant injection. On days 16 to 17 peritoneal exudate cells or spleen cells from normal or adjuvant-injected rats were isolated and tested[4].
Auranofin is dissolved in DMSO. Cells are treated with auranofin (0, 50, 100, 200 and 400 nM) for 72 h for the dose-dependent response assay and 100 nM of auranofin is added into the wells for 0, 24, 72 and 120 h for the time-dependent response assay. Control cultures are treated with DMSO. Cell viability is measured by the MTT assay[2].
IC50: 0.2 μM (TrxR)[1] In Vitro Auranofin is a drug that is approved for the treatment of rheumatoid arthritis but is being investigated for potential therapeutic application in a number of other diseases including cancer, neurodegenerative disorders. Auranofin induces apoptosis in cells through a Bax/Bak-dependent mechanism associated with selective disruption of mitochondrial redox homeostasis in conjunction with oxidation of Prx3[1].Auranofin inhibits proliferation and survival of SKOV3 cells in a dose- and time-dependent manner. Auranofin treatment activates the pro-apoptotic caspase-3, increases protein levels of apoptosis-inducing proteins Bax and Bim and reduces the expression of the anti-apoptotic mediator Bcl-2 in SKOV3 cells[2].Auranofin is a lipophilic gold compound with anti-inflammatory and immunosuppressive properties. Auranofin inhibits the cell growth and induction of mitochondrial apoptosis in PC3 human prostate cancer cells. Treatment with auranofin significantly inhibits cell viability with an IC50 value of 2.5 μM after 24 h[3]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Auranofin Related Antibodies
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[1]. Cox AG, et al. The thioredoxin reductase inhibitor auranofin triggers apoptosis through a Bax/Bak-dependent process that involves peroxiredoxin 3 oxidation. Biochem Pharmacol. 2008 Oct 30
76(9):1097-109. [Content Brief]
[2]. Park SH, et al. Auranofin displays anticancer activity against ovarian cancer cells through FOXO3 activation independent of p53. Int J Oncol. 2014 Oct
45(4):1691-8. [Content Brief]
[3]. Park N, et al. Auranofin promotes mitochondrial apoptosis by inducing annexin A5 expression and translocation in human prostate cancer cells. J Toxicol Environ Health A. 2014
77(22-24):1467-76. [Content Brief]
[4]. Lee JC, et al. Effect of auranofin treatment on aberrant splenic interleukin production in adjuvant arthritic rats. J Immunol. 1987 Nov 15
139(10):3268-74. [Content Brief]
[5]. Shuofeng Yuan, et al. Metallodrug ranitidine bismuth citrate suppresses SARS-CoV-2 replication and relieves virus-associated pneumonia in Syrian hamsters. Nat Microbiol. 2020 Oct 7. [Content Brief]
