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Auranofin

Catalog No. T1303 CAS 34031-32-8

Synonyms: SKF-39162

Auranofin (SKF-39162) is an antirheumatic agent, is used to treat rheumatoid arthritis, improves arthritis symptoms including painful or tender and swollen joints and morning stiffness.

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Auranofin, CAS 34031-32-8

Pack Size	Availability	Price/USD
5 mg	In stock	$ 37.00
10 mg	In stock	$ 59.00
25 mg	In stock	$ 113.00
50 mg	In stock	$ 189.00
100 mg	In stock	$ 289.00
1 mL * 10 mM (in DMSO)	In stock	$ 64.00

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Purity: 99.01%

Purity: 98.87%

Purity: 98%

Purity: 97.4%

Purity: 97%

Biological Description

Chemical Properties

Storage & Solubility Information

Description	Auranofin (SKF-39162) is an antirheumatic agent, is used to treat rheumatoid arthritis, improves arthritis symptoms including painful or tender and swollen joints and morning stiffness.
Targets&IC50	TrxR:0.2 μM
In vitro	Auranofin, an established rheumatoid arthritis treatment, also shows promise across a spectrum of other conditions such as cancer and neurodegenerative diseases. It triggers apoptosis via a Bax/Bak-dependent pathway by selectively disrupting mitochondrial redox balance and oxidizing Prx3[1]. Furthermore, auranofin hampers SKOV3 cell proliferation and survival in a dose- and time-specific manner, instigating caspase-3 activation, elevating pro-apoptotic Bax and Bim proteins, and diminishing the anti-apoptotic Bcl-2 in SKOV3 cells[2]. This lipophilic gold-based agent, known for its anti-inflammatory and immunosuppressive characteristics, notably impedes cell growth and induces mitochondrial apoptosis in PC3 human prostate cancer cells, with a noteworthy reduction in cell viability at an IC50 of 2.5 µM after 24 hours[3].
In vivo	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, without effect on the depressed IL-3 production[4].
Cell Research	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].

Synonyms	SKF-39162
Molecular Weight	678.49
Formula	C20H34AuO9PS
CAS No.	34031-32-8

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 22.5 mg/mL (33.16 mM)

References and Literature

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. 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. 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. 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. 5. Zhang Y, Zhou J, Ye Q, et al. 6-Dithio-2′-deoxyguanosine analogs induce reactive oxygen species-mediated tumor cell apoptosis via bi-targeting thioredoxin 1 and telomerase[J]. Toxicology and Applied Pharmacology. 2020: 115079. 6. Lu H, Lu W, Zhu Y, et al. Auranofin Has Advantages over First-Line Drugs in the Treatment of Severe Streptococcus suis Infections[J]. Antibiotics. 2021, 10(1): 26. 7. Xia Y, Chen J, Yu Y, et al. Compensatory combination of mTOR and TrxR inhibitors to cause oxidative stress and regression of tumors[J]. Theranostics. 2021, 11(9): 4335. 8. Zheng X, Yang Z, Gu Q, et al. The protease activity of human ATG4B is regulated by reversible oxidative modification[J]. Autophagy. 2019 (just-accepted).

Citations

1. Zheng X, Yang Z, Gu Q, et al. The protease activity of human ATG4B is regulated by reversible oxidative modification. Autophagy. 2019 2. Xia Y, Chen J, Yu Y, et al. Compensatory combination of mTOR and TrxR inhibitors to cause oxidative stress and regression of tumors. Theranostics. 2021, 11(9): 4335. 3. Lu H, Lu W, Zhu Y, et al. Auranofin Has Advantages over First-Line Drugs in the Treatment of Severe Streptococcus suis Infections. Antibiotics. 2021, 10(1): 26. 4. Zhang Y, Zhou J, Ye Q, et al. 6-Dithio-2′-deoxyguanosine analogs induce reactive oxygen species-mediated tumor cell apoptosis via bi-targeting thioredoxin 1 and telomerase. Toxicology and Applied Pharmacology. 2020: 115079 5. Zheng P, Xia Y, Shen X, et al.Combination of TrxR1 inhibitor and lenvatinib triggers ROS-dependent cell death in human lung cancer cells.International Journal of Biological Sciences.2024, 20(1): 249-264. 6. Shen X, Xia Y, Lu H, et al.Synergistic targeting of TrxR1 and ATM/AKT pathway in human colon cancer cells.Biomedicine & Pharmacotherapy.2024, 174: 116507.

Related compound libraries

This product is contained In the following compound libraries：

Anti-Cancer Drug Library Drug Repurposing Compound Library Inhibitor Library Anti-Cancer Approved Drug Library Anti-Cancer Clinical Compound Library ReFRAME Related Library Lipid Metabolism Compound Library Bioactive Compound Library Anti-Cancer Compound Library Drug-induced Liver Injury (DILI) Compound Library

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Keywords

Auranofin 34031-32-8 Microbiology/Virology Others Antibacterial SARS-CoV SARS coronavirus inhibit Bacterial SKF-39162 Inhibitor SKF39162 SKF 39162 inhibitor

Products are chemical reagents for research use only and are not intended for human use. We do not sell to patients.