Inhibitor of thioredoxin reductase (TrxR) (IC50 = 20 nM; Ki = 4 nM for the NADPH-reduced form of human cytosolic TrxR). Thought to induce the mitochondrial permeability transition via inhibition of mitochondrial TrxR. Also exhibits anti-inflammatory and immunosuppressive activities; inhibits 5-lipoxygenase at high concentrations and stimulates LTA hydrolase at low concentrations.
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 678.48. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.47 mL||7.37 mL||14.74 mL|
|5 mM||0.29 mL||1.47 mL||2.95 mL|
|10 mM||0.15 mL||0.74 mL||1.47 mL|
|50 mM||0.03 mL||0.15 mL||0.29 mL|
References are publications that support the products' biological activity.
Kim et al (2007) Auranofin blocks interleukin-6 signalling by inhibiting phosphorylation of JAK1 and STAT3. Immunology 122 607 PMID: 17645497
Rigobello et al (2002) Induction of mitochondrial permeability transition by auranofin, a gold(I)-phosphine derivative. Br.J.Pharmacol. 136 1162 PMID: 12163349
Gromer et al (1998) Human placenta thioredoxin reductase. Isolation of the selenoenzyme, steady state kinetics, and inhibition by therapeutic gold compounds. J.Biol.Chem. 273 20096 PMID: 9685351
Betts et al (1990) Auranofin stimulates LTA hydrolase and inhibits 5-lipoxygenase/LTA synthase activity of isolated human neutrophils. Biochem.Pharmacol. 39 1233 PMID: 2157444
If you know of a relevant reference for Auranofin, please let us know.
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Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.