Potent thioredoxin reductase (TrxR) inhibitor (EC50 = 2.8 nM, IC50 = 0.03 and 0.1 μM in MCF-7 cells and HT-29 cells, respectively). Highly stable in vivo; exhibits no significant ligand exchange with albumin. Inhibits tumor proliferation in vitro and in vivo by inducing cell death. Selectively kills cancer cells.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 596.43. 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||1.68 mL||8.38 mL||16.77 mL|
|5 mM||0.34 mL||1.68 mL||3.35 mL|
|10 mM||0.17 mL||0.84 mL||1.68 mL|
|50 mM||0.03 mL||0.17 mL||0.34 mL|
References are publications that support the biological activity of the product.
Zhang et al (2014) Synthesis and molecular recognition studies on small-molecule inhibitors for thioredoxin reductase. J.Med.Chem. 57 8132 PMID: 25249032
Lin et al (2015) pH-sensitive polymeric nanoparticles with gold(I) compound payloads synergistically induce cancer cell death through modulation of autophagy. Mol.Pharm. 12 2869 PMID: 26101892
If you know of a relevant reference for D9, please let us know.
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Keywords: D9, D9 supplier, Thioredoxin, reductase, TrxR, inhibitors, inhibits, anti-tumor, cancer, gold, Au, 5921, Tocris Bioscience
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
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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.