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说明： Potent thioredoxin reductase (TrxR) inhibitor
化学名： (Diphenyl-2-thienylphosphine-κP)[2-(4-methoxyphenyl)ethynyl]gold
纯度： ≥98% (HPLC)
生物活性 for D9
D9 is a 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.
技术数据 for D9
| 分子量 | 596.43 |
| 公式 | C25H20AuOPS |
| 储存 | Store at -20°C |
| 纯度 | ≥98% (HPLC) |
| CAS Number | 1527513-89-8 |
| PubChem ID | 127021039 |
| InChI Key | DROLHVHTLXUINH-UHFFFAOYSA-O |
| Smiles | [Au].COC1=CC=C(C=C1)C#C.S1C=CC=C1P(C1=CC=CC=C1)C1=CC=CC=C1 |
上方提供的技术数据仅供参考。批次相关数据请参见分析证书。
Tocris products are intended for laboratory research use only, unless stated otherwise.
产品说明书 for D9
参考文献 for D9
参考文献是支持产品生物活性的出版物。
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
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关键词: D9, D9 supplier, Thioredoxin, reductase, TrxR, inhibitors, inhibits, anti-tumor, cancer, gold, Au, Reductases, 5921, Tocris Bioscience
1 篇 D9 的引用文献
引用文献是使用了 Tocris 产品的出版物。 D9 的部分引用包括：
Wang et al (2019) Pyridine nucleotide regulation of hepatic endoplasmic reticulum calcium uptake. Physiol Rep 7 e14151 PMID: 31222964
D9 的评论
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该领域的文献
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*请注意，Tocris 仅会向正规科研企业/机构地址发送文献。
Autophagy Poster
Autophagy is a cellular process used by cells for degradation and recycling. Written by Patricia Boya and Patrice Codogno, this poster summarizes the molecular machinery, physiology and pathology of autophagy. Compounds available from Tocris are listed.
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.