Aurothiomalate sodium(Synonyms: 金硫丁二钠)

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Aurothiomalate sodium (Synonyms: 金硫丁二钠)

Aurothiomalate sodium 是一种有效的和选择性的致癌 PKCι 信号传导抑制剂。Aurothiomalate sodium 抑制肿瘤细胞增殖，而不抑制细胞凋亡。Aurothiomalate sodium 是一种有效的硫氧还蛋白还原酶 (TrxR) 抑制剂。Aurothiomalate sodium 是一种抗风湿剂，显示出有效的抗肿瘤活性。

Aurothiomalate sodium(Synonyms: 金硫丁二钠)

Aurothiomalate sodium Chemical Structure

CAS No. : 12244-57-4

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生物活性

Aurothiomalate sodium is a potent and selective oncogenic PKCι signaling inhibitor. Aurothiomalate sodium inhibits tumor cell proliferation and not cell apoptosis. Aurothiomalate sodium is a potent thioredoxin reductase (TrxR) inhibitor. Aurothiomalate sodium, an anti-rheumatoid agent, exhibits potent anti-tumor activity[1][2][3].

IC50 & Target[1][2]

PKCι

 

体外研究
(In Vitro)

Aurothiomalate sodium (0.001, 0.01, 0.1, 1, 10, 100, 1000 uM) induces dose-dependent inhibition of anchorage-independent growth in all cell lines tested (A549, H1437, H2170, H460, H510, H187, H1703 and A427 lung cancer cell lines) with IC50s ranging from 300 nM-107 µM. The lung adenocarcinoma (LAC) and small cell lung carcinoma (SCLC) cells tends to be more sensitive and lung adenocarcinomas (LACs) less sensitive to Aurothiomalate sodium[1].
Aurothiomalate sodium (25 uM; 6 hours) suppresses TNFa-induced activation of NF-kB and the expression of NF-kB-targeted proinflammatory genes such as E-selectin and cyclooxygenase-2[3].
Aurothiomalate sodium inhibits non-small lung cancer (NSCLC) growth by binding PKCι and blocking activation of a PKCι-Par6-Rac1-Pak-Mek 1,2-Erk 1,2 signaling pathway[1].
Aurothiomalate sodium inhibits Mek/Erk signaling and decreases proliferative index without effecting tumor apoptosis or vascularization in vivo[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis[1]

Cell Line: Bovine arterial endothelial cells (BAEC)
Concentration: 25 uM
Incubation Time: 6 hours
Result: Suppressed TNFa-induced NF-kB-dependent gene expression in a dose-dependent manner.
Did not affect TrxR1 mRNA level in COS7 cells.

体内研究
(In Vivo)

Aurothiomalate sodium (2, 6, 20 or 60 mg/kg/day; intramuscular injections; 40 days) exhibits statistically significant inhibition of tumor growth at all concentrations tested in A427 cell tumors because A427 cells are highly responsive[1].
Aurothiomalate sodium (20, 60 mg/kg/day; intramuscular injections; 15 days) shows a statistically significant response (~50% reduction in tumor size) only at the 60 mg/kg dose in H460 tumors because H460 cells are less responsive[1].
Aurothiomalate sodium (60 mg/kg/day; IP; for six weeks) exhibites a decrease in tumor growth in Three-week-old KrasLA2 mice. Aurothiomalate sodium inhibits Kras-mediated bronchioalveolar stem cells (BASCs) expansion and lung tumorigenesis in vivo[2].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: 4-6-week-old female nude mice with A427 or H460 cells[1]
Dosage: 2, 6, 20 or 60 mg/kg
Administration: Intramuscular injections; daily; 40 days
Result: Exhibited statistically significant inhibition of tumor growth at all concentrations tested in A427 cell tumors because A427 cells are highly responsive.

Formula

C4H6O4S.Au.xNa
CAS 号

12244-57-4
中文名称

金硫丁二钠；金硫苹果酸钠
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Roderick P Regala, et al. Atypical protein kinase C iota expression and aurothiomalate sensitivity in human lung cancer cells. Cancer Res. 2008 Jul 15;68(14):5888-95.

    [2]. Roderick P Regala, et al. Atypical protein kinase C{iota} is required for bronchioalveolar stem cell expansion and lung tumorigenesis. Cancer Res. 2009 Oct 1;69(19):7603-11.

    [3]. Atsuko Sakurai, et al. Overexpression of thioredoxin reductase 1 regulates NF-kappa B activation. J Cell Physiol. 2004 Jan;198(1):22-30.

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