Aurothiomalate sodium 

Aurothiomalate sodium is a potent and selective oncogenic PKC_ι 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].

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 PKC_ι and blocking activation of a PKC_ι-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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

C₄H₆O₄S.Au.xNa

12244-57-4

Solid

Off-white to light yellow

OC(CC(S)C(O)=O)=O.[x].[Na].[Au]

Room temperature in continental US; may vary elsewhere.

4°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

• [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.  [Content Brief]

  [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.  [Content Brief]

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