1. Epigenetics
    TGF-beta/Smad
  2. PKC
  3. Aurothiomalate sodium

Aurothiomalate sodium 

Cat. No.: HY-106381
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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.

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Aurothiomalate sodium Chemical Structure

Aurothiomalate sodium Chemical Structure

CAS No. : 12244-57-4

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Description

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

 

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].

MCE 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.
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].

MCE 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 No.
SMILES

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

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Keywords:

AurothiomalatePKCProtein kinase CthioredoxinreductaseTrxRanti-rheumatoidNSCLCA549H1437H2170H460H510H187H1703A427LACSCLCLACsNF-kBTNFaMekErkInhibitorinhibitorinhibit

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Aurothiomalate sodium
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