Aurothiomalate sodium
Based on 1 Customer Validation
Aurothiomalate sodium acts as an inhibitor of PKCI and TrxR1. Aurothiomalate sodium disrupts the PKCI-Par6-Rac1 signaling pathway, and also inhibits TrxR1 activity, TNFα-induced NF-κB activation, and the expression of pro-inflammatory genes. Aurothiomalate sodium blocks Kras-mediated BASC expansion and lung tumor growth, inhibits anchorage-independent growth and tumorigenicity of lung cancer cells, and suppresses neutrophil chemotaxis, phagocytosis, and leukocyte extravasation. Aurothiomalate sodium can be used in research related to rheumatoid arthritis and non-small cell lung cancer.
For research use only. We do not sell to patients.
- Purity: 98.0%
- CAS No.: 12244-57-4
- Formula: C4H6O4S.Au.xNa
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Storage:
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Biological Activity
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PKCι |
Aurothiomalate (20 μmol/L; in vitro culture duration) sodium blocks the proliferative expansion and morphological transformation of bronchoalveolar stem cells isolated from LSL-Kras mice that are mediated by oncogenic Kras in vitro[2].
Aurothiomalate sodium potently inhibits the activity of mouse liver thioredoxin reductase in vitro[3].
Aurothiomalate (25-50 μM; administered 48 h prior to 6 h TNFα stimulation) sodium inhibits TNFα-induced NF-κB-dependent gene expression in TrxR1-overexpressing COS7 cells in a dose-dependent manner[3].
Aurothiomalate (50 μM; administered 48 h prior to TNFα stimulation) sodium inhibits TNFα-induced NF-κB DNA-binding activity in TrxR1-overexpressing COS7 cells[3].
Aurothiomalate (25 μM; administered concurrently with TNFα stimulation for 6 h) sodium inhibits TNFα-induced expression of the NF-κB-targeted pro-inflammatory genes E-selectin and COX-2 in bovine arterial endothelial cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Bovine arterial endothelial cells (BAEC)
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Concentration:25 uM
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Incubation Time:6 hours
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Result:Suppressed TNFa-induced NF-kB-dependent gene expression in a dose-dependent manner.
Did not affect TrxR1 mRNA level in COS7 cells.
Aurothiomalate (0.7 μg/g body weight; administered via intravenous injection, intramuscular injection, or direct air pouch injection; dosed twice) sodium significantly reduces the leukocyte count in exudate in carrageenan-induced acute inflammation models in mice, with intravenous injection exerting the strongest inhibitory effect[4].
Aurothiomalate (0.7 μg/g body weight; tail vein injection; single administration) sodium significantly reduces the leukocyte count in exudate in a carrageenan-induced acute inflammation mouse model[4].
Aurothiomalate (0.7 μg/g body weight; intravenous injection, intramuscular injection, direct air pouch injection) sodium significantly inhibits phagocytosis and chemotaxis of neutrophils in carrageenan-induced acute inflammation in mice, with intravenous and intramuscular injections exerting stronger inhibitory effects on chemotaxis than direct air pouch injection[4].
Aurothiomalate (2-60 mg/kg; intramuscular injection; daily administration) sodium exerts potent antitumor activity against A427 lung cancer xenografts by inhibiting cell proliferation and the Mek/Erk signaling pathway[6].
Aurothiomalate (20-60 mg/kg; intramuscular injection; daily) sodium exhibits moderate antitumor activity against H460 lung cancer xenografts by inhibiting cell proliferation and the Mek/Erk signaling pathway[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Athymic nude mice (Harlan Sprague-Dawley, female, 4-6 weeks old, subcutaneous xenograft model via injection of human H460 lung cancer cells)[6]
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Dosage:20 mg/kg; 60 mg/kg
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Administration:i.m.; daily
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Result:Caused a statistically significant ~50% reduction in H460 tumor volume compared to controls at the 60 mg/kg dose.
Reduced BrdUrd-positive nuclei (proliferative index) from ~21% in controls to ~11% at the 60 mg/kg dose.
Reduced the ratio of phospho-Erk 1,2 to total Erk 1,2 compared to controls at the 60 mg/kg dose.
Did not significantly increase the apoptotic index (TUNEL-positive cells remained <1%) or alter tumor vascularization (PECAM1 staining/expression unchanged) at either dose.
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Animal Model:Athymic nude mice (Harlan Sprague-Dawley, female, 4-6 weeks old, subcutaneous xenograft model via injection of human A427 lung cancer cells)[6]
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Dosage:2 mg/kg; 6 mg/kg; 20 mg/kg; 60 mg/kg
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Administration:i.m.; daily
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Result:Caused statistically significant inhibition of A427 tumor growth, with final tumor volume far lower than control tumors.
Reduced BrdUrd-positive nuclei (proliferative index) from ~17% in controls to ~9% at 2 mg/kg, ~6% at 6 mg/kg, ~5% at 20 mg/kg, and ~9% at 60 mg/kg.
Reduced the ratio of phospho-Erk 1,2 to total Erk 1,2 compared to controls.
Did not significantly increase the apoptotic index (TUNEL-positive cells remained <1%) or alter tumor vascularization (PECAM1 staining/expression unchanged) at any dose.
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Animal Model:KrasLA2 (3-week-old; spontaneous activation of latent oncogenic KrasG12D allele via somatic recombination)[2]
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Dosage:60 mg/kg
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Administration:i.p.; daily; 3 weeks; 6 weeks
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Result:Blocked the significant increase in BASCs per terminal bronchiole seen in saline-treated KrasLA2 mice, with BASC number and distribution matching levels in nontransgenic mice.
Reduced lung tumor growth, with a mean fold-change in average tumor size of ~1.6, compared to ~2.5 in saline-treated mice.
Chemical Information
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CAS No. 12244-57-4
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Appearance Solid
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Formula C4H6O4S.Au.xNa
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Color Off-white to light yellow
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SMILES
OC(CC(S)C(O)=O)=O.[Na].[Au]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvent & Solubility
H2O : 250 mg/mL (Need ultrasonic)
For the following dissolution methods, please prepare the working solution directly:
It is recommended to prepare fresh solutions and use them promptly within a short period of time.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: PBS
Solubility: 50 mg/mL; Clear solution; Need ultrasonic
Purity & Documentation
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Data Sheet (281 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
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Handling Instructions (2659 KB)
References
[1]. Campbell JM, et al. Action of sodium aurothiomalate on erythrocyte membrane. Ann Rheum Dis. 1992;51(8):969-971. [Content Brief]
[3]. Sakurai A, et al. Overexpression of thioredoxin reductase 1 regulates NF-kappa B activation. J Cell Physiol. 2004;198(1):22-30. [Content Brief]
[4]. Sin YM, et al. Effect of sodium aurothiomalate on carrageenan induced inflammation of the air pouch in mice. Ann Rheum Dis. 1992;51(1):112-116. [Content Brief]
[5]. Lewis D, et al. Gold levels produced by treatment with auranofin and sodium aurothiomalate. Ann Rheum Dis. 1983;42(5):566-570. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)