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
Description
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PKCι |
In Vitro
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. Further protocols information, click here.
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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.
In Vivo
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
In Vitro:
H2O : 250 mg/mL (Need ultrasonic)
In Vivo:
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
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
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Patient-Derived Orthotopic Xenograft (PDOX)
Patient-derived orthotopic xenograft (PDOX) modeling implants fresh patient tumor tissue or patient-derived tumor cells into the anatomically corresponding organ or tissue site of immunodeficient mice, usually by surgical orthotopic implantation, to preserve patient tumor histology, local microenvironmental context, invasion, metastatic behavior, and treatment-response features better than subcutaneous implantation. PDOX readouts include tumor engraftment, orthotopic tumor growth, local invasion, metastasis, recurrence after resection, histologic similarity to the donor tumor, biomarker retention, molecular concordance, survival, and response or resistance to therapy. PDOX models are used for preclinical drug testing and individualized therapy evaluation, but engraftment success varies by tumor type and specimen quality.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Carcinogenicity Bioassay
A carcinogenicity bioassay detects whether long-term exposure to a test substance increases benign or malignant tumor incidence, changes tumor spectrum, or shortens tumor latency in experimental animals; the classical rodent design exposes rats and/or mice to multiple dose levels for most of their lifespan, followed by complete necropsy and histopathologic diagnosis of neoplastic and non-neoplastic lesions. The readout is tumor incidence by organ, sex, species, dose group, and survival status; interpretation requires concurrent controls, dose-response assessment, survival-adjusted tumor statistics, and pathology review because mortality, spontaneous tumor background, and body-weight effects can influence apparent tumor rates.
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Phagocytosis Functional Assay
A phagocytosis functional assay measures the ability of phagocytic cells, such as neutrophils, macrophages, monocytes, or microglia/macrophages, to bind and internalize particulate targets including bacteria, yeast particles, beads, or myelin particles. Fluorescent flow-cytometry assays detect target uptake as fluorescence associated with gated phagocytes, while pH-sensitive dyes such as pHrodo increase signal in acidic phagosomal compartments and therefore preferentially report internalized particles rather than particles remaining outside the cell. Microscopy or high-content imaging can be used to confirm intracellular localization and, in some protocols, to follow uptake kinetics.
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Collagen-Induced Arthritis
Collagen-induced arthritis (CIA) is an autoimmune murine model of rheumatoid arthritis in which immunization with type II collagen (CII) emulsified in an adjuvant induces a T cell- and autoantibody-driven inflammatory arthritis characterized by synovial hyperplasia, immune cell infiltration, and joint destruction. The model typically relies on genetically susceptible mouse strains (e. g. , DBA/1) and reproduces key features of human rheumatoid arthritis, including anti-collagen immune responses and progressive joint inflammation. Disease onset generally occurs within ~3-4 weeks after immunization, depending on antigen/adjuvant combinations and protocol variation. The immunopathology is driven by adaptive immune activation against CII, leading to systemic and local joint inflammation mediated by pro-inflammatory cytokines and effector immune cells, making CIA a standard preclinical platform for evaluating immunomodulatory and anti-arthritic interventions.
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Chemotaxis Gradient Chamber Assay 1
The chemotaxis gradient chamber assay is based on the principle of observing directional cell migration in response to a stable, linear or quasi-linear concentration gradient of a chemoattractant formed between two fluid reservoirs separated by a narrow observation chamber. Cells placed within the chamber respond to the gradient by polarized movement toward higher chemoattractant concentrations, allowing quantification of chemotactic behavior in real time under microscopy. The classic Zigmond chamber design enables simultaneous visualization of gradient formation and individual cell trajectories, making it suitable for studying leukocyte chemotaxis and other motile cell types in vitro.
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Under-Agarose Cell Migration Assay
The under-agarose cell migration assay is a classical in vitro chemotaxis method designed to evaluate directed cell movement through a semi-solid agarose matrix toward soluble chemoattractant gradients, enabling visualization and quantification of leukocyte or motile cell migration in a confined 2D-like environment. In this system, cells and chemoattractants are placed in separate wells cut into an agarose gel, allowing diffusion-driven gradient formation that guides directional migration, which is typically assessed by measuring migration distance, cell morphology changes, and accumulation toward the chemoattractant source. This assay has been widely used to study neutrophil and leukocyte chemotaxis as a simple alternative to filter-based migration systems and allows direct microscopic observation of migrating cells under near-physiological confinement conditions.
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Transwell/Boyden Chamber Migration Assay
The Transwell/Boyden chamber migration assay measures cell movement through a porous membrane separating an upper and lower chamber, usually after a chemoattractant gradient is established by placing cells in the upper chamber and chemoattractant-containing medium in the lower chamber. The readout is generated by quantifying cells that traverse the membrane and appear on the lower membrane surface or in the lower chamber, depending on whether the cell type is adherent or non-adherent. This assay reflects chemotactic or haptotactic migration rather than matrix invasion unless an extracellular-matrix barrier is added to the membrane.
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Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Soft Agar Colony Formation Assay
Soft agar colony formation assay measures anchorage-independent growth, in which transformed or tumorigenic cells proliferate as colonies in a semisolid agar matrix while many non-transformed adherent cells fail to proliferate without attachment; classic studies showed that growth in semisolid medium correlates with tumorigenicity in nude mice, and later protocol papers describe the method as a stringent in vitro assay for malignant transformation. The readout is the number, size, morphology, or signal intensity of colonies formed within agar after incubation; published formats include manual colony counting after staining, 96-well or 384-well quantitative formats, DNA-binding dye detection, MTT/tetrazolium-based detection, digital image analysis, and PCR-based marker detection from soft agar cultures.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Chemotaxis Gradient Chamber Assay 2
Chemotaxis gradient chamber assays measure directional cell migration in response to a soluble chemical gradient by imaging cells as they move across a defined observation region; the readout is generated from time-lapse cell trajectories, displacement toward the gradient, forward migration index, trajectory plots, rose/polar plots, and statistical tests of non-random directionality. The Dunn chamber is a direct-viewing glass chamber in which cells migrate across a bridge between control and chemoattractant wells, allowing observation of cells in a linear concentration gradient; related direct-viewing formats include the Insall chamber, which supports defined unidirectional gradients and high numerical-aperture microscopy, and the μ-Slide Chemotaxis chamber, which supports long-term live-cell imaging and gradient characterization with fluorescent dye.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
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)