Aurothiomalate tetramer sodium 

Aurothiomalate tetramer sodium is the tetrameric form of Aurothiomalate sodium (HY-106381). Aurothiomalate tetramer sodium acts as an inhibitor of PKCI and TrxR1. Aurothiomalate tetramer 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 tetramer 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 tetramer sodium can be used in research related to rheumatoid arthritis and non-small cell lung cancer^{[1][2][3][4][5][6]}.

Aurothiomalate tetramer sodium (20 μmol/L; in vitro culture duration) 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 tetramer sodium potently inhibits the activity of mouse liver thioredoxin reductase in vitro^[3].
Aurothiomalate tetramer sodium (25-50 μM; administered 48 h prior to 6 h TNFα stimulation) inhibits TNFα-induced NF-κB-dependent gene expression in TrxR1-overexpressing COS7 cells in a dose-dependent manner^[3].
Aurothiomalate tetramer sodium (50 μM; administered 48 h prior to TNFα stimulation) inhibits TNFα-induced NF-κB DNA-binding activity in TrxR1-overexpressing COS7 cells^[3].
Aurothiomalate tetramer sodium (25 μM; administered concurrently with TNFα stimulation for 6 h) 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.

Aurothiomalate tetramer sodium (intraperitoneal injection; administered daily for 3-6 weeks at a dose of 60 mg/kg) inhibits Kras-mediated BASC expansion and reduces lung tumor growth by approximately 36% in Kras^LA2 mice^[2].
Aurothiomalate tetramer sodium (0.7 μg/g body weight; administered via intravenous injection, intramuscular injection, or direct air pouch injection; dosed twice) 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 tetramer sodium (0.7 μg/g body weight; tail vein injection; single administration) significantly reduces the leukocyte count in exudate in a carrageenan-induced acute inflammation mouse model^[4].
Aurothiomalate tetramer sodium (0.7 μg/g body weight; intravenous injection, intramuscular injection, direct air pouch injection) 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 tetramer sodium (2-60 mg/kg; intramuscular injection; daily administration) exerts potent antitumor activity against A427 lung cancer xenografts by inhibiting cell proliferation and the Mek/Erk signaling pathway^[6].
Aurothiomalate tetramer sodium (20-60 mg/kg; intramuscular injection; daily) 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.

Solid

White to off-white

O=C(O[Na])C(S[Au])CC(O[Na])=O.[4]

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]. Campbell JM, et al. Action of sodium aurothiomalate on erythrocyte membrane. Ann Rheum Dis. 1992;51(8):969-971.  [Content Brief]

  [2]. Regala RP, 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]. 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]

  [6]. Regala RP, 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.