Aurothiomalate (sodium)

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^{[1][2][3][4][5][6]}. 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]. In Vivo:Aurothiomalate (intraperitoneal injection; administered daily for 3-6 weeks at a dose of 60 mg/kg) sodium inhibits Kras-mediated BASC expansion and reduces lung tumor growth by approximately 36% in Kras^LA2 mice^[2].
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].