Sodium thiosulfate (99%, water≤1.0%)

Sodium thiosulfate is an antioxidant. Sodium thiosulfate inhibits the expression of p-GSK-3β and β-catenin proteins, reduces IL-1β, COX-2, and Iba-1, and inhibits NFκB activation. Sodium thiosulfate promotes angiogenesis, inhibits inflammation, and improves acute lung injury. Sodium thiosulfate also exhibits anti-cancer activity against melanoma. Sodium thiosulfate also exerts renal protective effects. Sodium thiosulfate can be used in the research of osteoarthritis, brain inflammation, cancer (such as breast cancer, melanoma), and kidney disease^{[1][2][3][4][5][6][7][8][9]}. In Vitro:Sodium thiosulfate (1.2-120 μM; 48 h) does not affect MCF-7 viability^[1].
Sodium thiosulfate (3 mM; 8 h) stimulates proliferation of human umbilical vein endothelial cells (HUVEC)^[2].
Sodium thiosulfate (0.2-25 mM; 1-7 days) dose-dependently inhibits mineralization of murine joint chondrocytes^[3].
Sodium thiosulfate (1-500 μM; 8 h) reduces LPS/IFNγ-induced release of TNFα and IL-6 in microglia^[4].
Sodium thiosulfate (0.1-10 mM; 48 h) does not attenuate the anticancer activity of Doxorubicin (HY-15142A) in human breast cancer MCF-7 cells and human cervical cancer HeLa cells^[6].
In Vivo:Sodium thiosulfate (0.5-1 g/kg/day; p.o. via water bottle; changed three times a week) promotes hindlimb ischemia-induced revascularization and muscle recovery in WT C57BL/6JRj mice and hypercholesterolemic LDLR^-/- mice, increases capillary density, reduces muscle damage^[2].
Sodium thiosulfate (0.4 g/kg; i.p.; three times per week) reduces the volume and crystal content of new periarticular calcific deposits, attenuates tibial and femoral cartilage damage and proteoglycan loss, and shows a significant positive correlation between the volume of new mineralized structures and tibial cartilage degradation score in menisectomy-induced osteoarthritis model of female C57BL/6 mice^[3].
Sodium thiosulfate (2 g/kg; intraperitoneal injection, 0 and 12 h after LPS challenge; 0.5 g/kg; i.v., 10 min after CLP) attenuates LPS or CLP-induced acute lung injury in male C57BL6J mice by inhibiting lung inflammation, reducing lung permeability, and suppressing NFκB activation^[5].
Sodium thiosulfate (2-3 g/kg; once daily) inhibits tumor growth and EMT process by the Wnt/β-catenin signaling pathway in nude mice xenografted with B16 cells^[8].
Sodium thiosulfate (100-750 mg/kg; i.p.) reduces brain inflammation induced by systemic lipopolysaccharide administration in female C57BL/6J mice by decreasing IL-1β, COX-2, Iba-1, and TSPO levels ^[9].