JS-K

JS-K is a nitric oxide (NO) donor that reacts with glutathione to generate NO at physiological pH.¹ It inhibits proliferation of HL-60 cells (IC₅₀ = 0.5 µM), which is prevented by the glutathione precursor N-acetyl-L-cysteine (Item No. 20261), and inhibits growth of the solid tumor cell lines PPC-1, DLD-1, and Meth A. It decreases tumor volume by over 50% in an HL-60 mouse xenograft model when used at a dose of 4 µmol/kg, i.v., three times per week. JS-K inhibits proliferation, induces apoptosis, and disrupts the cell cycle of Jurkat T acute lymphoblastic leukemia cells.² It also induces S-nitrosylation of β-catenin followed by dose-dependent degradation of nuclear β-catenin and S-nitrosylated nuclear β-catenin levels.

WARNING This product is not for human or veterinary use.

1. Shami, P.J., Saavedra, J.E., Wang, L.Y., et al. JS-K, a glutathione/glutathione S-transferase-activated nitric oxide donor of the diazeniumdiolate class with potent antineoplastic activity. Mol. Cancer Ther. 2(4), 409-417 (2003).

2. Nath, N., Chattopadhyay, M., Pospishil, L., et al. JS-K, a nitric oxide-releasing prodrug, modulates β-catenin/TCF signaling in leukemic Jurkat cells: Evidence of an S-nitrosylated mechanism. Biochem. Pharmacol. 80(11), 1641-1649 (2010).