JS-K

JS-K is a NO donor that reacts with glutathione to generate NO at physiological pH. JS-K induces reactive oxygen species (ROS) to mediate apoptosis. JS-K induces autophagy. JS-K inhibits invasion. JS-K has a broad spectrum anti-proliferative activity in cancer cells. JS-K reduces tumor volume and causes necrosis of implanted tumors in mice[1][2].

Product Specifications

CAS Number

[205432-12-8]

UNSPSC

12352005

Target

Apoptosis; Autophagy; NO Synthase; Reactive Oxygen Species (ROS)

Type

Reference compound

Related Pathways

Apoptosis; Autophagy; Immunology/Inflammation; Metabolic Enzyme/Protease; NF-κB

Applications

Cancer-programmed cell death

Field of Research

Cancer

Assay Protocol

https://www.medchemexpress.com/js-k.html

Purity

99.59

Solubility

DMSO : 36 mg/mL (ultrasonic; warming)

Smiles

O=C(N1CCN(/[N+]([O-])=N/OC2=CC=C([N+]([O-])=O)C=C2[N+]([O-])=O)CC1)OCC

Molecular Formula

C13H16N6O8

Molecular Weight

384.30

References & Citations

[1]Shami PJ, et al. JS-K, a glutathione/glutathione S-transferase-activated nitric oxide donor of the diazeniumdiolate class with potent antineoplastic activity. Mol Cancer Ther. 2003 Apr;2 (4) :409-17. |[2]Liu B, et al. JS-K, a nitric oxide donor, induces autophagy as a complementary mechanism inhibiting ovarian cancer. BMC Cancer. 2019 Jul 1;19 (1) :645. |[3]Simeone AM, et al. TIMP-2 mediates the anti-invasive effects of the nitric oxide-releasing prodrug JS-K in breast cancer cells. Breast Cancer Res. 2008;10 (3) :R44.|[4]Dong R, et al. Effects of JS-K, a novel anti-cancer nitric oxide prodrug, on gene expression in human hepatoma Hep3B cells. Biomed Pharmacother. 2017 Apr;88:367-373.