JS-K

• Description:

  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].

• 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.

• Shipping Conditions:

  Blue Ice

• Storage Conditions:

  -20°C, 3 years (Powder)

• Scientific Category:

  Reference compound1

• Clinical Information:

  No Development Reported

• CAS Number:

  [205432-12-8]