GL-V9

• Description:

  GL-V9 inhibits proliferation of HepG2 cell (IC50 is 35.2 μM) through induction of apoptosis and cell cycle arrest at G2/M phase. GL-V9 regulates mitochondrial membrane potential and increases the production of intracellular reactive oxygen species. GL-V9 inhibits the pentose phosphate pathway (PPP), enhances fatty acid oxidation (FAO) through activation of AMPK, and thus inhibits the metastasis of cancer cells. GL-V9 exhibits antitumor efficacy in mouse model[1][2].

• UNSPSC:

  12352005

• Target:

  AMPK; Apoptosis; Reactive Oxygen Species (ROS)

• Type:

  Reference compound

• Related Pathways:

  Apoptosis; Epigenetics; Immunology/Inflammation; Metabolic Enzyme/Protease; NF-κB; PI3K/Akt/mTOR

• Applications:

  Cancer-Kinase/protease

• Field of Research:

  Cancer

• Assay Protocol:

  https://www.medchemexpress.com/gl-v9.html

• Smiles:

  O=C1C=C(C2=CC=CC=C2)OC3=C(OC)C(OCCCCN4CCCC4)=CC(O)=C13

• Molecular Formula:

  C24H27NO5

• Molecular Weight:

  409.47

• References & Citations:

  [1]Li L, et al., GL-V9, a newly synthetic flavonoid derivative, induces mitochondrial-mediated apoptosis and G2/M cell cycle arrest in human hepatocellular carcinoma HepG2 cells. Eur J Pharmacol. 2011 Nov 16;670 (1) :13-21.|[2]Yang L, et al., Regulation of AMPK-related glycolipid metabolism imbalances redox homeostasis and inhibits anchorage independent growth in human breast cancer cells. Redox Biol. 2018 Jul;17:180-191.

• Shipping Conditions:

  Room temperature

• Scientific Category:

  Reference compound1

• Clinical Information:

  No Development Reported

• CAS Number:

  [1178583-19-1]