E3330 is a potent and selective APE1(Ref-1) inhibitor, which suppressed NF-kappa B DNA-binding activity.

E3330 affects hemangioblast development in vitro via inhibition of Ape1 redox activity. [1] E3330 inhibits the growth of human pancreatic cancer cell line PANC1, XPA1, MIAPACA, BxPC3, and PK9. E3330 also promotes exit of cell cycle in PANC1 cells, inhibits the DNA-Binding activity of HIF-1α and migration of pancreatic cancer cells. [2] In JHH6 cells, E3330 prevents the functional activation of NF-κB via the alteration of APE1 subcellular trafficking and reduces IL-6 and IL-8 expression induced by TNF-α and FAs accumulation through blockage of the redox-mediated activation of NF-κB. [3]

In mice with endotoxin-mediated hepatitis, E3330 (300 mg/kg, p.o.) attenuates the elevation of plasma tumor necrosis factor activity and protectes mice from liver injury. [4] In Rat model, E3330 (100 mg/kg, p.o.) also protectes rats from severe liver injury induced with endotoxin plus galactosamine. [5]

PANC1 cells are placed in one well of a 12-well plate and treated with 5 to 30 μM E3330. After a 24, 48, and 72 h of culture, the cells are washed with PBS and stained with trypan blue, and cell viability is examined by counting the live cell numbers.(Only for Reference)

DMSO: 50 mg/mL (132.11 mM), Sonication is recommended.

H2O: < 1 mg/mL (insoluble or slightly soluble)

Ethanol: 70 mg/mL (184.96 mM), Sonication is recommended.

10% DMSO+40% PEG300+5% Tween 80+45% Saline: 2 mg/mL (5.28 mM), Sonication is recommended.