|1.||Kelley, Mark R: 7 articles (07/2014 - 12/2010)|
|2.||Zou, Gang-Ming: 3 articles (08/2015 - 07/2008)|
|3.||Maitra, Anirban: 3 articles (09/2011 - 07/2008)|
|4.||Vascotto, Carlo: 2 articles (01/2014 - 01/2013)|
|5.||Tell, Gianluca: 2 articles (01/2014 - 01/2013)|
|6.||Fishel, Melissa L: 2 articles (09/2011 - 12/2010)|
|7.||Luo, Meihua: 2 articles (04/2011 - 12/2010)|
|8.||Roy, Sashwati: 1 article (09/2015)|
|9.||Pan, Xueliang: 1 article (09/2015)|
|10.||Gordillo, Gayle M: 1 article (09/2015)|
07/01/1992 - "We examined the protective effects and possible mechanism of action of E3330 in three different endotoxin (lipopolysaccharide)-induced murine hepatitis models, in which tumor necrosis factor is suggested to play a critical role in the pathogenesis. "
07/01/1992 - "These findings suggest that the inhibition by E3330 of tumor necrosis factor production is the major mechanism of the protective effect of E3330 in these endotoxin-mediated hepatitis models in mice."
12/08/1992 - "Protective effects of E3330, a novel quinone derivative, on galactosamine/tumor necrosis factor-alpha-induced hepatitis in mice."
12/08/1992 - "These findings suggest that the protective effect of E3330 on galactosamine/tumor necrosis factor-alpha hepatitis is due at least in part to its inhibition of the generation of leukotrienes. "
|2.||Chronic Hepatitis (Chronic Active Hepatitis)
07/01/1997 - "E3330 therefore showed protective effects on MHV-2cc-induced chronic hepatitis in athymic nude mice, but further studies are needed to analyze the mechanism."
07/01/1997 - "Protective effects of a novel quinone derivative, E3330, on mouse hepatitis virus (MHV)-induced chronic hepatitis in athymic nude mice."
07/01/1997 - "In this experiment, we examined the protective effects of a novel quinone derivative, E3330, on MHV-2cc-induced chronic hepatitis in athymic nude mice for up to 3 weeks after virus infection. "
04/15/2011 - "Studies using cancer cell lines demonstrated that E3330 and one analogue, RN8-51, decreased the cell line growth with little apoptosis, whereas the third, RN7-60, caused a dramatic effect. "
02/01/2011 - "In conclusion, pharmacological inhibition of APE1 by E3330 suppresses inflammatory response in activated macrophages and can be considered as a novel therapeutic strategy for the inhibition of tumor-associated macrophages."
04/01/2009 - "The Ape-1/Ref-1 redox antagonist E3330 inhibits the growth of tumor endothelium and endothelial progenitor cells: therapeutic implications in tumor angiogenesis."
09/01/2011 - "Pharmacokinetic studies also show that E3330 attains more than10 μmol/L blood concentrations and is detectable in tumor xenografts. "
09/01/2015 - "Intraperitoneal injection of the small molecule inhibitor E3330, which specifically targets Apex-1 redox-sensitive functions, resulted in a 50% decrease in tumor volume compared with mice injected with vehicle control (n = 6 per group), indicating that endothelial cell tumor proliferation is dependent on Apex-1 expression. "
|5.||Pancreatic Neoplasms (Pancreatic Cancer)
07/01/2008 - "In the present study, we used E3330, a small-molecule inhibitor of APE1 redox domain function, to interrogate the functional relevance of sustained redox function in pancreatic cancer. "
08/01/2015 - "Finally, treatment of pancreatic cancer cells with the WNT/β-catenin inhibitor IWR-1 resulted in growth inhibition, which was greatly enhanced when combined with E3330 treatment. "
09/01/2011 - "These data indicate that E3330, inhibitor of APE1/Ref-1, has potential in pancreatic cancer and clinical investigation of APE1/Ref-1 molecular target is warranted."
04/01/2009 - "We demonstrate that E3330, a small molecule inhibitor of the Ape-1/Ref-1 redox domain, blocks the in vitro growth of pancreatic cancer-associated endothelial cells (PCECs) and EPCs, which is recapitulated by stable expression of a dominant-negative redox domain mutant. "
07/01/2008 - "Finally, E3330 treatment inhibits pancreatic cancer cell migration as assessed by in vitro chemokine assays. "
|1.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
|4.||Transcription Factors (Transcription Factor)
|5.||DNA (Deoxyribonucleic Acid)
|6.||DNA-(Apurinic or Apyrimidinic Site) Lyase (AP Endonuclease)
|7.||Vascular Endothelial Growth Factor A (Vascular Endothelial Growth Factor)
|8.||Small Interfering RNA (siRNA)
|10.||Reactive Oxygen Species (Oxygen Radicals)
|1.||Heterologous Transplantation (Xenotransplantation)