|Related Categories||Apoptosis and Cell Cycle, Bioactive Small Molecules, Biochemicals and Reagents, Cell Biology, Cell Signaling and Neuroscience,|
|color||white to beige|
|solubility||DMSO: soluble20 mg/mL, clear|
DiQ is a potent inhibitor of Poly(ADP-ribose) synthetase which is activated by nitric oxide; neuroprotective agent.
Butyrate-induced cell death and differentiation are associated with distinct patterns of ROS in HT29-derived human colon cancer cells. Domokos M, Jakus J, Szeker K, et al. Dig. Dis. Sci. 55(4), 920-30, (2010)
Inhibitors of poly (ADP-ribose) polymerase ameliorate myocardial reperfusion injury by modulation of activator protein-1 and neutrophil infiltration. Kaplan J, O'Connor M, Hake PW, et al. Shock 23(3), 233-8, (2005)
The effect of poly (adenosine diphosphate-ribose) polymerase inhibitors on biochemical changes in testicular ischemia-reperfusion injury. Bozlu M, Eskandari G, Cayan S, et al. J. Urol. 169(5), 1870-3, (2003)
Poly(ADP-ribose) polymerase-1 is a positive regulator of the p53-mediated G1 arrest response following ionizing radiation. Wieler S, Gagné JP, Vaziri H, et al. J. Biol. Chem. 278(21), 18914-21, (2003)
Effects of inhibitors of the activity of poly (ADP-ribose) synthetase on the organ injury and dysfunction caused by haemorrhagic shock. McDonald MC, Filipe HM, and Thiemermann C Br. J. Pharmacol. 128(6), 1339-45, (1999)
Poly(ADP-ribose) polymerase inhibition in oxidant-stressed endothelial cells prevents oncosis and permits caspase activation and apoptosis. Walisser JA and Thies RL Exp. Cell Res. 251(2), 401-13, (1999)
An inhibitor of poly (ADP-ribose) synthetase activity reduces contractile dysfunction and preserves high energy phosphate levels during reperfusion of the ischaemic rat heart. Docherty JC, Kuzio B, Silvester JA, et al. Br. J. Pharmacol. 127(6), 1518-24, (1999)
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