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About This Item
Empirical Formula (Hill Notation):
C9H7NO2
CAS Number:
Molecular Weight:
161.16
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352202
MDL number:
InChI
1S/C9H7NO2/c11-8-3-1-2-7-6(8)4-5-10-9(7)12/h1-5,11H,(H,10,12)
SMILES string
Oc1cccc2c(O)nccc12
InChI key
LFUJIPVWTMGYDG-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
mp
279-281 °C
solubility
DMSO: 20 mg/mL, clear
storage temp.
2-8°C
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Biochem/physiol Actions
DiQ is a potent inhibitor of Poly(ADP-ribose) synthetase which is activated by nitric oxide; neuroprotective agent.
Disclaimer
Light sensitive
Storage Class
11 - Combustible Solids
wgk
WGK 3
ppe
dust mask type N95 (US), Eyeshields, Gloves
Regulatory Information
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G M Shah et al.
Biochimica et biophysica acta, 1312(1), 1-7 (1996-06-05)
Activation of the poly(ADP-ribose) polymerase after oxidative damage is implicated in different responses of the cells, for example, cell recovery after sublethal damage or cell death after lethal damage. However, the extent and mechanism of involvement of the enzyme in
J C Docherty et al.
British journal of pharmacology, 127(6), 1518-1524 (1999-08-24)
The cardioprotective properties of inhibition of poly (ADP-ribose) synthetase (PARS) were investigated in the isolated perfused heart of the rat. Hearts were perfused in the Langendorff mode and subjected to 23 min total global ischaemia and reperfused for 60 min.
P K Chatterjee et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 14(5), 641-651 (2000-04-01)
The activation of poly (ADP-ribose) synthetase (PARS) subsequent to DNA damage caused by reactive oxygen or nitrogen species has been implicated in several pathophysiological conditions, including ischemia-reperfusion injury and shock. The aim of this study was to investigate whether PARS
J A Walisser et al.
Experimental cell research, 251(2), 401-413 (1999-09-02)
Endothelial cells (EC) are subject to oxidative-induced cell death. Activation of poly(ADP-ribose) polymerase (PARP) occurs early in oxidant-induced EC injury and putatively mediates cell death by depleting its substrate, NAD(+). In this study, the role of PARP in H(2)O(2)-induced EC
G M Wray et al.
Shock (Augusta, Ga.), 10(1), 13-19 (1998-08-04)
The nuclear enzyme poly(ADP-ribose) synthetase (PARS) is activated by DNA strand breakage, caused, for example by nitric oxide (NO), peroxynitrite, or oxygen-derived free radicals. Activation of PARS can cause intracellular energy depletion and cell death in vitro and may play
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