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I138

Sigma-Aldrich

1,5-Isoquinolinediol

≥98% (HPLC), powder

Synonym(s):

1,5-Dihydroxyisoquinoline, 5-Hydroxy-1(2H)-isoquinolinone, DiQ

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About This Item

Empirical Formula (Hill Notation):
C9H7NO2
CAS Number:
5154-02-9
Molecular Weight:
161.16
MDL number:
MFCD00006900
UNSPSC Code:
12352202
PubChem Substance ID:
24278174
NACRES:
NA.77

assay

≥98% (HPLC)

form

powder

color

white to beige

mp

279-281  °C

solubility

DMSO: 20 mg/mL, clear

storage temp.

2-8°C

SMILES string

Oc1cccc2c(O)nccc12

InChI

1S/C9H7NO2/c11-8-3-1-2-7-6(8)4-5-10-9(7)12/h1-5,11H,(H,10,12)

InChI key

LFUJIPVWTMGYDG-UHFFFAOYSA-N

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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.

Caution

Light sensitive

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

ppe

dust mask type N95 (US), Eyeshields, Gloves

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T Ruscetti et al.
The Journal of biological chemistry, 273(23), 14461-14467 (1998-06-11)
The DNA-dependent protein kinase (DNA-PK) is a heterotrimeric enzyme that binds to double-stranded DNA and is required for the rejoining of double-stranded DNA breaks in mammalian cells. It has been proposed that DNA-PK functions in this DNA repair pathway by
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
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
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