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Merck
CN

I2784

INH2BP

≥98% (HPLC), solid

Synonym(s):

5-Iodo-6-amino-1,2-benzopyrone

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About This Item

Empirical Formula (Hill Notation):
C9H6INO2
CAS Number:
Molecular Weight:
287.05
UNSPSC Code:
12352202
PubChem Substance ID:
MDL number:
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InChI

1S/C9H6INO2/c10-9-5-1-4-8(12)13-7(5)3-2-6(9)11/h1-4H,11H2

SMILES string

Nc1ccc2OC(=O)C=Cc2c1I

InChI key

WWRAFPGUBABZSD-UHFFFAOYSA-N

assay

≥98% (HPLC)

form

solid

solubility

DMSO: soluble 31 mg/mL, H2O: insoluble

storage temp.

2-8°C

Biochem/physiol Actions

Inhibitor of poly (ADP-ribose) polymerase-1 (PARP-1); anti-apoptotic.

Storage Class

11 - Combustible Solids

wgk

WGK 3

ppe

dust mask type N95 (US), Eyeshields, Gloves

Regulatory Information

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France Vaillancourt et al.
Arthritis research & therapy, 10(5), R107-R107 (2008-09-11)
4-Hydroxynonenal (HNE) is one of the most abundant and reactive aldehydes of lipid peroxidation products and exerts various effects on intracellular and extracellular signalling cascades. We have previously shown that HNE at low concentrations could be considered as an important
Allison B Haugrud et al.
Breast cancer research and treatment, 147(3), 539-550 (2014-09-13)
The unique metabolism of breast cancer cells provides interest in exploiting this phenomenon therapeutically. Metformin, a promising breast cancer therapeutic, targets complex I of the electron transport chain leading to an accumulation of reactive oxygen species (ROS) that eventually lead
G A Cole et al.
Biochemical and biophysical research communications, 180(2), 504-514 (1991-10-31)
The effects of two adenosine diphosphoribose transferase (ADPRT) enzyme inhibitory ligands, 6-amino-1,2-benzopyrone and its 5-iodo-derivative, were determined in AA-2 and MT-2 cell cultures on the replication of HIV-1 IIIb, assayed by an immunochemical test for the HIV protein p24, and
M Endres et al.
European journal of pharmacology, 351(3), 377-382 (1998-08-28)
Peroxynitrite triggers DNA single-strand breakage, which activates the nuclear enzyme poly(ADP-ribose) synthetase (PARS). Activation of PARS depletes its substrate, NAD+, slowing the rate of glycolysis, electron transport, and ATP formation, resulting in cell necrosis. Here, we demonstrate that inhibition of
J G Mabley et al.
British journal of pharmacology, 133(6), 909-919 (2001-07-17)
Activation of poly(ADP-ribose) synthetase (PARS, also termed polyADP-ribose polymerase or PARP) has been proposed as a major mechanism contributing to beta-cell destruction in type I diabetes. In the present study, we have investigated the role of PARS in mediating the

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