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SML1697

Sigma-Aldrich

OGG1 Inhibitor O8

≥98% (HPLC)

Synonym(s):

3,4-Dichloro-benzo[b]thiophene-2-carboxylic acid hydrazide

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About This Item

Empirical Formula (Hill Notation):
C9H6Cl2N2OS
CAS Number:
Molecular Weight:
261.13
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Quality Level

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 5 mg/mL, clear

storage temp.

2-8°C

SMILES string

ClC1=C(C(NN)=O)SC2=CC=CC(Cl)=C21

InChI

1S/C9H6Cl2N2OS/c10-4-2-1-3-5-6(4)7(11)8(15-5)9(14)13-12/h1-3H,12H2,(H,13,14)

InChI key

HSSHUDKWJRJKPV-UHFFFAOYSA-N

General description

Inhibition of 8-oxoguanine DNA glycosylase-1 (OGG1) can be used in monotherapy or in combination therapy to treat some types of cancer.

Biochem/physiol Actions

OGG1 Inhibitor O8 is a potent inhibitor of 8-Oxoguanine DNA Glycosylase-1 (OGG1), part of the DNA base excision repair (BER) pathway that is becoming a drug target for cancer therapy. OGG1 Inhibitor O8 has an IC50 value of 220 nM and >100-fold selectivity for OGG1 relative to several other DNA repair glycosylases. O8 acts through the inhibition of Schiff base formation during OGG1 catalysis. It does not prevent DNA binding of OGG1 to a 7,8-dihydro-8-oxoguanine (8-oxo-Gua)-containing substrate.

pictograms

Exclamation mark

signalword

Warning

Hazard Classifications

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

target_organs

Respiratory system

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Nathan Donley et al.
ACS chemical biology, 10(10), 2334-2343 (2015-07-29)
The DNA base excision repair (BER) pathway, which utilizes DNA glycosylases to initiate repair of specific DNA lesions, is the major pathway for the repair of DNA damage induced by oxidation, alkylation, and deamination. Early results from clinical trials suggest
Mingxin Chang et al.
Frontiers in pharmacology, 11, 610205-610205 (2021-02-02)
Background: Oncogenic transformation is associated with elevated oxidative stress that promotes tumor progression but also renders cancer cells vulnerable to further oxidative insult. Agents that stimulate ROS generation or suppress antioxidant systems can drive oxidative pressure to toxic levels selectively
Xu Zheng et al.
Journal of innate immunity, 1-22 (2022-05-06)
The primary cause of morbidity and mortality from infection with respiratory syncytial virus (RSV) is the excessive innate immune response(s) (IIR) in which reactive oxygen species (ROS) play key role(s). However, the mechanisms for these processes are not fully understood.
Hongge Wang et al.
Oncogene, 39(14), 2905-2920 (2020-02-08)
PARP1 and PARP2 play critical roles in regulating DNA repair and PARP inhibitors have been approved for the treatment of BRCA1/2-mutated ovarian and breast cancers. It has long been known that PARP inhibition sensitizes cancer cells to DNA-damaging cytotoxic agents
Wenjing Hao et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34(6), 7427-7441 (2020-05-08)
8-Oxoguanine DNA glycosylase1 (OGG1)-initiated base excision repair (BER) is the primary pathway to remove the pre-mutagenic 8-oxo-7,8-dihydroguanine (8-oxoG) from DNA. Recent studies documented 8-oxoG serves as an epigenetic-like mark and OGG1 modulates gene expression in oxidatively stressed cells. For this

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