25752-66-3

Basic information

• Product Name: 1-bromo-4-(tert-butylsulfonyl)benzene
• Synonyms: 1-bromo-4-(tert-butylsulfonyl)benzene
• CAS NO: 25752-66-3
• Molecular Weight: 277.182
• Mol File: 25752-66-3.mol
• Article Data: 5

Chemical Properties

• CAS DataBase Reference: 1-bromo-4-(tert-butylsulfonyl)benzene(CAS DataBase Reference)
• NIST Chemistry Reference: 1-bromo-4-(tert-butylsulfonyl)benzene(25752-66-3)
• EPA Substance Registry System: 1-bromo-4-(tert-butylsulfonyl)benzene(25752-66-3)

Safety Data

• Hazardous Substances Data: 25752-66-3(Hazardous Substances Data)

Upstream product

• 106-53-6 para-bromobenzenethiol 
• 25752-90-3 tert-butyl 4-bromophenyl sulfide 

Downstream Products

• 1286238-54-7 3-amino-6-(4-(tert-butylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide 

Relevant articles and documents

CYCLOALKYL NITRILE PYRAZOLO PYRIDONES AS JANUS KINASE INHIBITORS

Compounds of formula I are provided, which are JAK inhibitors and are useful for the treatment of JAK-mediated diseases such as rheumatoid arthritis, asthma, COPD and cancer.

ACYCLIC CYANOETHYLPYRAZOLO PYRIDONES AS JANUS KINASE INHIBITORS

The instant invention provides compounds of formula I which are JAK inhibitors, and as such are useful for the treatment of JAK-mediated diseases such as rheumatoid arthritis, asthma, COPD and cancer.

Discovery of Potent and Selective Inhibitors of Ataxia Telangiectasia Mutated and Rad3 Related (ATR) Protein Kinase as Potential Anticancer Agents

DNA-damaging agents are among the most frequently used anticancer drugs. However, they provide only modest benefit in most cancers. This may be attributed to a genome maintenance network, the DNA damage response (DDR), that recognizes and repairs damaged DNA. ATR is a major regulator of the DDR and an attractive anticancer target. Herein, we describe the discovery of a series of aminopyrazines with potent and selective ATR inhibition. Compound 45 inhibits ATR with a Ki of 6 nM, shows >600-fold selectivity over related kinases ATM or DNA-PK, and blocks ATR signaling in cells with an IC50 of 0.42 μM. Using this compound, we show that ATR inhibition markedly enhances death induced by DNA-damaging agents in certain cancers but not normal cells. This differential response between cancer and normal cells highlights the great potential for ATR inhibition as a novel mechanism to dramatically increase the efficacy of many established drugs and ionizing radiation.