25752-66-3Relevant academic research and scientific papers
CYCLOALKYL NITRILE PYRAZOLO PYRIDONES AS JANUS KINASE INHIBITORS
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Page/Page column 119, (2014/10/03)
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.
N-(2-CYANO HETEROCYCLYL)PYRAZOLO PYRIDONES AS JANUS KINASE INHIBITORS
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Page/Page column 51, (2014/10/03)
Provided are compounds of Formula I, a JAK inhibitor, and use thereof for the treatment of JAK-mediated diseases by the application.
ACYCLIC CYANOETHYLPYRAZOLO PYRIDONES AS JANUS KINASE INHIBITORS
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Page/Page column 49, (2014/10/03)
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.
GEMINALLY SUBSTITUTED CYANOETHYLPYRAZOLO PYRIDONES AS JANUS KINASE INHIBITORS
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Page/Page column 108; 109, (2014/10/03)
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
Charrier, Jean-Damien,Durrant, Steven J.,Golec, Julian M. C.,Kay, David P.,Knegtel, Ronald M. A.,MacCormick, Somhairle,Mortimore, Michael,O'Donnell, Michael E.,Pinder, Joanne L.,Reaper, Philip M.,Rutherford, Alistair P.,Wang, Paul S. H.,Young, Stephen C.,Pollard, John R.
supporting information; experimental part, p. 2320 - 2330 (2011/06/17)
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.
