4373-73-3Relevant academic research and scientific papers
COMPOUNDS USEFUL FOR INHIBITING CHK1
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Page/Page column 43, (2008/06/13)
Substituted urea compounds useful in the treatment of diseases and conditions related to DNA damage or lesions in DNA replication are disclosed. Methods of making the compounds, and their use as ther-apeutic agents, for example, in treating cancer and oth
QUINOLINE DERIVATIVES
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Page 51, (2010/02/07)
The present invention relates to compounds of Formula I, wherein R1, R2, R3, R4, and n are as defined, and to pharmaceutically acceptable salts of said compounds. Compounds of Formula I have activity in agonizing 5HT7 receptors and are useful in treating, for example, disorders that can be treated by modulating circadian rhythms.
A simple and efficient synthesis of 2,- 3-, or 4-(2-nitrophenyl)pyridine derivatives via palladium catalyzed ullmann cross-coupling reaction
Shimizu, Noboru,Kitamura, Takahiro,Watanabe, Koichiro,Yamaguchi, Takashi,Shigyo, Hiromichi,Ohta, Tomio
, p. 3421 - 3424 (2007/10/02)
The Ullmann cross-coupling reaction of halopyridines with 2-bromonitirobenzenes was successffully catalyzed by low valent palladium [Pd(PPh3)4, PdCl2(PPh3)2, PdCl2] to afford (2-nitrophenyl)pyridine derivatives in good to excellent yield.
Synthesis and antiarrhythmic activity of disubstituted phenylpyridine derivative
Shigyo,Sato,Shibuya,Takahashi,Yamaguchi,Sonoki,Ohta
, p. 1573 - 1582 (2007/10/02)
A series of disubstituted phenylpyridine derivatives was synthesized and their antiarrhythmic effects against chloroform-induced ventricular arrhythmias in mice were examined. Among them, 2- and 3-[2-(3- aminobutyramido)-4-(2,2,2-trifluoroethoxy)phenyl]pyridines (23h, 24h) and 3- [2-(3-aminobutyramido)-4-ethoxyphenyl]pyridine (24i) showed potent antiarrhythmic activity. They had approximately twice the potency of mexiletine (III). Compound 24i was selected from this series as a candidate for further development; it was found to have a class I B electrophysiological character and to show a slow kinetic rate-dependent block (RDB) of the sodium channel in cardiac muscle.
