20949-44-4Relevant academic research and scientific papers
Phosgene-free synthesis of N-Aryl-N'-(4-pyridinyl)ureas via selenium-catalyzed oxidative carbonylation of 4-Aminopyridine with aromatic amines
Zhang, Xiaopeng,Li, Zhengwei,Wang, Yan,Dong, Shuxiang,Niu, Xueli,Zhang, Guisheng
, p. 197 - 209 (2016/10/22)
A facile, phosgene-free approach with high atom economy has been developed for the synthesis of N-Aryl-N'-(4-pyridinyl)ureas. With cheap selenium as the catalyst, carbon monoxide (instead of phosgene) as the carbonyl reagent, N-Aryl-N'-(4-pyridinyl)ureas can be obtained in a one-pot manner mostly in moderate to good yields via oxidative cross-carbonylation of 4-Aminopyridine with a variety of aromatic amines in the presence of oxygen under atmospheric pressure. The mechanism for the synthesis of N-Aryl-N'-(4-pyridinyl)ureas is also proposed.
Design and synthesis of Rho kinase inhibitors (I)
Takami, Atsuya,Iwakubo, Masayuki,Okada, Yuji,Kawata, Takehisa,Odai, Hideharu,Takahashi, Nobuaki,Shindo, Kazutoshi,Kimura, Kaname,Tagami, Yoshimichi,Miyake, Mika,Fukushima, Kayoko,Inagaki, Masaki,Amano, Mutsuki,Kaibuchi, Kozo,Iijima, Hiroshi
, p. 2115 - 2137 (2007/10/03)
Several structurally unrelated scaffolds of the Rho kinase inhibitor were designed using pharmacophore information obtained from the results of a high-throughput screening and structural information from a homology model of Rho kinase. A docking simulation using the ligand-binding pocket of the Rho kinase model helped to comprehensively understand and to predict the structure-activity relationship of the inhibitors. This understanding was useful for developing new Rho kinase inhibitors of higher potency and selectivity. We identified several potent platforms for developing the Rho kinase inhibitors, namely, pyridine, 1H-indazole, isoquinoline, and phthalimide.
N-phenyl-N'-pyridinylureas as anticonvulsant agents
Pavia,Lobbestael,Taylor,Hershenson,Miskell
, p. 854 - 861 (2007/10/02)
A series of N-phenyl-N'-pyridinylureas was examined for anticonvulsant activity. Extensive structure/activity investigations revealed optimal activity in the N-(2,6-disubstituted-phenyl)-N'-(4-pyridinyl)urea series, with 37 exhibiting the best overall anticonvulsant profile. Compound 37 was effective against seizures induced by maximal electroshock but did not protect mice from clonic seizures produced by the convulsant pentylenetetrazol. The overall pharmacological profile suggests that 37 would be of therapeutic use in the treatment of generalized tonic-clonic and partial seizures. Compound 37 was selected for Phase 1 clinical trials.
