165806-89-3Relevant academic research and scientific papers
Imidazole compounds, use and process of making
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, (2008/06/13)
Novel 1,4,5-substituted imidazole compounds and compositions for use in therapy as cytokine inhibitors.
Pyridyl imidazole compounds and compositions
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, (2008/06/13)
Novel 1, 4, 5-substituted imidazole compounds and compositions for use in therapy as cytokine inhibitors.
Regulation of stress-induced cytokine production by pyridinylimidazoles inhibition of CSBP kinase
Gallagher, Timothy F.,Seibel, George L.,Kassis, Shouki,Laydon, Jeffrey T.,Blumenthal, Mary Jane,Lee, John C.,Lee, Dennis,Boehm, Jeffrey C.,Fier-Thompson, Susan M.,Abt, Jeffrey W.,Soreson, Margaret E.,Smietana, Juanita M.,Hall, Ralph F.,Garigipati, Ravi S.,Bender, Paul E.,Erhard, Karl F.,Krog, Arnold J.,Hofmann, Glenn A.,Sheldrake, Peter L.,McDonnell, Peter C.,Kumar, Sanjay,Young, Peter R.,Adams, Jerry L.
, p. 49 - 64 (2007/10/03)
Members of three classes of pyridinylimidazoles bind with varying affinities to CSBP (p38) kinase which is a member of a stress-induced signal transduction pathway. Based upon SAR and protein homology modeling, the pharmacophore and three potential modes of binding to the enzyme are presented. For a subset of pyridinylimidazoles, binding is shown to correlate with inhibition of CSBP kinase activity, whereas no significant inhibition of PKA, PKα and ERK kinase activity is observed.
1-Substituted 4-aryl-5-pyridinylimidazoles: A new class of cytokine suppressive drugs with low 5-lipoxygenase and cyclooxygenase inhibitory potency
Boehm, Jeffrey C.,Smietana, Juanita M.,Sorenson, Margaret E.,Garigipati, Ravi S.,Gallagher, Timothy F.,Sheldrake, Peter L.,Bradbeer, Jeremy,Badger, Alison M.,Laydon, Jeffrey T.,Lee, John C.,Hillegass, Leonard M.,Griswold, Donald E.,Breton, John J.,Chabot-Fletcher, Marie C.,Adams, Jerry L.
, p. 3929 - 3937 (2007/10/03)
A series of 1-alkyl- or -aryl-4-aryl-5-pyridinylimidazoles (A) were prepared and tested for their ability to bind to a recently discovered protein kinase termed CSBP and to inhibit lipopolysaccharide (LPS)-stimulated TNF production in mice. The kinase, CS
