3034-16-0Relevant academic research and scientific papers
Raf kinase inhibitor based on chromone structure, and preparation method and uses thereof
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Paragraph 0061; 0062; 0063, (2016/10/07)
The invention relates to the technical field of pharmaceutical chemistry, and more concretely relates to a group of chromone compounds (A), wherein R1-R10, X1 and X2 are defined in the description. The invention also discloses a preparation method of the
Design, synthesis, and biological evaluation of chromone-based p38 MAP kinase inhibitors
Dyrager, Christine,M?llers, Linda Nilsson,Kj?ll, Linda Karlsson,Alao, John Patrick,Dinér, Peter,Wallner, Fredrik K.,Sunnerhagen, Per,Gr?til, Morten
supporting information; experimental part, p. 7427 - 7431 (2011/12/16)
3-(4-Fluorophenyl)-2-(4-pyridyl)chromone derivatives were synthesized and evaluated as p38 MAP kinase inhibitors. Introduction of an amino group in the 2-position of the pyridyl moiety gave p38α inhibitors with IC50 in the low nanomolar range (
PHARMACEUTICAL COMPOSITIONS FOR THE PREVENTION AND TREATMENT OF COMPLEX DISEASES AND THEIR DELIVERY BY INSERTABLE MEDICAL DEVICES
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Page/Page column 60, (2008/06/13)
The present invention relates to polyphenol-like compounds that are useful for inhibiting VCAM-1 expression, MCP-1 expression and/or SMC proliferation in a mammal. The disclosed compounds are useful for regulating markers of inflammatory conditions, including vascular inflammation, and for treatment and prevention of inflammatory and cardiovascular diseases and related disease states.
Benzoflavone activators of the cystic fibrosis transmembrane conductance regulator: Towards a pharmacophore model for the nucleotide-binding domain
Springsteel, Mark F.,Galietta, Luis J. V.,Ma, Tonghui,By, Kolbot,Berger, Gideon O.,Yang, Hong,Dicus, Christopher W.,Choung, Wonken,Quan, Chao,Shelat, Anang A.,Guy, R. Kiplin,Verkman,Kurth, Mark J.,Nantz, Michael H.
, p. 4113 - 4120 (2007/10/03)
Our previous screen of flavones and related heterocycles for the ability to activate the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel indicated that UCCF-029, a 7,8-benzoflavone, was a potent activator. In the present study, we describe the synthesis and evaluation, using cell-based assays, of a series of benzoflavone analogues to examine structure-activity relationships and to identify compounds having greater potency for activation of both wild type CFTR and a mutant CFTR (G551D-CFTR) that causes cystic fibrosis in some human subjects. Using UCCF-029 as a structural guide, a panel of 77 flavonoid analogues was prepared. Analysis of the panel in FRT cells indicated that benzannulation of the flavone A-ring at the 7,8-position greatly improved compound activity and potency for several flavonoids. Incorporation of a B-ring pyridyl nitrogen either at the 3- or 4-position also elevated CFTR activity, but the influence of this structural modification was not as uniform as the influence of benzannulation. The most potent new analogue, UCCF-339, activated wild-type CFTR with a Kd of 1.7 μM, which is more active than the previous most potent flavonoid activator of CFTR, apigenin. Several compounds in the benzoflavone panel also activated G551D-CFTR, but none were as active as apigenin. Pharmacophore modeling suggests a common binding mode for the flavones and other known CFTR activators at one of the nucleotide-binding sites, allowing for the rational development of more potent flavone analogues.
