853139-10-3Relevant academic research and scientific papers
Sulfamoyl-4-oxoquinoline-3-carboxamides: Novel potentiators of defective ΔF508-cystic fibrosis transmembrane conductance regulator chloride channel gating
Suen, Yat Fan,Robins, Lori,Yang, Baoxue,Verkman,Nantz, Michael H.,Kurth, Mark J.
, p. 537 - 540 (2007/10/03)
The synthesis of a small collection of sulfamoyl-4-oxoquinoline-3- carboxamides is described for use as correctors of defective gating of the ΔF508-cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel. Several compounds with submicromolar potency were obtained. N-Ethyl 6-(ethylphenylsulfamoyl)-4-oxo-1,4-dihydroquinoline-3-carboxamide (7b) was found to be the most effective sulfonamide corrector of defective ΔF508-CFTR gating.
COMPOUNDS HAVING ACTIVITY IN INCREASING ION TRANSPORT BY MUTANT-CFTR AND USES THEREOF
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Page/Page column 48-49; figure 2, (2008/06/13)
The invention provides compositions, pharmaceutical preparations and methods for increasing activity (e.g., ion transport) of the mutant cystic fibrosis transmembrane conductance regulator protein (mutant-CFTR), e.g., DF508 CFTR, G551D-CFTR, G1349D-CFTR,
Phenylglycine and sulfonamide correctors of defective ΔF508 and G551D cystic fibrosis transmembrane conductance regulator chloride-channel gating
Pedemonte, Nicoletta,Sonawane,Taddei, Alessandro,Hu, Jie,Zegarra-Moran, Olga,Suen, Yat Fan,Robins, Lori I.,Dicus, Christopher W.,Willenbring, Dan,Nantz, Michael H.,Kurth, Mark J.,Galietta, Luis J. V.,Verkman, Alan S.
, p. 1797 - 1807 (2007/10/03)
Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel cause cystic fibrosis. The ΔF508 mutation produces defects in channel gating and cellular processing, whereas the G551D mutation produces primarily a gating defec
