uccf-029 and Cystic-Fibrosis

uccf-029 has been researched along with Cystic-Fibrosis* in 1 studies

Other Studies

1 other study(ies) available for uccf-029 and Cystic-Fibrosis

Article	Year
Activation of CFTR by UCCF-029 and genistein. Bioorganic & medicinal chemistry letters, 2008, Jul-15, Volume: 18, Issue:14 The mechanism of action of a novel CFTR activator UC(CF)-029 on NIH3T3 cells stably expressing DeltaF508-CFTR was investigated and its effects compared to those of genistein, a known CFTR activator. This study shows that UC(CF)-029 and genistein have differing efficacies. The efficacy of UC(CF)-029 in the presence of forskolin (10microM) is approximately 50% that of genistein; however, the EC(50)'s for both drugs are comparable; 3.5microM for UC(CF)-029 and 4.4muM for genistein. Using NIH3T3 cells stably transfected with K1250A-CFTR we find that CFTR channel open time is unaffected by UC(CF)-029 or genistein, supporting the hypothesis that these compounds stabilize the open state by inhibiting ATP hydrolysis at NBD2. Our data suggest that the ability of UC(CF)-029 to augment DeltaF508-CFTR channel activity necessitates further interest. Topics: Adenosine Triphosphate; Animals; Benzoflavones; Colforsin; Cystic Fibrosis; Cystic Fibrosis Transmembrane Conductance Regulator; Dose-Response Relationship, Drug; Drug Design; Genistein; Hydrolysis; Mice; Models, Chemical; NIH 3T3 Cells; Protein Kinase Inhibitors; Transfection	2008

Article

Year

Activation of CFTR by UCCF-029 and genistein.

Bioorganic & medicinal chemistry letters, 2008, Jul-15, Volume: 18, Issue:14

The mechanism of action of a novel CFTR activator UC(CF)-029 on NIH3T3 cells stably expressing DeltaF508-CFTR was investigated and its effects compared to those of genistein, a known CFTR activator. This study shows that UC(CF)-029 and genistein have differing efficacies. The efficacy of UC(CF)-029 in the presence of forskolin (10microM) is approximately 50% that of genistein; however, the EC(50)'s for both drugs are comparable; 3.5microM for UC(CF)-029 and 4.4muM for genistein. Using NIH3T3 cells stably transfected with K1250A-CFTR we find that CFTR channel open time is unaffected by UC(CF)-029 or genistein, supporting the hypothesis that these compounds stabilize the open state by inhibiting ATP hydrolysis at NBD2. Our data suggest that the ability of UC(CF)-029 to augment DeltaF508-CFTR channel activity necessitates further interest.

Topics: Adenosine Triphosphate; Animals; Benzoflavones; Colforsin; Cystic Fibrosis; Cystic Fibrosis Transmembrane Conductance Regulator; Dose-Response Relationship, Drug; Drug Design; Genistein; Hydrolysis; Mice; Models, Chemical; NIH 3T3 Cells; Protein Kinase Inhibitors; Transfection

2008