80309-04-2

Basic information

• Product Name: 4H-Naphtho[1,2-b]pyran-4-one, 6-bromo-2-(4-methoxyphenyl)-
• CAS NO: 80309-04-2
• Molecular Formula: C20H13BrO3
• Molecular Weight: 381.225
• Mol File: 80309-04-2.mol
• Article Data: 2

Chemical Properties

• CAS DataBase Reference: 4H-Naphtho[1,2-b]pyran-4-one, 6-bromo-2-(4-methoxyphenyl)-(CAS DataBase Reference)
• NIST Chemistry Reference: 4H-Naphtho[1,2-b]pyran-4-one, 6-bromo-2-(4-methoxyphenyl)-(80309-04-2)
• EPA Substance Registry System: 4H-Naphtho[1,2-b]pyran-4-one, 6-bromo-2-(4-methoxyphenyl)-(80309-04-2)

Safety Data

• Hazardous Substances Data: 80309-04-2(Hazardous Substances Data)

Upstream product

• 623-11-0 1-methyl-4-nitrosobenzene 
• 30508-15-7 (2RS:3SR)-2,3-dibromo-1-(4-bromo-1-hydroxy-[2]naphthyl)-3-(4-methoxy-phenyl)-propan-1-one 
• 67-64-1 acetone 
• 80309-02-0 4-bromo-2-hydroxy-3,4-benzoacetophenone anisoate 
• 52220-64-1 1-(4-bromo-1-hydroxynaphthalen-2-yl)ethanone 
• 80309-03-1 5-bromo-2-hydroxy-4'-methoxy-3,4-benzodibenzoylmethane 

Relevant articles and documents

Benzoflavone activators of the cystic fibrosis transmembrane conductance regulator: Towards a pharmacophore model for the nucleotide-binding domain

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.