Docking-based analysis and modeling of the activity of bile acids and their synthetic analogues on large conductance Ca2+ activated K channels in smooth muscle cells.

Abstract

Molecular docking suggested that the pharmacophore for maximizing the activity of BK(Ca) channels in the steroid skeleton of bile acids is the C3 quasi-axial α-OH group and the C24 carboxyl function. Derived neural network model successfully predicted activities of tested bile acids on Ca2+ activated K+ channels in smooth muscle cells.