Wilson’s disease or hepatolenticular degeneration in an autosomal recessive genetic disorder in which copper accumulates in tissues. The condition is due to mutations in Wilson disease protein (ATP7B). A special feature of WD is that medical therapy is used to treat presymptomatic as well as symptomatic individuals, and hepatic transplantation can reverse the metabolic abnormality. In the present research work, an attempt has been made to map the binding site residues of ATP7B protein (receptor). The 3D structure of the monomeric protein was not yet not been experimentally elucidated for which the theoretical structure was determined by homology modeling using 2UVC as template and the structure was validated and refined by SAVS and MODELLER. The generated 3D structure of ATP7B protein was solvated at 310k and energy minimized using Gromacs. Similarly, 2D structures of several diuretic compounds were retrieved, refined and energy minimized using Arguslab software. The diuretic compounds were then subjected to analyze their adsorption, distribution, metabolism, excretion and their toxicity properties. This analysis was done using the online server PREADME/TOX. The protein- ligand interactions between the ATP7B protein and the diuretic compounds were analyzed using Autodock - PyRx and the docking models were visualized and analyzed by PyMol. Based on the output of the docking models and the binding energies the best lead compound was determined which can be used for fighting against the Wilson disease.
