Due to the power and high prevalence of infection and the lack of suitable medicine for the Ebola virus, research has been conducted on the discovery and introduction of anti-Ebola drugs. The purpose of the present study was to investigate the bioinformatic inhibition of Ebola virus entry and proliferation by licensed non-viral drugs. This research is a descriptive-analytical method and to carry out this investigation, first, the chemical structure of the compounds was drawn using ChemDraw Ultra 10.0 software, and then it was transferred to Hyperchem8 software to optimize the energy. Docking studies were carried out by AutoDock4.2 software and were analyzed in the final stage. The results obtained from the present study showed that the bonds involved in drug binding with receptors are hydrophobic, π-π, hydrogen bonds, and cation-π. Among all studied compounds, the best docking results were related to chloroquine, diphenoxylate, and amodiaquine drugs. These three drugs with the most negative binding energy level had a greater tendency to bind to the amino acids of the binding site of GP and VP40 proteins. The weakest docking results were related to the two drugs erythromycin and dirithromycin, because the hydrophilicity of these two drugs is very high. In general, the presence of hydrophobic parts, optimal hydrogen bonds, and tertiary amine increases the anti-Ebola potency of drugs. Based on the results obtained from bioinformatics studies, all drugs show good inhibitory effects in the receptor binding site and can be considered effective inhibitors of Ebola virus entry and proliferation
