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The Ebola virus is a highly infectious pathogen with no effective antiviral treatments currently available, prompting ongoing research into potential therapeutic options. This study evaluated the inhibitory effects of licensed non-viral drugs on Ebola virus entry and replication using bioinformatic tools. A descriptive-analytical approach was used, in which the chemical structures of selected drugs were first generated in ChemDraw Ultra 10.0 and then energy-optimized in Hyperchem 8.0. Molecular docking was performed using AutoDock4.2 to simulate interactions between the drugs and viral proteins. The analysis revealed that the interactions involved primarily hydrophobic, π-π stacking, hydrogen bonding, and cation-π interactions. Chloroquine, diphenoxylate, and amodiaquine showed the strongest binding affinity, with the most negative docking energies, indicating their potential as effective inhibitors of the GP and VP40 proteins. Conversely, erythromycin and dirithromycin, due to their high hydrophilicity, exhibited weaker binding results. Overall, the study highlighted that drugs with hydrophobic components, effective hydrogen bonding, and tertiary amines tend to show enhanced anti-Ebola properties. The bioinformatic analysis suggests that these drugs could serve as promising candidates for inhibiting Ebola virus entry and replication.