The mechanism of action of alpha toxin begins with the binding of the toxin monomers to specific receptors on the surface of susceptible host cells. Once bound, seven monomers oligomerize to form a heptameric pre-pore complex on the cell membrane. This complex undergoes a conformational change, inserting into the lipid bilayer to form a transmembrane pore. The pore allows uncontrolled ions, small molecules, and water flux across the membrane, leading to osmotic imbalance and cell swelling. This results in cell lysis and death. In immune cells, alpha toxin can also trigger pro-inflammatory responses, exacerbating tissue damage and promoting an environment conducive to bacterial invasion and dissemination. The ability of alpha toxin to target multiple cell types and disrupt various cellular processes makes it a critical factor in the virulence of Staphylococcus aureus. The protein and ligand structures are prepped for molecular docking using AutoDock by adding charges and hydrogen atoms. The protein structure is often obtained from the Protein Data Bank (PDB), which must be filtered of unnecessary components like water.(9) Furthermore, the ligand must be suitable for docking, which means it must have the proper shape and format.