BACE-1 is involved in the production of beta-amyloid peptides, and inhibiting its activity is a potential therapeutic strategy for managing Alzheimer’s disease, as excessive beta-amyloid accumulation is a characteristic feature of the disease.Computational results suggest that hypericin has the potential to act as an inhibitor of BACE-1. The Molecular Docking results indicate a high binding affinity between hypericin and BACE-1, with a notable binding energy score of -10.3 kcal/ mol. Additionally, the formation of various chemical bonds, including hydrogen bonds and hydrophobic bonds, further supports the idea that hypericin may effectively interact with the active site of BACE-1. It is important to note that while the in silico Molecular Docking results are promising, further in vitro and in vivo studies would be necessary to validate and better understand the inhibitory potential of hypericin against BACE-1. Additionally, the practical application of hypericin as a BACE-1 inhibitor in a therapeutic context would require careful consideration of factors such as bioavailability, safety, and efficacy.