Esophageal cancer (EC) is a cancer with high lethality and poor prognosis, and it was responsible for the death of 0.54 million people in 2020. Its treatment is often challenged by the side effects of the drugs used and the development of resistance mechanisms by EC cells. In this study, the potential of rosmarinic acid (RA) to serve as a therapeutic regimen for the treatment of EC was evaluated using network pharmacology approach. Firstly, the putative targets of RA were identified using small molecule target prediction platforms, while the genes commonly dysregulated in EC were identified by microarray data analysis. Subsequently, common targets were identified and their interaction network was delineated using the STRING database, while the core targets of the network were identified using the CytoHubba plug-in of Cystoscope. Further analysis conducted included the gene ontology, pathways enrichment analysis, and molecular docking of RA with the core targets. The results of the study revealed that CDK2, CHEK1, ERBB2, GSK3β, HSP90AA1, MMP9, NFKβ1, and STAT1 to be the core targets via which RA might exhibit its anti-EC potential, and the molecular function mediated by these core targets include ATP binding and protein kinase activity. Critical pathways such as the interleukin-17 and PI3K-Akt signaling pathways which are commonly dysregulated in EC were also identified as the pathways RA may restore. Molecular docking simulation also revealed RA possess high binding affinities for the core targets. Ultimately, further confirmation of the anti-EC activity of RA should be conducted in experimental studies.