University Archives

Minoxidil is a drug commonly used to treat androgenetic alopecia and has been shown to interact with hormone receptor signaling pathways that regulate cellular proliferation. Previous studies have demonstrated that minoxidil can influence estrogen receptor alpha (ERα) activity and stimulate growth in estrogen-dependent breast cancer cells. In this study, the biological activity of a synthetic intermediate of minoxidil, 6-chloropyrimidine-2,4-diamine-3-oxide, was evaluated to determine whether structural components of the parent compound retain biological function. Estrogen-dependent breast cancer cells from cell lines MCF-7 and T47D were cultured under estrogen-depleted conditions and treated with estradiol or increasing concentrations of the minoxidil intermediate. Cellular proliferation was assessed using an Alamar Blue metabolic assay, which measures fluorescence produced by metabolically active cells. In parallel, computational docking studies were performed to evaluate potential interactions between ligands and ERα using molecular docking simulations. Experimental results showed that estradiol treatment produced the strongest proliferative response, while treatment with the minoxidil intermediate produced fluorescence values close to control conditions in both cell lines. Docking analysis was used to examine potential ligand interactions within the ERα binding pocket. These findings suggest that the minoxidil intermediate does not strongly stimulate estrogen-dependent proliferation under the tested conditions and highlight the importance of structural features present in the fully formed drug.