University Archives

 Minoxidil (MXD) has been used to treat androgenic alopecia (AGA) for decades. AGA is genetic and caused by a disruption in androgen-androgen receptor pathways in the hair follicles, but MXDs interactions with the pathway are still not fully understood. One possible method involves MXD interacting with estrogen receptor alpha (ER⍺) and stimulating growth of the hair follicles. This study focuses on the estrogenic effects of MXD and how its structure affects this. AutoDock Vina from SwissDock was used to simulate molecular docking comparing how MXD and estradiol (E2) would interact with ER⍺, showing that both ligands could bind to the same site on the receptor protein. A less nonpolar MXD intermediate (MXDI), 6-chloropyrimidine-2 4-diamine- 3-oxide, was developed to see if it retained similar functionality to the complete MXD. To test this, a cell proliferation assay was conducted on two estrogen dependent breast cancer tissue cell lines, MCF-7 and T47D, to see if replication would occur when exposed to MXDI, which resulted in very minor levels of growth. This suggests that MXD’s structure is crucial to its effectiveness and that without its nonpolar segments its ability to bind well to ER⍺ is diminished. This matters greatly because it means an MXD derivative containing more nonpolar segments could be more effective and treat AGA more efficiently.