Minoxidil
Minoxidil was first introduced as an oral medication for the treatment of severe and recalcitrant hypertension in the 1970s. Coincidentally, physicians observed hair regrowth and generalized hypertrichosis in balding patients, which led to the development of a topical minoxidil formulation for treating androgenetic alopecia (AGA) first in male and then in female individuals. The 2% minoxidil solution was first launched in the market in 1986, followed by the 5% solution in 1993.
Minoxidil is a potent arteriolar vasodilator that opens potassium channels located on the smooth muscles of the peripheral artery, causing hyperpolarization of the cell membrane. The positive effect of minoxidil on hair growth is mainly due to its metabolite, minoxidil sulfate, and the enzyme responsible for this conversion is sulfotransferase, which is located in hair follicles and varies in production among individuals. There are two phenol sulfotransferases responsible for minoxidil sulfation in the human scalp, and patients with higher enzyme activity responded better to topical minoxidil than those with lower enzyme activity did.
Finasteride
Finasteride is a 5α-reductase inhibitor, and therefore an antiandrogen. It works by decreasing the production of dihydrotestosterone (DHT) by about 70%, including in the prostate gland and the scalp.
Taking finasteride leads to a reduction in scalp and serum DHT levels; by lowering scalp levels of DHT, finasteride can maintain or increase the amount of terminal hairs in the anagen phase by inhibiting and sometimes reversing miniaturization of the hair follicle. Finasteride is most effective on the vertex but can reduce hair loss in all areas of the scalp.