Testosterone is the most abundant androgen in serum. Intracellularly, testosterone is converted to dihydrotestosterone, the preferred ligand for androgen receptor transactivation, by the enzyme 5α-reductase. Three 5α-reductase isozymes have been discovered and they are expressed ubiquitously in human tissues. Testosterone and dihydrotestosterone have different but complimentary functions. Dihydrotestosterone has 2-5 times higher binding affinity for the androgen receptor than testosterone, and 10-fold higher potency of inducing androgen receptor signaling than testosterone. The role of dihydrotestosterone was discovered after the description of 5α-reductase type 2 deficiency in 1974, where affected males have normal internal but ambiguous external genitalia. Neither BPH nor prostate cancer has been reported in these patients. Currently, two 5α-reductase inhibitors are available for clinical use. This review will discuss the important clinical trials of 5α-reductase inhibitors in the treatment of benign prostatic diseases.