In the prostate, the testosterone content accounts for 20% of the total testosterone content in the body, while dihydrotestosterone (DHT) accounts for 90%, the latter being the main androgen in the prostate. In addition, because the prostate is rich in 5-reductase enzymes, which can convert testosterone entering from the blood circulation into DHT. the effect of DHT is significantly stronger than testosterone, and is a decisive factor in tissue hyperplasia in the prostate. The application of 5-reductase inhibitors inhibits the activity of 5-reductase and reduces the amount of testosterone converted to dihydrotestosterone, thereby inhibiting DHT from promoting prostate growth. Finasteride is a potent and reproducible 5-reductase inhibitor with a molecular structure similar to testosterone, which competes with testosterone to inhibit 5-reductase. The application of this drug can lead to 80%-90% inhibition of DHT in the prostate. The average reduction in prostate size was 26% after 6 months of medication. A study has confirmed that the lack of 5-reductase in the prostate can’t convert testosterone into dihydrotestosterone, thus preventing the prostate from developing normally, not to mention the possibility of prostate hyperplasia. Because of the important role of 5-reductase and dihydrotestosterone in the pathogenesis of prostatic hyperplasia, the use of the 5-reductase inhibitor finasteride, which blocks the conversion of testosterone to dihydrotestosterone, can then block prostatic hyperplasia. The use of finasteride in the treatment of prostate enlargement can be effective, but the drug does not work quickly and must be taken for several years, probably because of the slow development of prostate enlargement itself.