Translational andrology and urology · 2026
Low-dose finasteride in benign prostatic hyperplasia: a comprehensive narrative review of efficacy, safety, and preventative potential.
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Farooqi Mustafa, Bird Paige, Lassiter Samuel, Stroie Florian A
Аннотация
BACKGROUND AND OBJECTIVE: Finasteride 5 mg is a well-established therapy for benign prostatic hyperplasia (BPH). Lower doses, such as finasteride 1 mg-commonly prescribed for androgenic alopecia-also produce measurable suppression of dihydrotestosterone (DHT) and prostate-specific antigen (PSA). This review examines the available evidence related to finasteride 1 mg with respect to prostate biology, safety, and its theoretical potential in modifying BPH risk when initiated earlier in life and its hypothesis-generating potential for preventive use.
METHODS: A structured review of PubMed, EMBASE, and the Cochrane Library from January 1990 through January 2026 was performed to identify studies evaluating finasteride 1 mg with prostate-relevant biologic or surrogate outcomes, including PSA suppression and androgen modulation. Pharmacodynamic dose-response studies were reviewed, and landmark randomized controlled trials (RCTs) of finasteride 5 mg in men with BPH were included for clinical context regarding established prostate volume, symptoms, and progression outcomes.
KEY CONTENT AND FINDINGS: Observational and secondary analyses evaluating long-term exposure to finasteride 1 mg demonstrate consistent biologic effects on prostate-related pathways, most notably suppression of serum PSA. Prostate volume, lower urinary tract symptoms (LUTS), and progression-related outcomes were not predefined primary endpoints in available studies evaluating finasteride 1 mg, and direct evidence demonstrating clinical benefit for these outcomes at the 1 mg dose is lacking.
CONCLUSIONS: Finasteride 1 mg produces measurable biologic effects on prostate-related pathways, including suppression of DHT and PSA. However, clinical prostate outcomes-such as reductions in prostate volume, improvement in LUTS, and prevention of disease progression-are supported only by randomized trials evaluating finasteride 5 mg. Finasteride 1 mg may therefore be best considered a hypothesis-generating option for early or preventive strategies in selected younger men. Large RCTs are warranted to determine whether these biologic effects translate into clinically meaningful benefits.
METHODS: A structured review of PubMed, EMBASE, and the Cochrane Library from January 1990 through January 2026 was performed to identify studies evaluating finasteride 1 mg with prostate-relevant biologic or surrogate outcomes, including PSA suppression and androgen modulation. Pharmacodynamic dose-response studies were reviewed, and landmark randomized controlled trials (RCTs) of finasteride 5 mg in men with BPH were included for clinical context regarding established prostate volume, symptoms, and progression outcomes.
KEY CONTENT AND FINDINGS: Observational and secondary analyses evaluating long-term exposure to finasteride 1 mg demonstrate consistent biologic effects on prostate-related pathways, most notably suppression of serum PSA. Prostate volume, lower urinary tract symptoms (LUTS), and progression-related outcomes were not predefined primary endpoints in available studies evaluating finasteride 1 mg, and direct evidence demonstrating clinical benefit for these outcomes at the 1 mg dose is lacking.
CONCLUSIONS: Finasteride 1 mg produces measurable biologic effects on prostate-related pathways, including suppression of DHT and PSA. However, clinical prostate outcomes-such as reductions in prostate volume, improvement in LUTS, and prevention of disease progression-are supported only by randomized trials evaluating finasteride 5 mg. Finasteride 1 mg may therefore be best considered a hypothesis-generating option for early or preventive strategies in selected younger men. Large RCTs are warranted to determine whether these biologic effects translate into clinically meaningful benefits.