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Last Update: March 27, 2021.

Continuing Education Activity

Finasteride is an FDA-approved pharmacologic agent for treating benign prostate hyperplasia and androgenic alopecia (male pattern hair loss) in men. Finasteride has also been used to treat signs of hyperandrogenism, such as hirsutism, and may be used in transgender women in combination with estrogen for its anti-androgen properties. This activity outlines the indications, mechanism of action, dosing, significant adverse effects, contraindications, monitoring, and toxicity of finasteride so that providers can direct patient therapy to optimal outcomes.


  • Identify the mechanism of action of finasteride.
  • Summarize the indications and appropriate dosing of finasteride.
  • Review the adverse events profile of finasteride.
  • Outline interprofessional team strategies for improving care coordination and communication to advance improved outcomes when using finasteride for its indicated purposes.
Earn continuing education credits (CME/CE) on this topic.


In 1947, James Hamilton of Yale University published an article on male hormone stimulation as a prerequisite to common baldness after examining 104 men with testicular insufficiency. In 1974, Julianne Imperato-McGinley, of Cornell University published reports on Caribbean children with a mutation leading to deficiencies in 5-alpha-reductase and dihydrotestosterone. When these male children matured, they had smaller prostate sizes and a lack of male pattern baldness. These observations and findings ultimately led to the development of finasteride.[1][2][3]

Finasteride is an FDA-approved pharmacologic agent for treating benign prostate hyperplasia and androgenic alopecia (male pattern hair loss) in men. Finasteride was first used in 1992 to treat benign prostate hyperplasia at a dose of 5 mg. In 1998, it received approval to treat male pattern hair loss at a dose of 1 mg. Finasteride has also been used to treat signs of hyperandrogenism, such as hirsutism, and may find use in transgender women in combination with estrogen for its anti-androgen properties.

Mechanism of Action

Finasteride is a competitive inhibitor of types II and III 5-alpha-reductase isoenzyme, resulting in inhibition of testosterone conversion to dihydrotestosterone (DHT). Finasteride has minimal selectivity for the type I 5-alpha-reductase enzyme. The type I 5-alpha-reductase isomer is present in sebaceous glands, sweat glands, dermal papillae cells, and epidermal and follicular keratinocytes. Type II is in the outer root sheaths of hair follicles, the epididymis, vas deferens, seminal vesicles, and the prostate.[4][5][6]

Research has shown finasteride to reduce prostatic DHT levels by upwards of 90% and serum DHT levels by upwards of 70%. However, increasing the dose does not necessarily result in greater serum reduction. Dutasteride, in comparison, inhibits all three 5-alpha-reductase isoenzymes leading to a 99% reduction in serum DHT levels. In the treatment of androgenic alopecia, where finasteride does not lead to a 100% reduction in DHT, hair loss is slowed but not completely halted. In the treatment of benign prostate hyperplasia, long-term use of finasteride has been associated with a reduction in prostatic volume, thereby providing relief from bothersome urinary symptoms attributed to an enlarged gland. Previously published literature has demonstrated a reduced risk of urinary retention and delayed the need for surgical intervention.


The bioavailability of finasteride is approximately 65% and is not affected by food. Finasteride is approximately 90% protein bound with a volume of distribution of 76 L at a steady state. Upon discontinuation of finasteride, DHT levels return to normal within 14 days. In patients treated for benign prostate hyperplasia, the prostate volume returns to baseline within three months; patients receiving treatment for androgenic alopecia have a reversal of hair count within 12 months.

Finasteride undergoes extensive metabolism in the liver (hepatic metabolism) via the cytochrome P450 enzyme system, specifically CYP3A4, into two active metabolites with less than 20% of the activity of finasteride. Finasteride has a half-life of elimination from the serum of 5 to 6 hours, ranging from 3 to 16 hours. In elderly patients (greater than 70 years of age), the half-life can be prolonged to 8 hours. In comparison to dutasteride, the half-life of finasteride is markedly shorter. Dutasteride has a half-life of 4 to 5 weeks. 

Finasteride is eliminated as metabolites, 57% in the feces and 39% in the urine.


Finasteride is available as a 1 mg tablet or a 5 mg tablet for oral use. Each dose has a different indication. As much as six months of continued treatment may be necessary to assess the benefit of treatment.

Recommended Dosages

  • Benign prostatic hyperplasia: 5 mg once daily (as a single agent or combined with an alpha-blocker).
  • Androgenic alopecia (male pattern baldness): 1 mg once daily.
  • Hirsutism (female, idiopathic, and related to polycystic ovary syndrome): 5 mg once daily or 2.5 mg once daily; this is an off-label use.

Adverse Effects

Common adverse effects associated with finasteride include loss of libido, erectile dysfunction (2% to 4%), decreased ejaculatory volume, and gynecomastia. It also correlates with orthostatic hypotension. This adverse event can be additive in patients who are taking concomitant alpha-blockers. Finasteride reportedly causes orthostatic hypotension in approximately 9% of users as monotherapy and as high as 18% with combined therapy. Therefore, appropriate patient counseling is necessary.

Post-finasteride syndrome (PFS) has been a recently reported issue. This term refers to the continuation of adverse effects despite the discontinuation of therapy. Further investigational studies to better understand post-finasteride syndrome are currently underway.

The impact of finasteride on fertility has also been examined by the urologic and dermatologic practitioners that utilize the medication using different doses for various indications). Thus far, there is minimal data to support the association of permanent infertility using a low dose of 1 mg finasteride. The effects of low-dose finasteride on fertility appear to be reversible as various studies have demonstrated improved fertility and sperm parameters in those who discontinued therapy. However, fertility may suffer a negative impact from the use of the higher 5-mg dose. Not all users experience fertility issues, and many users of the medication are still able to conceive. 

Additionally, finasteride has correlations to symptoms of dizziness, weakness, dyspnea, rhinitis, and skin rash.


Finasteride is contraindicated in those with hypersensitivity to any component of the formulation. Finasteride is contraindicated in children. Furthermore, finasteride is contraindicated in pregnant women or women of childbearing age.

Pregnant women should avoid contact with tablets that have been crushed or broken as animal reproduction studies resulted in an abnormality of external male genitalia. If used for the off-label management of hirsutism in female patients with polycystic ovary syndrome, adequate contraception is the recommendation from the American College of Gynecology.

Blood donation is contraindicated in those currently taking finasteride and for up to 6 months following the last dose of finasteride.


No specific laboratory monitoring guidelines exist for finasteride. However, prostate-specific antigen is a routine assessment in men with benign prostate hyperplasia and surveillance for prostate cancer. Due to the decrease in prostatic volume at the 5-mg dose, there is an expected decrease in serum prostate-specific antigen levels. Therefore, the recommendation is to obtain baseline prostate-specific antigen levels before initiating therapy. Practitioners should be cognizant of serum prostate-specific antigen values in patients using finasteride. Serum lab values are often multiplied by 2 to estimate a more accurate approximation of levels.[7][8]

There has been some controversy regarding the role of finasteride in the development of prostate cancer. The Prostate Cancer Prevention Trial (PCPT) was a landmark study that compared daily finasteride to placebo therapy in over 18,000 men aged 55 and older, who researchers followed for seven years. The study ultimately concluded that finasteride was associated with a 25% reduction in the prevalence of prostate cancer. However, it was also associated with an increased rate of detection of high-grade prostate cancer. The FDA eventually placed a black box warning on the medication safety label, resulting in a negative impact on the prescribing patterns of the drug. There is a considerable consensus in the field that the increased rate of high-grade cancer in the PCPT may result from confounding factors and detection bias. However, it cannot be excluded with certainty.

The American Society of Clinical Oncology (ASCO) and American Urological Association (AUA) released a joint statement in 2008 and developed a clinical practice guideline to assist physicians and patients with making informed decisions after reviewing the risks and benefits of the medication.

The AUA supports the use of finasteride as a treatment option for men with benign prostate hyperplasia and shared decision-making.


There are no reports of overdoses of finasteride, resulting in clinically significant toxicity. However, overdoses could occur as an extension of previously reported adverse drug effects, including orthostatic hypotension.

Enhancing Healthcare Team Outcomes

Finasteride is an FDA-approved pharmacologic agent for treating benign prostate hyperplasia and androgenic alopecia (male pattern hair loss) in men. The drug is also sometimes used to treat hyperandrogenism and hirsutism. All male patients should receive prostate cancer while on this agent; when prescribing this medication, all interprofessional healthcare team members, including clinicians, mid-level practitioners, nurses, and pharmacists, should share information and coordinate their efforts to optimize patient outcomes. [Level 5]

Continuing Education / Review Questions


Zabkowski T, Saracyn M. Drug adherence and drug-related problems in pharmacotherapy for lower urinary tract symptoms related to benign prostatic hyperplasia. J Physiol Pharmacol. 2018 Aug;69(4) [PubMed: 30552307]
Andrade C. Why Odds Ratios Can Be Tricky Statistics: The Case of Finasteride, Dutasteride, and Sexual Dysfunction. J Clin Psychiatry. 2018 Nov 27;79(6) [PubMed: 30549493]
Dai JY, LeBlanc M, Goodman PJ, Lucia MS, Thompson IM, Tangen CM. Case-only Methods Identified Genetic Loci Predicting a Subgroup of Men with Reduced Risk of High-grade Prostate Cancer by Finasteride. Cancer Prev Res (Phila). 2019 Feb;12(2):113-120. [PMC free article: PMC6365187] [PubMed: 30538099]
Shin JW, Chung EH, Kim MB, Kim TO, Kim WI, Huh CH. Evaluation of long-term efficacy of finasteride in Korean men with androgenetic alopecia using the basic and specific classification system. J Dermatol. 2019 Feb;46(2):139-143. [PMC free article: PMC6587453] [PubMed: 30536893]
Almohanna HM, Perper M, Tosti A. Safety concerns when using novel medications to treat alopecia. Expert Opin Drug Saf. 2018 Nov;17(11):1115-1128. [PubMed: 30318935]
Azarchi S, Bienenfeld A, Lo Sicco K, Marchbein S, Shapiro J, Nagler AR. Androgens in women: Hormone-modulating therapies for skin disease. J Am Acad Dermatol. 2019 Jun;80(6):1509-1521. [PubMed: 30312645]
Shin YS, Karna KK, Choi BR, Park JK. Finasteride and Erectile Dysfunction in Patients with Benign Prostatic Hyperplasia or Male Androgenetic Alopecia. World J Mens Health. 2019 May;37(2):157-165. [PMC free article: PMC6479090] [PubMed: 30209896]
Andy G, John M, Mirna S, Rachita D, Michael K, Maja K, Aseem S, Zeljana B. Controversies in the treatment of androgenetic alopecia: The history of finasteride. Dermatol Ther. 2019 Mar;32(2):e12647. [PubMed: 30253001]
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Bookshelf ID: NBK513329PMID: 30020701


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