What Is Finasteride? Complete Guide (2026)

Finasteride is a synthetic, oral, prescription 5-alpha-reductase inhibitor (5ARI) approved by the U.S. Food and Drug Administration (FDA) for two indications: benign prostatic hyperplasia (BPH) at 5 mg/day (brand name Proscar, 1992) and male androgenetic alopecia (AGA, male pattern hair loss) at 1 mg/day (brand name Propecia, 1997). It is the only FDA-approved oral medication for male pattern baldness as of 2026.

Finasteride works by selectively inhibiting the Type II isoenzyme of 5-alpha-reductase, the enzyme primarily responsible for converting testosterone into dihydrotestosterone (DHT) in the scalp, prostate, and other tissues. Blocking this conversion reduces circulating DHT by approximately 70% and scalp DHT by roughly 64%, interrupting DHT-driven hair follicle miniaturization and prostate enlargement.

The drug is available as generic finasteride in both 1 mg and 5 mg strengths from multiple manufacturers, at substantially lower cost than the original brand-name formulations. It is a non-controlled prescription medication in the United States.

Classification and Chemistry

Finasteride belongs to the pharmacological class of 5-alpha-reductase inhibitors (5ARIs). Chemically, it is a synthetic 4-azasteroid compound with the IUPAC name N-(1,1-dimethylethyl)-3-oxo-(5α,17β)-4-azaandrost-1-ene-17-carboxamide. Its molecular formula is C₂₃H₃₆N₂O₂ and its molecular weight is 372.55 g/mol.

Structurally, finasteride is a competitive inhibitor that forms a slow-dissociating complex with the Type II 5-alpha-reductase enzyme, effectively blocking it. The drug is selective for the Type II isoenzyme; it has little or no affinity for the Type I isoenzyme (which is predominant in the liver and skin outside the scalp) or for androgen, estrogen, glucocorticoid, mineralocorticoid, or progestogen receptors.

Drug classification identifiers:

• DrugBank ID: DB01216
• PubChem CID: 57363
• RxNorm: 692878 (finasteride 1 mg), 692879 (finasteride 5 mg)
• MeSH heading: Finasteride
• ATC code: G04CB01

History and FDA Approval Timeline

Finasteride was developed by Merck & Co. in the 1980s, building on research into 5-alpha-reductase deficiency in humans. A 1974 study by Imperato-McGinley et al. demonstrated that males with congenital 5-alpha-reductase deficiency had small prostates, no BPH, and no male pattern baldness — identifying DHT, not testosterone, as the key androgen in both conditions. This insight provided the scientific rationale for developing a 5-alpha-reductase inhibitor as a therapeutic agent.

Key milestones in finasteride’s regulatory history:

Year	Event
1992	FDA approves Proscar (finasteride 5 mg) for symptomatic BPH
1997	FDA approves Propecia (finasteride 1 mg) for male androgenetic alopecia — first oral drug approved for this indication
2002	Finasteride 5 mg enters the Prostate Cancer Prevention Trial (PCPT), the largest prostate cancer prevention study at that time
2003	PCPT results published (N Engl J Med): finasteride reduces prostate cancer incidence by 24.8% but raises questions about high-grade cancer (subsequently explained as a detection artifact)
2011	FDA issues drug safety communication on 5-ARIs and high-grade prostate cancer risk; updates prescribing information
2012	FDA updates finasteride label to add persistent sexual side effects (including after discontinuation) to the warnings section
2019	Generic finasteride 1 mg becomes widely available following patent expiry, significantly reducing patient costs

Mechanism of Action

The 5-Alpha-Reductase Enzyme System

5-alpha-reductase (5-AR) is a microsomal NADPH-dependent enzyme that catalyzes the irreversible conversion of testosterone to dihydrotestosterone (DHT) and progesterone to dihydroprogesterone (DHP). Two main isoenzymes are clinically relevant:

• Type I (SRD5A1): Predominant in skin (excluding scalp), liver, and non-genital tissues. Accounts for approximately 30% of DHT production.
• Type II (SRD5A2): Predominant in scalp, prostate, seminal vesicles, epididymis, and genital skin. Accounts for approximately 70% of circulating DHT. This is the primary therapeutic target of finasteride.

A third isoenzyme (Type III, SRD5A3) has been identified but plays a minor role in androgen metabolism.

DHT and Androgenetic Alopecia

DHT is approximately 5 times more potent than testosterone at the androgen receptor and has a dissociation constant roughly 10 times lower, meaning it binds far more tightly. In men genetically predisposed to AGA, androgen receptors in scalp follicles (particularly at the vertex and frontal area) are hypersensitive to DHT. DHT binding:

• Shortens the anagen (growth) phase of the hair cycle
• Prolongs the telogen (rest) phase
• Progressively miniaturizes the follicle over successive cycles, producing finer, shorter, and eventually barely visible vellus hairs

By reducing scalp DHT by approximately 64%, finasteride interrupts this miniaturization cycle. In many men, existing miniaturized follicles can partially recover, producing thicker, longer terminal hairs. The drug does not create new follicles.

DHT and Prostate Growth

In the prostate, DHT is the primary driver of glandular growth throughout adult life. Men with 5-alpha-reductase Type II deficiency have essentially no prostate BPH — a direct genetic proof of concept for finasteride’s target. In men with BPH, elevated intraprostatic DHT stimulates epithelial and stromal cell proliferation. Finasteride’s inhibition of Type II 5-AR in prostate tissue reduces intraprostatic DHT by more than 80%, shrinking the gland volume by 20–30% over 6–12 months and improving urinary flow parameters.

Pharmacokinetics

Parameter	Value	Notes
Oral bioavailability	~63%	Not significantly affected by food
Time to peak plasma (Tmax)	1–2 hours	After single oral dose
Protein binding	~90%	Primarily albumin and alpha-1-acid glycoprotein
Volume of distribution (Vd)	76 L	Distributes into prostatic tissue
Metabolism	Hepatic, CYP3A4	Two inactive metabolites; not CYP1A2, 2D6, or 2C9
Half-life	6–8 hours (young men); 8 hours (elderly)	Steady state in ~5 days
Elimination	57% feces (metabolites), 39% urine (metabolites)	Less than 0.1% as unchanged drug in urine

Finasteride achieves steady-state plasma concentrations within approximately 5 days of daily dosing. At the standard 1 mg/day dose for AGA, mean steady-state plasma concentrations are approximately 9.2 ng/mL. The drug crosses the blood-brain barrier to some extent; semen concentrations are detectable but extremely low (less than 1% of a 1 mg dose in ejaculate) and not considered sufficient to affect a fetus in the partner.

Elderly patients: In men over 70, finasteride’s half-life extends to approximately 8 hours, but no dose adjustment is required for age alone.

Renal impairment: In patients with chronic renal failure (creatinine clearance 9–55 mL/min), pharmacokinetics are not significantly altered. No dose adjustment is needed for renal impairment.

Hepatic impairment: Finasteride is metabolized by the liver. In patients with hepatic dysfunction, finasteride exposure may be increased. Finasteride is not recommended in patients with liver disease or abnormal liver function tests, as clinical data in this population are insufficient.

Approved Indications

Male Pattern Hair Loss (Androgenetic Alopecia)

Finasteride 1 mg daily (Propecia) is FDA-approved for the treatment of male androgenetic alopecia in adult men only. AGA is a hereditary, androgen-dependent progressive miniaturization of scalp hair follicles. It affects an estimated 50% of men by age 50 and up to 70% by age 70, following characteristic patterns (Norwood–Hamilton scale, Types I–VII).

The approved indication specifies:

• Adult men (18 years or older)
• Hair loss at the vertex (crown) or anterior mid-scalp region
• Norwood–Hamilton Type II to Type V AGA patterns

Finasteride is not approved for use in women (not approved for female AGA in the US, and contraindicated in pregnant women).

Benign Prostatic Hyperplasia (BPH)

Finasteride 5 mg daily (Proscar) is FDA-approved for the treatment of symptomatic BPH in adult men with an enlarged prostate, to:

• Improve symptoms and reduce the risk of acute urinary retention
• Reduce the risk of surgery related to BPH

Clinical benefit is most pronounced in men with prostate volumes of 40 mL or greater. For smaller prostates, clinical guidelines (AUA 2021) suggest that alpha-blockers alone may be preferred as initial therapy.

Clinical Evidence: Male Pattern Hair Loss

The pivotal clinical program supporting finasteride’s 1997 AGA approval comprised two large, 1-year randomized, double-blind, placebo-controlled trials (Study 1: n=1,553; Study 2: n=1,215) and a 5-year extension study.

Primary 1-Year Trials (Kaufman et al., 1998)

Hair count method (standardized 1-inch diameter scalp disk photographic technique):

Endpoint	Finasteride 1 mg	Placebo
Hair count change at 1 year (vertex)	+7.1 hairs/cm²	−10.6 hairs/cm²
Improvement in hair growth (investigator-assessed)	48%	7%
No further hair loss (stabilized)	83%	28%
Hair loss continued (worsened)	17%	72%

5-Year Extension Study (Kaufman et al., 1999; Whiting et al., 2003)

In the 5-year extension study (n=279 completers in the finasteride arm):

• Mean hair count remained above baseline throughout 5 years in the finasteride group
• In the placebo group, hair count continued to decline, resulting in a mean difference of 277 hairs/cm² (in a 1-inch disk) between groups at 5 years
• 65% of finasteride-treated men showed scalp hair growth greater than baseline at 5 years vs. 7% in the placebo group
• Men who switched from placebo to finasteride at year 1 recovered hair count, but never fully caught up to men who had been on finasteride for 5 years — underlining the value of early treatment

Long-Term Real-World Data

An open-label 10-year prospective study (Rossi et al., 2011; n=118) found that 99.1% of men maintained or increased their hair count over 10 years of continuous finasteride 1 mg therapy, with no significant change in efficacy profile. A 2012 Japanese study (Yanagisawa et al.) of 801 men over 10 years reported that 91.5% of patients showed hair growth improvement with continuous finasteride use.

Clinical Evidence: BPH

PLESS Trial (McConnell et al., 1998)

The Proscar Long-term Efficacy and Safety Study was a 4-year, randomized, double-blind, placebo-controlled multicenter trial (n=3,040 men with symptomatic BPH and prostate volume ≥40 mL). Key outcomes at 4 years:

Outcome	Finasteride 5 mg	Placebo	Risk Reduction
Acute urinary retention	3.0%	6.6%	57% reduction
BPH-related surgery	4.2%	8.9%	55% reduction
Prostate volume change	−20% (−18 mL)	+14% (+14 mL)	34 mL absolute difference
Maximum urinary flow (Qmax)	+1.9 mL/s	+0.2 mL/s	Net gain 1.7 mL/s

MTOPS Trial (McConnell et al., 2003)

The Medical Therapy of Prostatic Symptoms trial (n=3,047) compared finasteride 5 mg, doxazosin 8 mg, combination therapy, and placebo over 4–6 years. Combination finasteride + doxazosin was superior to either monotherapy alone in reducing the risk of overall clinical BPH progression (66% risk reduction vs. placebo, compared to 39% for doxazosin alone and 34% for finasteride alone). Combination therapy also provided the greatest reduction in AUA symptom score improvement.

Dosage and Administration

Indication	Recommended Dose	Formulation	Frequency
Male AGA (hair loss)	1 mg	Film-coated tablet	Once daily
BPH	5 mg	Film-coated tablet	Once daily

Administration: Tablets may be taken with or without food. There is no evidence that taking finasteride with food affects its efficacy or bioavailability. The tablet should be swallowed whole and not chewed, crushed, or divided by female patients (see teratogenicity section).

Time to effect:

• AGA: Minimum 3 months before any assessment is meaningful; most clinical improvement occurs between months 6–12. If no benefit after 12 months of continuous treatment, further benefit is unlikely.
• BPH: At least 6 months of treatment before assessing whether finasteride has produced a satisfactory response.

Missed dose: Take the missed dose as soon as remembered. If it is nearly time for the next scheduled dose, skip the missed dose. Do not take an extra dose to compensate. There is no evidence that occasional missed doses reduce long-term efficacy.

Stopping treatment: Discontinuing finasteride leads to reversal of benefit in both AGA and BPH within 6–12 months, as DHT levels return to pre-treatment concentrations.

Side Effects and Safety

Sexual Side Effects

The most frequently reported adverse effects of finasteride are sexual in nature. The following table presents data from the pivotal 1-year and 4-year Propecia and Proscar trials:

Adverse Effect	Propecia 1 mg (AGA)	Placebo	Proscar 5 mg (BPH)	Placebo
Decreased libido	1.8%	1.3%	3.7%	2.1%
Erectile dysfunction	1.3%	0.7%	8.1%	3.7%
Ejaculation disorder	0.8%	0.4%	7.7%	2.1%
Gynecomastia	0.4%	0.2%	Not reported separately	—

In most men who experience sexual side effects in clinical trials, effects resolved on discontinuation of treatment. However, the 2012 label update acknowledged reports of persistence (see below).

Post-Finasteride Syndrome (PFS)

Post-Finasteride Syndrome (PFS) is a term used to describe a constellation of reported persistent side effects — primarily sexual (erectile dysfunction, loss of libido, ejaculatory dysfunction), but also neuropsychological (depression, cognitive impairment, emotional blunting) and physical (genital numbness, gynecomastia) — that some men report experiencing after stopping finasteride.

What the evidence shows:

• The FDA updated the Propecia and Proscar labels in 2012 to include a warning that sexual side effects may persist after discontinuation
• The frequency of persistent PFS-type symptoms remains uncertain; most large clinical trials were not designed to capture post-discontinuation persistence
• Several case series (Traish et al., 2015; Ganzer et al., 2015) and a registry study (Khera et al., 2021) document persistent symptoms; methodological limitations (recall bias, lack of pre-treatment baselines) affect interpretation
• Proposed biological mechanisms include persistent epigenetic changes affecting androgen receptor signaling, neurosteroid disruption, and altered GABAergic function in the brain — none definitively proven as of 2026
• The PFS Foundation (pfsfoundation.org) supports ongoing research and patient advocacy

Read our complete Post-Finasteride Syndrome evidence review

PSA Effects and Prostate Cancer Monitoring

Finasteride reduces serum PSA (prostate-specific antigen) concentrations by approximately 50% in men treated for BPH. This effect occurs regardless of the indication for treatment.

For PSA interpretation in men on finasteride:

• The PSA value should be doubled to estimate the “expected” PSA in the absence of finasteride treatment
• Any confirmed increase in PSA while on finasteride — even if within the normal range — should be evaluated for possible underlying prostate cancer
• PSA velocity (rate of change) remains a useful monitoring parameter and is not affected by finasteride adjustment

Teratogenicity (Pregnancy Category X)

Animal studies at finasteride doses as low as 0.03 mg/kg/day in pregnant rats caused dose-dependent reduction in prostatic and seminal vesicular weight and feminization of external genitalia in male offspring. This is expected based on the mechanism of action (DHT is required for normal male genital development in utero).

Regarding semen: Finasteride concentrations in ejaculate of men on finasteride 1 mg daily are extremely low (median 0.26 ng/mL, maximum 1.52 ng/mL). Assuming 5 mL of ejaculate absorbed transvaginally, the maximum estimated fetal dose would be 7.6 ng/day — roughly 750 times lower than the lowest dose causing fetal effects in animal studies. However, given the absolute contraindication in pregnancy, physicians commonly advise patients to inform partners about finasteride use.

Drug Interactions

Finasteride has a relatively benign drug-drug interaction profile. It is metabolized by CYP3A4 but does not inhibit or induce CYP enzymes at therapeutic concentrations. Major pharmacokinetic interactions are uncommon. Key considerations:

Drug / Drug Class	Interaction	Clinical Significance
CYP3A4 strong inhibitors (e.g., ketoconazole, itraconazole, ritonavir)	May increase finasteride plasma levels	Low significance; no dose adjustment typically required
CYP3A4 inducers (e.g., rifampicin, carbamazepine)	May decrease finasteride plasma levels	Unclear clinical relevance; monitor therapeutic effect
Dutasteride	Additive 5-ARI effect (combined Type I and II inhibition)	Not a standard combination; limited clinical data
Warfarin	No clinically significant pharmacokinetic interaction in studies	Minimal concern
Digoxin	No clinically significant pharmacokinetic interaction	Minimal concern

Always inform your prescribing physician of all current medications, including over-the-counter drugs, herbal supplements (particularly saw palmetto, which has mild 5-ARI activity), and vitamins.

Contraindications and Special Populations

Contraindications:

• Pregnancy (Pregnancy Category X; absolute contraindication)
• Hypersensitivity to finasteride or any excipient in the formulation
• Pediatric patients (not evaluated; not indicated)

Elderly patients (≥70 years): Half-life is slightly extended (to ~8 hours), but no dose adjustment is required. Efficacy and safety data are available from BPH trials including large numbers of elderly patients.

Hepatic impairment: Finasteride is hepatically metabolized. No dose adjustment guidance exists for mild impairment; use with caution and consider avoidance in patients with clinically significant liver disease, as finasteride exposure may be markedly increased.

Renal impairment: No dose adjustment required. Pharmacokinetics not significantly altered even in severe renal failure.

Women (postmenopausal use, off-label): Postmenopausal women are sometimes prescribed finasteride off-label for AGA (see Off-Label Uses). The teratogenicity concern is irrelevant in postmenopausal women who cannot become pregnant, but safety data are more limited than in men, and this use is not FDA-approved.

Finasteride vs. Dutasteride

Dutasteride (Avodart, GlaxoSmithKline) is the only other approved 5ARI. Key differences:

	Finasteride	Dutasteride
5-AR isoenzymes inhibited	Type II only	Type I + Type II (dual inhibitor)
DHT suppression (serum)	~70%	~90%
DHT suppression (scalp)	~64%	~51% Type I + ~79% combined (approximated)
FDA-approved for AGA	Yes (1997)	No (not approved in the US for AGA)
FDA-approved for BPH	Yes	Yes
Half-life	6–8 hours	~5 weeks
Time to steady state	~5 days	~6 months
Generic available?	Yes	Yes
Pregnancy caution	Category X	Category X (higher exposure risk due to long half-life)

Several head-to-head trials (Olsen et al., 2006; Stough et al., 2006) have compared finasteride and dutasteride for AGA. Results are mixed: some studies show marginal superiority of dutasteride for hair density, while others show comparable efficacy. The clinical significance is modest, and finasteride remains the preferred first-line option for AGA due to its established safety record, longer approved use history, and FDA indication.

Full comparison: Finasteride vs. dutasteride for hair loss and BPH

Brand Names, Generics, and Global Availability

Finasteride is available under several brand names globally and as generic finasteride from multiple manufacturers:

Brand Name	Strength	Indication	Originator
Propecia	1 mg	Male AGA	Merck & Co. (US), Merck MSD (elsewhere)
Proscar	5 mg	BPH	Merck & Co. (US), Merck MSD (elsewhere)
Finpecia	1 mg	AGA (non-US)	Cipla (India)
Appecia	1 mg	AGA (non-US)	Dr. Reddy’s
Generic finasteride 1 mg	1 mg	AGA	Multiple manufacturers (Aurobindo, Dr. Reddy’s, Apotex, etc.)
Generic finasteride 5 mg	5 mg	BPH	Multiple manufacturers

Finasteride is available by prescription in all major markets. Its regulatory status:

• United States: Prescription only; not a controlled substance; finasteride 1 mg (AGA) and 5 mg (BPH) FDA-approved
• United Kingdom (NHS): Available on NHS prescription for BPH; Propecia (1 mg) for AGA is available by private prescription; NHS does not routinely fund hair loss treatment
• European Union: EMA-approved; available by prescription in all EU member states
• India: Available by prescription; widely sold as generic finasteride at significantly lower cost than Western markets
• Canada: Health Canada approved; available by prescription

Off-Label Uses

Several uses of finasteride are not FDA-approved but have evidence supporting consideration under physician guidance:

Off-Label Use	Evidence Level	Key Considerations
Female androgenetic alopecia (postmenopausal)	Moderate (RCTs; inconsistent results)	Not approved; teratogenicity not a concern in postmenopausal women; benefit vs. spironolactone unclear
Topical finasteride (compounded)	Growing (several Phase II/III RCTs)	Not an FDA-approved topical formulation; compounded by specialty pharmacies; aims to minimize systemic DHT suppression
Hirsutism (excess hair in women)	Limited (small trials)	Spironolactone is generally preferred; finasteride is not first-line
Prostate cancer prevention	Strong (PCPT; see above)	Not an FDA-approved indication; standard of care guidelines do not recommend routine chemoprevention with finasteride
Female-to-male gender-affirming therapy	Expert consensus; limited RCT data	Used in some protocols as DHT-blocker; not a standard component of WPATH guidelines

Off-label use of any medication should occur only under the supervision of a licensed prescribing physician who has assessed the individual patient’s risks and benefits.

Regulatory History and Label Changes

• 1992: FDA approves Proscar (5 mg) for symptomatic BPH
• 1997: FDA approves Propecia (1 mg) for male androgenetic alopecia
• 2011: FDA updates both Propecia and Proscar labels to add information about male breast cancer (cases reported post-marketing, causal relationship not established) and to revise information on prostate cancer risk following PCPT analysis
• 2012: FDA updates labels to add that reports exist of sexual adverse events persisting after discontinuation, including decreased libido, erectile dysfunction, and ejaculation disorders; this information is added to the “Adverse Reactions” section
• 2019: EMA (European Medicines Agency) updates finasteride information to strengthen warnings on sexual side effects, depression, and suicidal ideation following postmarketing reports

Frequently Asked Questions

Is finasteride safe for long-term use?

Clinical trial data and long-term observational studies (up to 10+ years) support the safety of continuous finasteride use in the majority of men, with no evidence of cumulative toxicity or increased cancer risk beyond what is discussed above. The most common side effects (sexual function) occur early in treatment and resolve in most men who experience them. Men with known hepatic impairment or hypersensitivity should not use finasteride.

Does finasteride affect testosterone levels?

Finasteride does not meaningfully reduce testosterone levels. By blocking the conversion of testosterone to DHT, it may cause a minor compensatory increase in circulating testosterone (typically within the normal range), but it does not reduce testosterone below normal. Finasteride also does not affect the conversion of testosterone to estradiol (aromatase pathway), so estrogen levels are not directly altered.

Can finasteride affect fertility or sperm?

Case reports document reversible reductions in semen parameters (volume, sperm count, motility, morphology) in some men taking finasteride, particularly at the 5 mg dose. In most published series, these changes resolved after stopping finasteride. Men planning to conceive should discuss finasteride use with their physician. Finasteride is not considered a reliable contraceptive method.

Can I drink alcohol while taking finasteride?

There is no known clinically significant pharmacokinetic or pharmacodynamic interaction between finasteride and moderate alcohol consumption. Alcohol is not listed as a contraindication or precaution in the finasteride prescribing information. Heavy, chronic alcohol use may affect hepatic function and thus finasteride metabolism; discuss with your physician if you have concerns about alcohol use.

Is topical finasteride as effective as oral?

Topical finasteride is not an FDA-approved formulation; it is compounded by specialty pharmacies and prescribed off-label. Phase II and Phase III trials (Mazzarella et al., 1997; Dhurat et al., 2020; Caserini et al., 2016) have shown efficacy comparable to or slightly lower than oral finasteride 1 mg for AGA, with significantly less systemic DHT suppression (scalp DHT reduced comparably, but serum DHT reduced by only 5–25% vs. ~70% with oral). This is considered advantageous for men concerned about systemic side effects. Topical finasteride remains an evolving area of research with no FDA approval as of 2026.

What is the difference between Propecia and generic finasteride?

Generic finasteride 1 mg is therapeutically equivalent to Propecia (the innovator brand). Generic formulations must demonstrate bioequivalence to the reference listed drug in FDA’s approval process, meaning they deliver the same amount of active drug to the bloodstream within acceptable pharmacokinetic limits. The difference is cost: generic finasteride 1 mg typically costs $15–$35/month, compared to $70–$100+ for brand-name Propecia. Both are manufactured to FDA current Good Manufacturing Practice (cGMP) standards.

Will my hair loss come back if I stop finasteride?

Yes. Finasteride suppresses DHT only while taken. When discontinued, DHT returns to pre-treatment levels within weeks, and hair follicles re-enter the miniaturization process. Hair loss typically returns to approximately where it would have been without treatment within 6–12 months of stopping finasteride. Any regrowth achieved during treatment is gradually lost. There is no evidence of a “rebound” acceleration of hair loss beyond the expected baseline rate.

Does finasteride work better for some people than others?

Yes. Several factors are associated with better response to finasteride: starting treatment earlier in the course of AGA (before extensive miniaturization), younger age, vertex/crown hair loss (as opposed to frontal hairline), and higher baseline hair density. Genetic factors likely play a role, but no validated pharmacogenomic test is yet in routine clinical use to predict individual response. Non-response or poor response affects a meaningful minority of men; combination with minoxidil often produces better outcomes than either agent alone in these cases.

Sources and References

• Imperato-McGinley J, et al. “Steroid 5alpha-reductase deficiency in man: an inherited form of male pseudohermaphroditism.” Science. 1974;186(4170):1213–1215.
• Merck & Co. Propecia (finasteride 1 mg) US Prescribing Information. Revised 2022.
• Merck & Co. Proscar (finasteride 5 mg) US Prescribing Information. Revised 2022.
• Dallob AL, et al. “The effect of finasteride, a 5 alpha-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations.” J Clin Endocrinol Metab. 1994;79(3):703–706.
• Kaufman KD, et al. “Finasteride in the treatment of men with androgenetic alopecia.” J Am Acad Dermatol. 1998;39(4):578–589.
• Kaufman KD, et al. “Long-term (5-year) multinational experience with finasteride 1 mg in the treatment of men with androgenetic alopecia.” Eur J Dermatol. 2002;12(1):38–49.
• McConnell JD, et al. “The effect of finasteride on the risk of acute urinary retention.” N Engl J Med. 1998;338(9):557–563. (PLESS)
• McConnell JD, et al. “The long-term effect of doxazosin, finasteride, and combination therapy.” N Engl J Med. 2003;349(25):2387–2398. (MTOPS)
• Thompson IM, et al. “The influence of finasteride on the development of prostate cancer.” N Engl J Med. 2003;349(3):215–224. (PCPT)
• Lucia MS, et al. “Finasteride and high-grade prostate cancer in the Prostate Cancer Prevention Trial.” J Natl Cancer Inst. 2007;99(18):1375–1383.
• Rossi A, et al. “Finasteride, 1 mg daily administration on male androgenetic alopecia in different age groups: 10-year follow-up.” Dermatol Ther. 2011;24(4):455–461.
• Traish AM, et al. “Adverse side effects of 5α-reductase inhibitors therapy: persistent diminished libido and erectile dysfunction and depression in a subset of patients.” J Sex Med. 2011;8(3):872–884.
• U.S. FDA. Drug Safety Communication: 5-alpha reductase inhibitors (5-ARIs) may increase the risk of a more serious form of prostate cancer. June 9, 2011.
• U.S. FDA. Drug Safety Communication: Update — 5-alpha reductase inhibitors: FDA adds labeling changes regarding risk of persistent sexual side effects. April 11, 2012.
• Badri T, Nessel TA, Kumar D. “Finasteride.” StatPearls. Treasure Island (FL): StatPearls Publishing; 2024.