Finasteride is a specific inhibitor of steroid 5α-reductase, an intracellular enzyme necessary for conversion of testosterone to 5α-dihydrotestosterone (DHT).1,2,3,5,6,7,8,9,10,11,12,13
Finasteride is used as monotherapy for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to improve symptoms (e.g., urinary hesitancy and/or urgency, nocturia), reduce the risk of acute urinary retention, and reduce the risk for surgery (including transurethral resection of the prostate [TURP] and prostatectomy).1,8,15,16,17,19
Finasteride is not indicated for use in female patients or pediatric patients.1 Finasteride is not approved for the prevention of prostate cancer.1
Results of a long-term (4-year) controlled clinical study in patients with moderate to severe symptoms of BPH indicate that finasteride (5 mg daily) reduces symptoms of BPH, reduces prostatic size, increases urinary flow rate, and reduces the risk of acute urinary retention and the need for surgery.1,19 In this study, treatment with finasteride or placebo for 4 years reduced symptom scores by a mean of 3.3 or 1.3 points, respectively, from an average baseline score of 15 (as measured on a scale of 0-34, with the total score equal to the sum of the scores for 7 measures of obstructive or irritative symptoms).1,19 A difference in symptom scores between treatment groups was evident within the first year of treatment and continued throughout the 4-year study.1,19 In general, at least 6 months of therapy was required to determine whether a beneficial reduction in symptoms had been achieved, although some patients experienced earlier improvement.1,19 Prostatic volume decreased during the first year of the study in patients receiving finasteride and then remained stable during the subsequent 2-4 years, whereas values in the placebo group increased steadily over the 4 years of the study.1,19 Acute urinary retention requiring catheterization of the bladder occurred in 2.8 or 6.6% of patients receiving finasteride or placebo, respectively; 4.6 or 10.1% of patients receiving finasteride or placebo, respectively, underwent surgery for BPH.1,19
Results of a meta-analysis of 1 year of data from 7 similarly designed controlled studies indicate that improvements in symptoms and maximum urinary flow rates associated with finasteride therapy are greater in patients with prostatic enlargement at baseline.1
Finasteride therapy in BPH appears to be suppressive rather than curative, and eventual return of the hyperplasia likely will occur if the drug is withdrawn.1,5
Finasteride may be used concomitantly with an α1-adrenergic blocking agent (e.g., doxazosin) to decrease the risk of symptomatic progression of BPH (i.e., an increase from baseline of at least 4 on the American Urological Association [AUA] symptom score).1,20,25 Although studies of up to 1 year in duration generally have found combination therapy with a 5α-reductase inhibitor (e.g., finasteride) and an α1-adrenergic blocker to be no more effective than α1-adrenergic blocker monotherapy in providing symptomatic relief of BPH, a long-term (mean follow-up: 4.5 years), double-blind study (Medical Therapy of Prostatic Symptoms [MTOPS]) found that combined therapy with finasteride (5 mg daily) and doxazosin (4-8 mg daily) was more effective than therapy with either drug alone in preventing symptom progression (defined as an increase from baseline of at least 4 points in the AUA symptom score, acute urinary retention, urinary incontinence, renal insufficiency, or recurrent urinary tract infection).1,20,25 The percent reduction in the risk of symptom progression (generally manifested as an increase in AUA symptom score) relative to placebo was 34% with finasteride, 39% with doxazosin, and 67% with combination therapy.1,20,25 The risks of long-term acute urinary retention and the need for invasive therapy were reduced by combination therapy and by finasteride monotherapy but not by doxazosin monotherapy.1,20,25 Combination therapy or doxazosin or finasteride monotherapy each were effective in providing improvement in symptom scores, with combination therapy providing greater improvement than either drug alone.1,20,25 Adverse effects associated with combined 5α-reductase inhibitor and α1-adrenergic blocker therapy generally reflect the combined toxicity profile of each drug alone, although certain adverse effects (e.g., effects on sexual function and libido, postural hypotension, peripheral edema, dizziness, asthenia, rhinitis) may be more common with combined therapy.1,20,25
Finasteride also may be used in combination with tadalafil, a phosphodiesterase (PDE) type 5 inhibitor, for the treatment of signs and symptoms of BPH.32,33 A fixed combination preparation (finasteride/tadalafil; Entadfi®) is commercially available for the initial treatment of signs and symptoms of BPH in men with an enlarged prostate for up to 26 weeks; the incremental benefit of tadalafil beyond 26 weeks is unknown.32 Efficacy and safety of finasteride/tadalafil for the symptomatic management of BPH are based on the results of a 26-week, double-blind, placebo-controlled study of tadalafil coadministered with finasteride in men with BPH.32 Patients ≥45 years of age with International Prostate Symptom Score (IPSS) ≥13 and prostate volume ≥30 mL who did not previously receive treatment with an 5α-reductase inhibitor were randomized to tadalafil 5 mg plus finasteride 5 mg or placebo plus finasteride 5 mg.32 Treatment with tadalafil plus finasteride resulted in a statistically significant improvement in the signs and symptoms of BPH as measured by the total symptom score (IPSS) at 12 weeks (the primary study endpoint) compared with finasteride plus placebo.32 However, the magnitude of treatment difference between placebo/finasteride and tadalafil/finasteride decreased from 1.7 points at week 4 to 1 point at week 26; the incremental benefit of combination therapy beyond 26 weeks is unknown.32 The combinaton therapy improved erectile function in patients in the study who had comorbid erectile dysfunction.32,33
Interventions for BPH include behavioral/lifestyle modifications, pharmacologic therapy, and/or surgical options.25 An assessment of prostate size and shape is recommended prior to initiating therapy to guide the most appropriate course of treatment.25 Pharmacologic options for the treatment of lower urinary tract symptoms of BPH include α1-adrenergic blockers, 5α-reductase inhibitors, PDE type 5 inhibitors, and anticholinergic agents.25
The American Urological Association (AUA) has published guidelines on the management of lower urinary tract symptoms in patients with BPH.25 The guideline considers 5α-reductase inhibitor monotherapy to be an appropriate option for the symptomatic treatment of lower urinary tract symptoms in patients with BPH who have evidence of prostatic enlargement (prostate volume >30 g on imaging, a prostate specific antigen [PSA] >1.5 ng/dL, or palpable prostate enlargement on digital rectal exam).25 Patients with larger prostate glands appear to benefit the most from treatment with 5α-reductase inhibitors.25 A 5α-reductase inhibitor, alone or in combination with an α1-adrenergic blocker, is recommended as a treatment option to prevent progression of lower urinary tract symptoms and/or reduce the risks of urinary retention and need for future prostate-related surgery in patients with demonstrable prostatic enlargement.25,25 Because of the slow onset of action of 5α-reductase inhibitors, other drug classes such as α1-blockers may provide more immediate relief of symptoms.25
The AUA guidelines state that clinicians may offer the combination of low-dose daily tadalafil 5 mg with finasteride for the treatment of lower urinary tract symptoms of BPH; however, there is a lack of long-term data with this combination and such combination therapy is thought to offer little to no advantages in symptom improvement over finasteride alone in the short term.25
In a study comparing finasteride to dutasteride for the treatment of BPH, no differences were observed between the drugs in regards to prostate volume, lower urinary tract symptoms, and obstruction.25
Dispensing and Administration Precautions
Finasteride is administered orally without regard to meals.1 The fixed combination of finasteride/tadalafil is administered orally on an empty stomach.32
The recommended adult dosage of finasteride, administered alone or in combination with an α1-adrenergic blocking agent (e.g., doxazosin), is 5 mg once daily without regard to meals.1 While early symptomatic improvement may occur, 6 months or more of therapy with finasteride may be necessary to determine clinical benefit.1
The usual adult dosage of the fixed-combination preparation of finasteride/tadalafil is 5 mg of finasteride and 5 mg of tadalafil taken once daily on an empty stomach at approximately the same time every day for up to 26 weeks; use is not recommended for more than 26 weeks because the incremental benefit of tadalafil after this time period is not known.32
Use caution in patients with hepatic impairment; the manufacturer makes no specific dosage adjustment recommendations.1
Dosage adjustment is not necessary in patients with renal impairment.1
Dosage adjustment is not necessary in geriatric patients.1
Effects on Prostate Specific Antigen (PSA)
The possibility that finasteride could interfere with interpretation of serum PSA determinations should be considered.1,12 Serum concentrations of PSAa serine protease secreted exclusively by prostatic epithelial cellsmay be elevated in patients with BPH, prostate cancer, or other prostatic disease.4,12 Finasteride causes a decrease in serum PSA concentrations of approximately 50% in patients with BPH; decreases in PSA can occur even in those with prostate cancer.1 However, the effect of finasteride on serum PSA concentrations has not been demonstrated to provide clinical benefit in patients with prostate cancer and should not be interpreted as a therapeutic effect of the drug on the disease.1,12,15 The effect of finasteride on serum PSA concentrations is predictable over the entire range of PSA values, although there is evidence of interindividual variation.1 For clinical interpretation of PSA values in men who have been receiving finasteride for 6 months or longer, a new PSA baseline should be established.1 The reported PSA value should be doubled for comparison with normal values in men not receiving the drug.1 This adjustment will preserve the utility of the serum PSA assay and maintain its usefulness in the detection of prostate cancer.1 Finasteride does not substantially alter the ratio of free to total PSA (percentage of free PSA).1 If clinicians elect to use this ratio in the detection of prostate cancer, no adjustment of the reported value of the ratio appears to be necessary.1 Any confirmed increase in serum PSA concentration during finasteride therapy should be evaluated carefully, even if PSA values are within the normal range for men not receiving 5α-reductase inhibitor therapy.1,29 Noncompliance with finasteride may affect PSA concentrations and should be considered when evaluating test results.1
Increased Risk of High-grade Prostate Cancer with 5-Reductase Inhibitors
5α-reductase inhibitors may increase the risk of development of high-grade prostate cancer.1,29 The efficacy of finasteride for prevention of prostate cancer occurrence was evaluated in a 7-year placebo-controlled trial (Prostate Cancer Prevention Trial; PCPT) in men 55 years of age or older with baseline serum PSA concentrations of 3 ng/mL or less and normal digital rectal examinations.1,22,29,31 Although results showed that finasteride (5 mg daily) was associated with an overall reduction in prostate cancer occurrence (which reflected a reduction in lower-grade [Gleason score of 6 or less] tumors), high-grade tumors (Gleason score of 8-10) were detected more frequently in men receiving finasteride (1.8%) than in those receiving placebo (1.1%).1,22,29 Similar results were reported in a 4-year placebo-controlled trial (Reduction by Dutasteride of Prostate Cancer Events; REDUCE) evaluating preventive therapy with the 5α-reductase inhibitor dutasteride; in this trial, high-grade prostate cancer occurred in 1% of men receiving dutasteride compared with 0.5% of those receiving placebo, and the reduction in risk of prostate cancer was limited to tumors with a Gleason score of 6 or less.1,29 It is not known whether detection bias (e.g., 5α-reductase inhibitors potentially could increase the number of biopsy-detected tumors by reducing prostate volume, since this would result in a greater proportion of the prostate being sampled) or study-related factors influenced the results of these studies.1,30,31 Finasteride is not labeled by the FDA for prevention of prostate cancer.29
Finasteride is not indicated for use in women.1 Based on animal findings and the drug's mechanism of action, finasteride may cause abnormal development of external genitalia in a male fetus if administered to a pregnant female.1 (See Pregnancy under Cautions.) Women should not handle crushed or broken finasteride tablets if they are pregnant or potentially pregnant because of the possibility of absorption of finasteride and the riskto a male fetus.1 Finasteride tablets are coated and will prevent contact with the active ingredient during normal handling, provided the tablets have not been broken or crushed.1 If a pregnant woman comes in contact with crushed or broken finasteride tablets, the contact area should be washed immediately with soap and water.1
In healthy male volunteers who received finasteride for 24 weeks, no clinically meaningful effects on sperm parameters (e.g., concentration, mobility, morphology, or pH) were observed.1 Ejaculate volume decreased by a median of 22% with a concomitant reduction in total sperm per ejaculate.1 These parameters remained within the normal range and were reversible upon discontinuation of therapy with an average time to return to baseline of 84 weeks.1
Consideration of Other Urological Conditions
Prior to initiating treatment with finasteride, consideration should be given to other urological conditions that may cause similar symptoms.1 In addition, prostate cancer and BPH may coexist.1
Since not all patients exhibit a response to finasteride, patients with a large residual urinary volume and/or severely diminished urinary flow should be monitored carefully for obstructive uropathy; such patients may not be candidates for finasteride therapy.1
When finasteride is used in fixed combination with tadalafil, the usual cautions, precautions, and contraindications associated with tadalafil must be considered in addition to those associated with finasteride.32
Finasteride is not indicated for use in women and is contraindicated in women who are pregnant or may potentially be pregnant.1 Because of the ability of 5α-reductase inhibitors to inhibit the conversion of testosterone to DHT, finasteride may cause abnormalities of the external genitalia of male fetuses exposed to the drug during pregnancy.1 Studies have shown that low doses of finasteride administered to female rats during pregnancy can produce abnormalities of the external genitalia in male offspring.1 If finasteride is administered during pregnancy, the patient should be apprised of the potential fetal hazard.1 In addition, because of the possibility of drug absorption and subsequent risk to a male fetus, women who are pregnant or who potentially may be pregnant should not handle broken or crushed finasteride tablets; if such contact occurs, the affected area should be washed immediately with soap and water and the woman should inform her clinician.1 Intact finasteride tablets are coated, and the coating will prevent contact with finasteride during normal handling.1
Reproduction studies in pregnant rats receiving finasteride dosages ranging from 100 mcg/kg daily to 100 mg/kg daily (up to 86 times the maximum recommended human dosage [MRHD]) resulted in dose-dependent development of hypospadias in 3.6-100% of male offspring.1 Pregnant rats produced male offspring with decreased prostatic and seminal vesicular weights, delayed preputial separation, and transient nipple development when given dosages of 30 mcg/kg daily (0.03 times the MRHD) and decreased anogenital distance when given dosages of 3 mcg/kg daily (0.003 times the MRHD).1 The critical period during which these effects can be induced in male rats has been determined to be days 16-17 of gestation.1 These effects are expected pharmacologic effects of 5α-reductase inhibitors and are similar to those reported in male infants with a genetic deficiency of 5α-reductase.1 No abnormalities were observed in female offspring exposed to any finasteride dosage in utero.1
No developmental abnormalities were observed in first filial generation (F1) male or female offspring resulting from mating of male rats receiving finasteride 80 mg/kg daily (61 times the MRHD) with untreated females.1 Administration of the drug at a dosage of 3 mg/kg daily (30 times the MRHD) during the late gestation and lactation period resulted in slightly decreased fertility in F1 male offspring.1 No effects were seen in female offspring.1 No evidence of malformations was observed in rabbit fetuses exposed to finasteride in utero from days 6-18 of gestation at dosages up to 100 mg/kg daily; however, effects on male genitalia would not be expected as the exposure did not occur during the critical period of genital system development in rabbits.1
No abnormalities were observed in male fetuses when pregnant rhesus monkeys were given finasteride IV at dosages up to 800 ng daily (143 times the highest estimated exposure of a pregnant woman to finasteride via the semen of a sexual partner receiving finasteride 5 mg daily) during days 20-100 of gestation.1 However, external genital abnormalities were observed in male rhesus monkey fetuses in studies using an oral finasteride dosage of 2 mg/kg daily (18,000 times the highest estimated blood levels of finasteride from semen in men receiving 5 mg daily).1 No other abnormalities were observed in male fetuses, and no abnormalities were observed in female fetuses exposed to finasteride at any dosage in utero.1
It is not known whether finasteride is distributed into human milk, but the drug is not indicated for use in women.1
Females and Males of Reproductive Potential
In healthy male volunteers treated with finasteride for 24 weeks, there was no clinically meaningful effect on sperm concentration, mobility, morphology, or pH.1 A 0.6 mL (22.1%) median decrease in ejaculate volume with a concomitant reduction in total sperm per ejaculate was observed.1 These parameters remained within the normal range and were reversible upon discontinution, with an average time to return to baseline of 84 weeks.1 There have been postmarking reports of male infertility and/or poor seminal quality; normalization or improvement of seminal quality has been reported after discontinuation.1
Finasteride is not indicated for use in pediatric patients; safety and efficacy have not been established.1
Because BPH occurs mainly in men 55 years of age or older, efficacy and safety of finasteride in this age group have been established, although only limited data are available on use of the drug in men older than 80 years of age.8,15,17 Of the 3040 patients enrolled in a long-term (4 years) controlled clinical trial of the drug, 1480 (49%) were 65 years of age or older and 105 (3.5%) were 75 years of age or older.1 No overall differences in efficacy or safety were observed in this trial between geriatric and younger patients, and other clinical experience has revealed no evidence of age-related differences.1 Generally, finasteride is well tolerated in geriatric men.1,3,8,15,16,17
The elimination rate of finasteride is decreased in geriatric individuals; however, the findings are not clinically significant and dosage adjustment is not necessary.1 The mean terminal half-life of finasteride in individuals 70 years of age or older was approximately 8 hours (range: 6-15 hours) compared with 6 hours (range: 4-12 hours) in individuals 45-60 years of a consequently, the mean daily AUC after 17 days of dosing was 15% higher in individuals 70 years of age or older.1
The effect of hepatic impairment on finasteride pharmacokinetics has not been studied.1 Because finasteride is metabolized extensively in the liver, the drug should be used with caution in patients with hepatic impairment.1
The pharmacokinetics of finasteride following a single dose in patients with chronic renal impairment (i.e., creatinine clearance of 9-55 mL/minute) was similar to that observed in healthy individuals, although the proportion of the dose excreted as metabolites in feces versus urine was increased in those with renal impairment.1
The most common adverse effects of finasteride reported in ≥1% of patients in clinical studies include impotence, decreased libido, decreased volume of 1
Finasteride does not affect the cytochrome P-450 (CYP) enzyme system.1 No clinically meaningful drug interactions have been identified.1 Drugs that have been tested for drug interaction potential with finasteride include digoxin, propranolol, theophylline, and warfarin.1
Although specific drug interaction studies have not been performed, in clinical studies, finasteride was used concomitantly with acetaminophen, acetylsalicylic acid, α-blockers, analgesics, angiotensin-converting enzyme (ACE) inhibitors, anticonvulsants, benzodiazepines, beta-blockers, calcium-channel blockers, cardiac nitrates, diuretics, H2 antagonists, HMG-CoA reductase inhibitors, nonsteroidal anti-inflammatory agents, and quinolone anti-infectives without evidence of clinically significant adverse interactions.1
Finasteride is a synthetic 4-azasteroid compound.1,2,13 The drug is a specific inhibitor of steroid Type II 5α-reductase, an intracellular enzyme present in high concentrations in the liver, skin, and prostate gland.1,2,3,5,6,7,8,9,10,11,12,13 The conversion of testosterone to 5α-dihydrotestosterone (DHT) depends on the presence of this enzyme, and DHT appears to be the principal androgen responsible for stimulation of prostatic growth.1,2,13 1,2,3,5,6,7,8,9,10,11,12,13
Finasteride inhibits 5α-reductase by forming a stable enzyme complex; turnover from the complex is slow (half-life of about 30 days).1 Inhibition of 5α-reductase by finasteride, in a dose-dependent fashion, reduces serum and prostatic DHT concentrations substantially (by 70%), increases serum testosterone concentrations (by 10-20%, remaining within the physiologic range), and increases prostatic tissue testosterone concentrations (by up to 10 times over pretreatment levels).1,2,3,6,7,8,9,10,11,12,13,15 In healthy men receiving finasteride for 2 weeks, serum DHT concentrations returned to pretreatment levels approximately 2 weeks after discontinuance of the drug.1 In most patients with benign prostatic hypertrophy (BPH), prostatic volume decreases by an average of about 20-30% after 6-24 months of finasteride treatment and returns to baseline volume within several months after discontinuance of the drug; in one study of patients receiving finasteride for 3 months, prostatic volume declined by approximately 20% and returned to close to baseline value approximately 3 months following discontinuance of treatment.1,2,5,8,15,16,17 The drug also decreases serum and prostatic levels of prostate-specific antigen (PSA).1,12,15,16,17
The mean bioavailability of finasteride 5-mg tablets is 63%; bioavailability is not affected by food.1 Peak plasma concentrations of the drug are achieved in 1-2 hours following a dose.1 Approximately 90% of circulating finasteride is bound to plasma proteins.1 The drug has been shown to cross the blood brain barrier, but does not appear to distribute preferentially into the CSF.1 Finasteride is extensively metabolized in the liver, primary by cytochrome P-450 (CYP) 3A4.1 The mean elimination half-life of the drug in healthy individuals was 6 hours (range 3 to 16 hours).1 Following administration of an oral dose, approximately 39% of the dose is excreted in urine as metabolites and 57% is ecreted in feces.1
Additional Information
The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer's labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care.
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
---|---|---|---|---|
Oral | Tablets, film-coated | 5 mg* | Finasteride Tablets | |
Organon |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
---|---|---|---|---|
Oral | Capsules | 5 mg of finasteride with 5 mg of tadalafil | Entadfi® | Veru |
AHFS® Drug Information. © Copyright, 1959-2024, Selected Revisions June 10, 2024. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
Only references cited for selected revisions after 1984 are available electronically.
1. Organon. Proscar® (finasteride) tablets prescribing information. Jersey City, NJ; 2023 Nov.
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3. Gormley GJ, Stoner E. The role of 5α-reductase inhibitors in the treatment of benign prostatic hyperplasia. Probl Urol . 1991; 5:436-440..
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6. De Schepper PJ, Imperato-McGinley J, Van Hecken A et al. Hormonal effects, tolerability, and preliminary kinetics in men of MK-906, a 5 alpha-reductase inhibitor. Steroids . 1991; 56:469-71.. [PubMed 1666698]
7. McConnell JD, Wilson JD, George FW et al. Finasteride, an inhibitor of 5 alpha-reductase, suppresses prostatic dihydrotestosterone in men with benign prostatic hyperplasia. J Clin Endocrinol Metab . 1992; 74:505-8.. [PubMed 1371291]
8. The MK-906 (Finasteride) Study Group. One-year experience in the treatment of benign prostatic hyperplasia with finasteride. J Androl . 1991; 12:372-5.. [PubMed 1722792]
9. Vermeulen A, Giagulli VA, De Schepper P et al. Hormonal effects of a 5 alpha-reductase inhibitor (finasteride) on hormonal levels in normal men and in patients with benign prostatic hyperplasia. Eur Urol . 1991; 20(Suppl 1):82-6.. [PubMed 1722168]
10. Gormley GJ, Stoner E, Rittmaster RS et al. Effects of finasteride (MK-906), a 5 alpha-reductase inhibitor, on circulating androgens in male volunteers. J Clin Endocrinol Metab . 1990; 70:1136-41.. [PubMed 2156887]
11. Rittmaster RS, Stoner E, Thompson DL et al. Effect of MK-906, a specific 5 alpha-reductase inhibitor, on serum androgens and androgen conjugates in normal men. J Androl . 1989; 10:259-62. [PubMed 2550402]
12. Geller J. Effect of finasteride, a 5 alpha-reductase inhibitor on prostate tissue androgens and prostate-specific antigen. J Clin Endocrinol Metab . 1990; 71:1552-5.. [PubMed 1699965]
13. Vermeulen A, Giagulli VA, De Schepper P et al. Hormonal effects of an orally active 4-azasteroid inhibitor of 5 alpha-reductase in humans. Prostate . 1989; 14:45-53.. [PubMed 2538808]
14. Chapple C. Medical treatment for benign prostatic hyperplasia. BMJ . 1992; 304:1198-9.. [PubMed 1381250]
15. Gormley GJ, Stoner E, Bruskewitz RC et al. The effect of finasteride in men with benign prostatic hyperplasia. N Engl J Med . 1992; 327:1185-91. [PubMed 1383816]
16. Steiner JF. Finasteride: a 5α-reductase inhibitor. Clin Pharm . 1993; 12:15-23.. [PubMed 7679063]
17. Peters DH, Sorkin EM. Finasteride: a review of its potential in the treatment of benign prostatic hyperplasia. Drugs . 1993; 46:177-208.. [PubMed 7691505]
19. McConnell JD, Bruskewitz R, Walsh P et al. The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hyperplasia. N Engl J Med . 1998; 338:557-63.. [PubMed 9475762]
20. McConnell JD, Claus G, Roehrborn MD et al. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Engl J Med . 2003; 349:2387-98.. [PubMed 14681504]
22. Thompson IM, Goodman PJ, Tangen CM et al. The influence of finasteride on the development of prostate cancer. N Engl J Med . 2003; 349:215-24.. [PubMed 12824459]
24. Scardino PT. The prevention of prostate cancerthe dilemma continues. N Engl J Med . 2003; 349:297-9.. [PubMed 12824458]
25. Sandhu JS, Bixler BR, Dahm P, et al. Management of lower urinary tract symptoms attributed to benign prostatic hyperplasia (BPH): AUA Guideline amendment 2023. J Urol. 2023;10.1097/JU.0000000000003698. From the AUA website. [Web]
26. Vaughan ED. Medical management of benign prostatic hyperplasiaare two drugs better than one? N Engl J Med . 2003; 349:2440-51. Editorial.
27. de la Rossette JJ, Alivizatos G, Madersbacher S et al. EAU guidelines on benign prostatic hyperplasia (BPH). Eur Urol . 2001; 40:256-63.. [PubMed 11684840]
28. Agency for Health Care Policy and Research. Benign prostatic hyperplasia: diagnosis and treatment. J Am Geriatric Soc . 1998; 46:1163-5..
29. Food and Drug Administration. FDA drug safety communication: 5-alpha reductase inhibitors (5-ARIs) may increase the risk of a more serious form of prostate cancer. Rockville, MD; 2011 Jun 9. From FDA website. [Web]
30. Theoret MR, Ning YM, Zhang JJ et al. The risks and benefits of 5α-reductase inhibitors for prostate-cancer prevention. N Engl J Med . 2011; 365:97-9.. [PubMed 21675880]
31. Lucia MS, Epstein JI, Goodman PJ et al. Finasteride and high-grade prostate cancer in the Prostate Cancer Prevention Trial. J Natl Cancer Inst . 2007; 99:1375-83.. [PubMed 17848673]
32. Veru, Inc.. Entadfi® (finasteride and tadalafil) capsules prescribing information. Miami, Fl; 2021 Dec
33. Casabé A, Roehrborn CG, Da Pozzo LF et al. Efficacy and safety of the coadministration of tadalafil once daily with finasteride for 6 months in men with lower urinary tract symptoms and prostatic enlargement secondary to benign prostatic hyperplasia. J Urol. 2014; 191:727-33.