Finasteride

Class: 5-alpha-Reductase Inhibitors
VA Class: HS900
Chemical Name: (5α,17β)-N-(1,1-dimethylethyl)-3-oxo-4-azaandrost-1-ene-17-carboxamide
CAS Number: 98319-26-7
Brands: Propecia, Proscar

Special Alerts:

[Posted 06/09/2011] ISSUE: FDA notified healthcare professionals that the Warnings and Precautions section of the labels for the 5-alpha reductase inhibitor (5-ARI) class of drugs has been revised to include new safety information about the increased risk of being diagnosed with a more serious form of prostate cancer (high-grade prostate cancer).

BACKGROUND: The new safety information is based on FDA’s review of two large, randomized controlled trials––the Prostate Cancer Prevention Trial (PCPT) and the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial. Finasteride (Proscar), dutasteride (Avodart), and dutasteride in combination with tamsulosin (marketed combination product as Jalyn) are approved to improve symptoms of an enlarged prostate gland (benign prostatic hyperplasia or BPH). Proscar and Avodart are also approved to reduce the risk of urinary retention or surgery related to an enlarged prostate. Finasteride (Propecia) is approved to treat male pattern hair loss.

RECOMMENDATION: Prior to initiating therapy with 5-ARIs, perform appropriate evaluation to rule out other urological conditions, including prostate cancer, that might mimic benign prostatic hyperplasia (BPH). See Drug Safety Communication for a Data Summary and additional information. For more information visit the FDA website at: and .

Introduction

Specific inhibitor of steroid 5α-reductase; blocks conversion of testosterone by type 2 5α-reductase to 5α-dihydrotestosterone (DHT).^{1 2 3 5 6 7 8 9 10 11 12 13 d f g k l m n o}

Uses for Finasteride

Pending revision, the material in this section should be considered in light of more recently available information in the MedWatch notification at the beginning of this monograph.

Benign Prostatic Hypertrophy (BPH)

Treatment of symptomatic BPH to improve symptoms and reduce the risk of acute urinary retention and the need for surgery.^{1 8 15 16 17 19} Ineffective in patients who do not have evidence of prostatic enlargement.²⁵

Used alone or in combination with an α₁-adrenergic blocking agent (e.g., doxazosin).^{1 20 25} Combination therapy with a 5α-reductase inhibitor and an α₁-blocker has been more effective than therapy with either drug alone in preventing long-term BPH symptom progression.^{1 20 25} Men at risk for BPH progression are most likely to benefit from combination therapy.^{20 25}

Steroid 5α-reductase inhibitors may be a useful alternative to surgery in patients with obstructive manifestations who are awaiting or unwilling to undergo surgical correction of BPH; may aid those who are at increased risk from or are not candidates for prostate surgery.^{3 14 25} Also may be considered in patients who have symptomatic prostatic enlargement but whose symptoms are not bothersome (i.e., do not interfere with activities of daily living) in order to prevent progression of the disease.²⁵

Although drug therapy usually is not as effective as surgical therapy, it may provide adequate symptomatic relief with fewer and less serious adverse effects compared with surgery.²⁵

Androgenetic Alopecia

Stimulates regrowth of hair in men with mild to moderate androgenetic alopecia (male pattern alopecia, hereditary alopecia, common male baldness).^{d f}

Effective in promoting hair regrowth in young and middle-aged men (18–41 years of age) with mild to moderate androgenetic alopecia and hair loss on the vertex of the scalp and/or anterior mid-scalp area; the effects on bitemporal recession are not established.^d

Recommended only for use in men;^d not indicated for use in women or children.^d Ineffective for treatment of hair loss in postmenopausal women with androgenetic alopecia.^d

Withdrawal of the drug leads to reversal of clinical benefit within 1 year.^d Therapy must be continued to sustain initial regrowth and subsequent slowing of hair loss.^d Maximum improvement in hair count occurs during first 2 years of therapy.^d

Finasteride Dosage and Administration

Administration

Administer orally without regard to meals.^{1 d}

Dosage

Pending revision, the material in this section should be considered in light of more recently available information in the MedWatch notification at the beginning of this monograph.

Adults

BPH

Oral

5 mg once daily, alone or in combination with doxazosin mesylate.¹

While early symptomatic improvement may occur, ≥6 months of therapy may be necessary to determine clinical benefit.^{1 21}

Androgenetic Alopecia

Oral

1 mg once daily.^d

Generally administered for ≥3 months before benefit is observed.^{f d} If improvement does not occur within 1 year, further treatment with the drug is unlikely to provide benefit.^r

Continued use recommended to sustain benefit, which should be re-evaluated periodically.^d

Discontinuance leads to reversal of effect within 12 months.^d

Special Populations

Hepatic Impairment

No specific dosage recommendations for hepatic impairment.^{1 d} (See Hepatic Impairment under Cautions.)

Renal Impairment

Dosage adjustment not required.^{1 d}

Geriatric Patients

Dosage adjustment not required.^{1 d}

Cautions for Finasteride

Contraindications

• 
  

  Known or suspected pregnancy.^{1 d} (See Fetal/Neonatal Morbidity and also Pregnancy under Warnings/Precautions.)

  
  


• 
  

  Known hypersensitivity to finasteride or any ingredient in the formulation.^{1 d}

  
  

Warnings/Precautions

Warnings

Fetal/Neonatal Morbidity

May cause fetal harm; teratogenicity demonstrated in animals.¹

Animal studies indicate adverse effects on embryofetal development of male fetuses exposed to the drug during pregnancy (e.g., abnormalities of the external genitalia, decreased prostatic and seminal vesicular weights, delayed preputial separation, and transient nipple development).¹

No abnormalities were observed in female offspring exposed to any finasteride dosage in utero.¹

Because of the potential for absorption through the skin and the subsequent potential risk to a male fetus, pregnant women or women who potentially may be pregnant should avoid direct contact with broken (e.g., crushed) tablets of the drug.^{1 21 d}

If used during pregnancy or if pregnancy occurs, apprise the pregnant woman of potential fetal hazard to the male fetus.¹

General Precautions

Patient Assessment

Evaluate candidates for finasteride therapy for other urologic conditions that might mimic BPH, such as infection, prostate cancer, stricture disease, hypotonic bladder, other neurogenic disorders.¹

Perform digital rectal examinations, as well as other screening tests for prostate cancer before initiating therapy for BPH and periodically thereafter.^{27 28}

Monitor patients with a large residual urinary volume and/or severely diminished urinary flow carefully for obstructive uropathy.¹ Such patients may not be candidates for finasteride therapy.¹

Prostate Cancer

Pending revision, the material in this section should be considered in light of more recently available information in the MedWatch notification at the beginning of this monograph.

No clinical benefit has been demonstrated in patients with prostate cancer.^{1 12 15}

No effect on rate of prostate cancer detection in clinical studies in patients with BPH and elevated serum PSA concentrations.¹

Prostate-specific Antigen (PSA)

Decreases PSA concentrations; may interfere with interpretation of serum PSA determinations.^{1 12 d} (See Specific Drugs and Laboratory Tests under Interactions.)

Carefully evaluate sustained increases in serum PSA concentration during finasteride therapy, including consideration that the patient is not compliant.¹

Breast Changes

Breast enlargement and tenderness reported in men receiving finasteride 5 mg daily for BPH or 1 mg daily for androgenetic alopecia.^{1 d}

Breast neoplasm was reported in several men receiving finasteride 5 mg daily (alone or in combination with doxazosin) in a clinical trial of 4–6 years’ duration;^{1 20} however, breast neoplasm was reported in placebo recipients only in another long-term trial of finasteride.^{1 19} Not known whether a causal relationship exists between long-term finasteride use and breast neoplasia in men.^{1 d}

Specific Populations

Pregnancy

Category X.¹ (See Fetal/Neonatal Morbidity and also see Contraindications under Cautions.)

Lactation

Not known whether finasteride is distributed into milk, but the drug is not indicated for use in women.^{1 d}

Pediatric Use

Safety and efficacy not established, but the drug is not indicated for use in children.^{1 d}

Geriatric Use

No substantial differences in safety and efficacy for treatment of BPH in men ≥65 or ≥75 years of age relative to younger men.¹ Efficacy for promoting hair regrowth in geriatric men with androgenetic alopecia not established.^d

Hepatic Impairment

Not studied in patients with hepatic impairment.^{1 d} Extensively metabolized in the liver.^{1 d} Use with caution.^{1 d}

Common Adverse Effects

Impotence, decreased libido, ejaculation disorder (e.g., decreased volume of ejaculate), breast enlargement.^{1 8 15 17 d}

Interactions for Finasteride

Extensively metabolized by CYP3A4; apparently does not affect CYP isoenzymes.^{1 d}

Specific Drugs and Laboratory Tests

Drug or Test	Interaction	Comments
Antipyrine	Pharmacokinetic or pharmacodynamic interaction unlikely1 d
Digoxin	Pharmacokinetic or pharmacodynamic interaction unlikely1 d
Propranolol	Pharmacokinetic or pharmacodynamic interaction unlikely1 d
Test for PSA	50% decrease in serum PSA concentration in patients with BPH receiving 5 mg daily, even in those with prostate cancer1 12 15 d PSA decreased from 0.7 ng/mL at baseline to 0.5 ng/mL at 12 months with 1-mg daily dosage for androgenetic alopeciad No substantial change in ratio of free to total PSA (percentage of free PSA)1	Do not interpret decrease in PSA value as a therapeutic effect on prostate cancer1 12 15 Take decrease into account for interpretation of PSA values in men receiving finasterided For clinical interpretation of PSA values in men with BPH receiving finasteride 5 mg daily for ≥6 months, double the reported value for PSA for comparison with normal values in men not receiving the drug1 No adjustment of reported values of ratio appears to be required1
Theophylline	Pharmacokinetic or pharmacodynamic interaction unlikely1 d
Warfarin	Pharmacokinetic or pharmacodynamic interaction unlikely1 d

Finasteride Pharmacokinetics

Absorption

Bioavailability

Mean bioavailability is 63–65%.^{1 d}

Onset

Rapid, with maximum decrease in serum DHT concentrations at 8 hours following oral administration of first dose of 5 mg, and 65% suppression of serum DHT within 24 hours after oral administration of 1 mg.^{1 d}

Duration

DHT suppression maintained throughout 24-hour dosage interval; DHT decreased by about 70% with 5-mg daily dosage for at least 4 years.¹

Food

Food does not appear to affect absorption.^{1 d}

Distribution

Extent

Crosses blood-brain barrier, but is not preferentially distributed into CSF.^{1 d}

Distributed into semen in amounts estimated to be 50- to 100-fold less than the dose (5 mcg) that had no effect on circulating DHT concentrations in men.¹

Crosses the placenta in rats.^{1 d}

Not known whether distributed into human milk.^{1 d}

Plasma Protein Binding

Approximately 90%. ^{1 d}

Elimination

Metabolism

Extensively metabolized, principally in the liver, via CYP3A4; 2 metabolites identified with ≤20% of activity of finasteride.^{1 d}

Elimination Route

Principally excreted in the feces (57%) and in urine (39%) as metabolites.^{1 d}

Half-life

Males 18–60 years of age: 5–6 hours.^{1 d}

Special Populations

Half-life in males ≥70 years of age: 8 hours; increase not clinically important.^{1 d}

Effect of hepatic impairment on pharmacokinetics not studied; extensively metabolized in the liver.^{1 d}

In patients with chronic renal impairment (Cl_cr 9–55 mL/minute), pharmacokinetics after single-dose administration appear to be similar to those in healthy individuals except that the proportion excreted in feces versus urine is increased in those with impairment.¹

Stability

Storage

Oral

Tablets

5-mg tablets: Tight, light resistant containers at room temperature <30°.¹

1-mg tablets: Tight, light resistant containers at 15–30°C.^d

ActionsActions

• 
  

  Competitive specific inhibitor of type 2 isoenzyme of steroid 5α-reductase.^{1 2 3 5 6 7 8 9 10 11 12 13 d f g h i j k l m n o}

  
  


• 
  

  100-fold more selective for type 2 5α-reductase than for type 1 isoenzyme;^{d g k l m} chronic treatment may have some effect on the type 1 isoenzyme.^{g h}

  
  


• 
  

  Type 2 steroid 5α-reductase isoenzyme converts testosterone to DHT in the prostate gland, seminal vesicles, epididymides, liver, and the inner root sheath of hair follicles and is responsible for the formation of about two-thirds of circulating DHT.^{d g k l m n o}

  
  


• 
  

  Reduces serum and tissue (e.g., prostate, scalp) DHT concentrations substantially.^{1 2 3 6 7 8 9 10 11 12 13 15 d g k l m o}

  
  


• 
  

  Increases serum testosterone concentrations minimally to moderately (usually within the normal range) and prostatic testosterone concentrations substantially.^{1 2 3 6 7 8 9 10 11 12 13 15}

  
  


• 
  

  Decreases prostatic volume by an average of about 20–30% after 6–24 months of continued therapy in most patients with BPH.^{1 2 5 8 15 16 17}

  
  


• 
  

  In men with androgenetic alopecia, decreases scalp DHT concentrations to levels found in hairy scalp, reduces serum DHT, increases hair regrowth, and slows hair loss.^{d g k l m o} However, exact mechanism of action not fully elucidated.^{g l}

  
  

Advice to Patients

Pending revision, the material in this section should be considered in light of more recently available information in the MedWatch notification at the beginning of this monograph.

• 
  

  Importance of obtaining and reading patient information on finasteride before initiation of therapy and with each new prescription refill.^{1 21 d r}

  
  


• 
  

  Importance of advising pregnant women or women who may be pregnant to avoid direct contact with broken or crushed tablets of the drug.^{1 21 d f r} (See Fetal/Neonatal Morbidity under Cautions.)

  
  


• 
  

  Importance of pregnant women informing a clinician if they swallow the drug or have skin contact from handling broken or crushed finasteride tablets;^{1 21 d r} necessity for clinicians to advise pregnant women of risk to male fetus.^{1 21 d r}

  
  


• 
  

  Advise patients that a decrease in the volume of ejaculate may occur but that this does not appear to interfere with normal sexual function.^{1 21 r}

  
  


• 
  

  Advise patients of the possibility of impotence and decreased libido.^{1 8 15 17 21 r}

  
  


• 
  

  Importance of promptly informing clinician of any changes in breasts (e.g., lumps, pain, nipple discharge), since breast changes (enlargement, tenderness, neoplasm) have been reported.^{1 21 d r}

  
  


• 
  

  Advise that ≥6 months of continuous therapy may be required before improvement in BPH symptoms occurs and a decrease in prostate size may not noticeably improve urine flow or symptoms.²¹

  
  


• 
  

  Advise that ≥3 months of continuous therapy may be required before improvement in androgenetic baldness occurs, and if no improvement is observed after 12 months, further treatment is unlikely to be of benefit.^r

  
  


• 
  

  Advise that hair growth gained during treatment for androgenetic baldness will likely be lost within 12 months after discontinuing the drug.^r

  
  


• 
  

  Importance of informing clinician about finasteride therapy if a PSA test is performed.^r

  
  


• 
  

  Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.^{1 d}

  
  


• 
  

  Importance of advising patients of other important precautionary information.^{1 d} (See Cautions.)

  
  

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Finasteride

Routes	Dosage Forms	Strengths	Brand Names	Manufacturer
Oral	Tablets, film-coated	1 mg	Propecia (available in regular and Pro-Pak)	Merck
		5 mg	Proscar	Merck

Comparative Pricing

This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 07/2011. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.

Propecia 1MG Tablets (MERCK SHARP &amp; DOHME): 90/$184.99 or 120/$242.98

Proscar 5MG Tablets (MERCK SHARP &amp; DOHME): 30/$112.99 or 90/$308.97

Disclaimer

This report on medications is for your information only, and is not considered individual patient advice. Because of the changing nature of drug information, please consult your physician or pharmacist about specific clinical use.

The American Society of Health-System Pharmacists, Inc. and Drugs.com represent that the information provided hereunder was formulated with a reasonable standard of care, and in conformity with professional standards in the field. The American Society of Health-System Pharmacists, Inc. and Drugs.com make no representations or warranties, express or implied, including, but not limited to, any implied warranty of merchantability and/or fitness for a particular purpose, with respect to such information and specifically disclaims all such warranties. Users are advised that decisions regarding drug therapy are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and the information is provided for informational purposes only. The entire monograph for a drug should be reviewed for a thorough understanding of the drug's actions, uses and side effects. The American Society of Health-System Pharmacists, Inc. and Drugs.com do not endorse or recommend the use of any drug. The information is not a substitute for medical care.

AHFS Drug Information. © Copyright, 1959-2011, Selected Revisions June 09, 2011. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.

References

1. Merck & Co, Inc. Proscar (finasteride) tablets prescribing information. Whitehouse Station, NJ; 2006 Jan.

2. Stoner E. The clinical development of a 5α-reductase inhibitor, finasteride. J Steroid Biochem Mol Biol. 1990; 37:375-8. [PubMed 1701660]

3. Gormley GJ, Stoner E. The role of 5α-reductase inhibitors in the treatment of benign prostatic hyperplasia. Probl Urol. 1991; 5:436-40.

4. Catalone WJ, Smith DS, Ratliff TL et al. Measurement of prostate-specific antigen in serum as a screening test for prostate cancer. N Engl J Med. 1991; 324:1156-61. [PubMed 1707140]

5. Stoner E. The clinical effects of a 5 alpha reductase inhibitor, finasteride, on benign prostatic hyperplasia. J Urol. 1992; 147:1298-302. [IDIS 296030] [PubMed 1373779]

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. [IDIS 292954] [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. [IDIS 285920] [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. [IDIS 304508] [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. [IDIS 296671] [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. [IDIS 304089] [PubMed 1383816]

16. Steiner JF. Finasteride: a 5α-reductase inhibitor. Clin Pharm. 1993; 12:15-23. [IDIS 307042] [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]

18. Merck Sharpe & Dohme. Proscar (finasteride) tablets prescribing information. West Point, PA; 1992 Sep.

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, Roehrborn CG, Bautista OM 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. [IDIS 508413] [PubMed 14681504]

21. Merck & Co, Inc. Patient information about Proscar (finasteride). Whitehouse Station NJ; 2006 Jan.

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]

23. Prostate cancer. From: PDQ. Physician data query (database). Bethesda, MD: National Cancer Institute; 2006 Jul 21.

24. Scardino PT. The prevention of prostate cancer—the dilemma continues. N Engl J Med 2003; 349:297-9. [PubMed 12824458]

25. American Urological Association. Guideline on the management of benign prostatic hyperplasia (BPH)(2003/updated 2006). Available at: . Accessed 2006 Aug 10.

26. Vaughan ED. Medical management of benign prostatic hyperplasia—are 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.

a. AHFS drug information 2005. McEvoy GK, ed. Finasteride. Bethesda, MD: American Society of Health-System Pharmacists; 2005:3561-2.

b. AHFS drug information 2005. McEvoy GK, ed. Finasteride. Bethesda, MD: American Society of Health-System Pharmacists; 2005:3472-3.

d. Merck & Co. Propecia (finasteride) tablets prescribing information. Whitehouse Station, NJ; 2006 Jan.

f. Anon. Propecia and Rogaine Extra Strength for alopecia. Med Lett Drugs Ther. 1998; 40:25-7. [PubMed 9505960]

g. Dallob AL, Sadick NS, Unger W. The effect of finasteride, a 5α-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations in patients with male pattern baldness. J Clin Endocrinol Metab. 1994; 79:703-6. [IDIS 336768] [PubMed 8077349]

h. Stoner E. The clinical development of a 5α-reductase inhibitor, finasteride. J Steroid Biochem Mol Biol. 1990; 37:375-8. [PubMed 1701660]

i. Gormley GJ, Stoner E, Rittmaster RS et al. Effects of finasteride (MK-906), a 5 α- reductase inhibitor, on circulating androgens in male volunteers. J Clin Endocrinol Metab. 1990; 70:1136-41. [IDIS 285920] [PubMed 2156887]

j. 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]

k. Rittmaster RS. Finasteride. New Engl J Med. 1994; 330:120-5. [IDIS 323829] [PubMed 7505051]

l. Walsh DS, Dunn CL, James WD. Improvement in androgenetic alopecia (stageV) using topical minoxidil in a retinoid vehicle and oral finasteride. Arch Dermatol. 1995; 131:1373-5. [IDIS 357195] [PubMed 7492124]

m. Chen W, Zouboulis CC, Orfanos CE. The 5α-reductase system and its inhibitors: recent development and its perspective in treating androgen-dependent skin disorders. Dermatology. 1996; 193:177-84. [PubMed 8944337]

n. Gormley GJ. Finasteride: a clinical review. Biomed Pharmacother. 1995; 49:319-24. [PubMed 8562856]

o. Amichai B, Grunwald MH, Sobel R. 5α-reductase inhibitors—a new hope in dermatology. Int J Dermatol. 1997; 36:182-4. [PubMed 9158996]

p. Drake LA, Dinehart SM, Farmer ER et al for the American Academy of Dermatology. Guidelines of care for andogenetic alopecia. J Am Acad Dermatol. 1996; 35:465-8. [IDIS 372685] [PubMed 8784287]

r. Merck & Co. Propecia (finasteride) patient information. Whitehouse Station, NJ; 2006 Jan.

More Finasteride resources

• Finasteride Side Effects (in more detail)
• Finasteride Dosage
• Finasteride Use in Pregnancy & Breastfeeding
• Drug Images
• Finasteride Drug Interactions
• Finasteride Support Group
• 11 Reviews for Finasteride - Add your own review/rating

• Finasteride MedFacts Consumer Leaflet (Wolters Kluwer)


• Finasteride Prescribing Information (FDA)


• Finasteride Professional Patient Advice (Wolters Kluwer)


• finasteride Advanced Consumer (Micromedex) - Includes Dosage Information


• Propecia Prescribing Information (FDA)


• Propecia Consumer Overview


• Propecia MedFacts Consumer Leaflet (Wolters Kluwer)


• Proscar Prescribing Information (FDA)


• Proscar Consumer Overview

Compare Finasteride with other medications

• Androgenetic Alopecia
• Benign Prostatic Hyperplasia