Finasteride

Finasteride, sold under the brand names Proscar and Propecia among others, is a medication used to treat pattern hair loss and benign prostatic hyperplasia (BPH) in men.^[6] It can also be used to treat excessive hair growth in women.^[7][8] It is usually taken orally but there are topical formulations for patients with hair loss, designed to minimize systemic exposure by acting specifically on hair follicles.^[9]

Finasteride

Clinical data
Trade names	Proscar, Propecia, Finide, others
Other names	MK-906; YM-152; L-652,931; 17β-(N-tert-Butylcarbamoyl)-4-aza-5α-androst-1-en-3-one; N-(1,1-Dimethylethyl)-3-oxo-4-aza-5α-androst-1-ene-17β-carboxamide
AHFS/Drugs.com	Monograph
MedlinePlus	a698016
License data	US DailyMed: Finasteride
Pregnancy category	AU: X (High risk)
Routes of administration	By mouth
Drug class	5α-Reductase inhibitor
ATC code	G04CB01 (WHO) D11AX10 (WHO)
Legal status
Legal status	AU: S4 (Prescription only) CA: ℞-only UK: POM (Prescription only)^[1]^[2] US: ℞-only^[3]^[4]
Pharmacokinetic data
Bioavailability	65%^[5]
Protein binding	90%^[5]
Metabolism	Liver (CYP3A4, ALDH)^[5]
Elimination half-life	Adults: 5–6 hours^[5] Elderly: >8 hours^[5]
Excretion	Feces: 57%^[5] Urine: 40%^[5]
Identifiers
IUPAC name (1S,3aS,3bS,5aR,9aR,9bS,11aS)-N-tert-butyl-9a,11a-dimethyl-7-oxo-1,2,3,3a,3b,4,5,5a,6,9b,10,11-dodecahydroindeno[5,4-f]quinoline-1-carboxamide
CAS Number	98319-26-7^Y
PubChem CID	57363
IUPHAR/BPS	6818
DrugBank	DB01216^Y
ChemSpider	51714^Y
UNII	57GNO57U7G
KEGG	D00321^Y
ChEBI	CHEBI:5062^Y
ChEMBL	ChEMBL710^Y
CompTox Dashboard (EPA)	DTXSID3020625
ECHA InfoCard	100.149.445
Chemical and physical data
Formula	C23H36N2O2
Molar mass	372.553 g·mol^−1
3D model (JSmol)	Interactive image
SMILES O=C(NC(C)(C)C)[C@@H]2[C@]1(CC[C@H]3[C@H]([C@@H]1CC2)CC[C@H]4NC(=O)\C=C/[C@]34C)C
InChI InChI=1S/C23H36N2O2/c1-21(2,3)25-20(27)17-8-7-15-14-6-9-18-23(5,13-11-19(26)24-18)16(14)10-12-22(15,17)4/h11,13-18H,6-10,12H2,1-5H3,(H,24,26)(H,25,27)/t14-,15-,16-,17+,18+,22-,23+/m0/s1^Y Key:DBEPLOCGEIEOCV-WSBQPABSSA-N^Y
(verify)

Finasteride is a 5α-reductase inhibitor and therefore an antiandrogen.^[10] It works by decreasing the production of dihydrotestosterone (DHT) by about 70%.^[6]

In addition to DHT, finasteride also inhibits the production of several anticonvulsant neurosteroids including allopregnanolone, androstanediol, and THDOC.^[11]

Adverse effects from finasteride are rare;^[12] however, some men experience sexual dysfunction, depression, and breast enlargement.^[13][14] In some men, sexual dysfunction may persist after stopping the medication.^[15][16] It may also hide the early symptoms of certain forms of prostate cancer.^[14]

Finasteride was patented in 1984 and approved for medical use in 1992.^[17] It is available as a generic medication.^[18] In 2021, it was the 88th most commonly prescribed medication in the United States, with more than 8 million prescriptions.^[19][20]

Medical uses

Finasteride has been used for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate^[3] and for the treatment of male pattern hair loss (androgenetic alopecia) in men.^[4]

Enlarged prostate

Physicians sometimes prescribe finasteride for the treatment of benign prostatic hyperplasia (BPH), informally known as an enlarged prostate.^[21] Finasteride may improve the symptoms associated with BPH such as difficulty urinating, getting up during the night to urinate, hesitation at the start and end of urination, and decreased urinary flow.^[22]

The use of the drug showed significant sexual adverse effects such as erectile dysfunction and less sexual desire, in particular when obstructive symptoms due to an enlarged prostate were present.^[23]

Scalp hair loss

Finasteride is also used to treat male pattern baldness (androgenic alopecia) in men, a condition that develops in up to 80% of Caucasian men aged 70 and over.^[24][4] In the United States, finasteride and minoxidil are the only two FDA approved drugs for the treatment of male pattern hair loss as of 2017.^[25] Treatment with finasteride slows further hair loss^[26] and provides about 30% improvement in hair loss after six months of treatment, with effectiveness persisting as long as the drug is taken.^[14] Taking finasteride leads to a reduction in scalp and serum DHT levels; by lowering scalp levels of DHT, finasteride can maintain or increase the amount of terminal hairs in the anagen phase by inhibiting and sometimes reversing miniaturization of the hair follicle. Finasteride is most effective on the crown but can reduce hair loss in all areas of the scalp.^[27][28] Finasteride has also been tested for pattern hair loss in women; however, the results were no better than placebo.^[29] Finasteride is less effective in the treatment of scalp hair loss than dutasteride.^[30][31]

Prostate cancer

In males aged 55 years old and over finasteride decreases the risk of low-grade prostate cancer but may increase the risk of high-grade prostate cancer and has no effect on overall survival.^[32]

A 2010 review found a 25% reduction in the risk of prostate cancer with 5α-reductase inhibitor.^[33] A follow-up study of the Medicare claims of participants in a 10-year Prostate Cancer Prevention Trial suggests the reduction in prostate cancer is maintained even after discontinuation of treatment.^[34] However, 5α-reductase inhibitors have been found to increase the risk of developing certain rare but aggressive forms of prostate cancer (27% risk increase), although not all studies have observed this.^[35] No impact of 5-α-reductase inhibitor on survival has been found in people with prostate cancer.^[35]

Excessive hair growth

Finasteride has been found to be effective in the treatment of hirsutism (excessive facial and/or body hair growth) in women. In a study of 89 women with hyperandrogenism due to persistent adrenarche syndrome, finasteride produced a 93% reduction in facial hirsutism and a 73% reduction bodily hirsutism after 2 years of treatment. Other studies using finasteride for hirsutism have also found it to be clearly effective.^[7]

Transgender hormone therapy

Finasteride is sometimes used in hormone replacement therapy for transgender women due to its antiandrogenic effects, in combination with a form of estrogen. However, little clinical research of finasteride use for this purpose has been conducted and evidence of safety or efficacy is limited.^[8] Moreover, caution has been recommended when prescribing finasteride to transgender women, as finasteride may be associated with side effects such as depression, anxiety, and suicidal ideation, symptoms that are particularly prevalent in the transgender population and in others at high risk already.^[36]

Adverse effects

A 2010 Cochrane review of finasteride for BPH found that, in men with a weighted mean age of 62.4, adverse effects are "rare; nevertheless, men taking finasteride are at increased risk for impotence, erectile dysfunction, decreased libido, and ejaculation disorder, versus placebo."^[12] As of 2016^[update] fresh evidence suggested such effects, along with disturbed neurosteroid production, may persist after finasteride use is stopped.^[37]

Finasteride is contraindicated in pregnancy.^[38][39] The Food and Drug Administration advises that donation of blood or plasma be deferred for at least one month after taking the last dose of finasteride.^[40]

The FDA has added a warning to 5α-reductase inhibitors concerning an increased risk of high-grade prostate cancer, as the treatment of BPH lowers PSA (prostate-specific antigen), which could mask the development of prostate cancer.^[41][42] Although overall incidence of male breast cancer in clinical trials for finasteride 5 mg was not increased, there are post-marketing reports of breast cancer in association with its use, though available evidence does not provide clarity as to whether there is a causative relationship between finasteride and these cancers.^[4][43] A 2018 meta-analysis found no higher risk of breast cancer with 5α-reductase inhibitors.^[44] Some men develop gynecomastia (breast development or enlargement) following finasteride usage.^{[45][46][47][48]} The risk of gynecomastia with 5α-reductase inhibitors is low at about 1.5%.^[49] Depressive symptoms and suicidality have been reported.^[50]

Sexual adverse effects

Use of finasteride is associated with an increased risk of sexual dysfunction including erectile dysfunction, decreased libido and ejaculatory dysfunction.^[51][13] Sexual adverse effects of finasteride and dutasteride have been linked to lower quality of life and ability to maintain an intimate relationship, and can cause stress in relationships.^[52]

The adverse effect profiles of finasteride are somewhat different for its indications of hair loss and BPH.

Finasteride for androgenetic alopecia (hair loss in men)

The most common adverse effects of finasteride taken for hair loss are: decrease in sex drive, erectile dysfunction and decrease in amount of semen.^[38]: 17

In addition, finasteride has been reported in case reports to cause sexual problems which persist after stopping the medication.^[16][15] A 2012 update to the FDA label noted reports of decreased sex drive, problems with ejaculation and difficulty achieving an erection which continued after stopping the medication. The update also referenced reports of testicular pain and "male infertility and/or poor quality of semen."^{[38]: 17 [14][53][49]}

Finasteride for BPH

The most common adverse sexual effects of finasteride for BPH are: trouble getting or keeping an erection, decrease in sex drive, decreased volume of ejaculate and ejaculation disorders.^[39]: 16

A 2010 Cochrane review found that men taking finasteride for BPH (with a mean age of 62.4) are at increased risk for impotence, erectile dysfunction, decreased libido, and ejaculation disorder for the first year of treatment. The rates became indistinguishable from placebo after 2–4 years and these side effects usually got better over time.^[12]

Long-term

Finasteride may cause persistent adverse sexual, neurological and physical effects in a subset of men.^[15] A 2019 metastudy surveyed the literature on the reversibility of finasteride's side effects. It identified three studies which demonstrated full reversibility of side effects and eleven that describe patients with irreversible adverse events. The findings were most convincing in a retrospective review of about 12,000 patients that 1.4% of the cohort developed persistent ED^[15] (ED lasting longer than 90 days post-withdrawal).^[54]

Post-finasteride syndrome

Reports of long-term, post-discontinuation adverse effects in some fraction of former finasteride users have led to a proposed post-finasteride syndrome, although some within the medical community question whether there is enough evidence to support a causal relationship between finasteride usage and PFS.^[55]

Individuals claiming to experience PFS report sexual, neurological, hormonal and psychological side effects that persist for an extended period after stopping the drug.^[56] Reported symptoms include penile atrophy and tissue changes, decreased ejaculate volume and quality, reduced libido, erectile dysfunction, loss of penile sensitivity, decreased orgasm sensation, dry skin, metabolic changes, muscle and strength loss, gynecomastia, depression, anxiety, panic attacks, insomnia, anhedonia, concentration problems, memory impairment and suicidal ideation.^[57] A meta-analysis found significant association between finasteride use and post-discontinuation depression, suicidal ideation, and sexual dysfunction, but the quality of evidence was limited.^[58]

The status of PFS as a legitimate and distinct medical pathology remains a subject of debate. A 2019 editorial in The BMJ called post-finasteride syndrome "ill defined and controversial".^[59] Some have argued that it has common features with other self-diagnosed "mystery syndromes" such as Morgellons or multiple chemical sensitivity, while others, including some in the biomedical research community, have concluded based on the available evidence that it represents a real and serious condition.^[16] There is no known underlying biological mechanism for the proposed syndrome, and its incidence is unclear.^[60] A lack of clear diagnostic criteria and the variable reporting fraction in different health-care settings make the problem challenging to evaluate.^[57]

As of 2016, Merck was a defendant in approximately 1,370 product liability lawsuits which had been filed by customers alleging they have experienced persistent sexual side effects following cessation of treatment with finasteride.^[61] Most cases were settled by 2018 when Merck paid a lump sum of $4.3 million USD to be distributed. As of September 2019^[update], 25 cases remained outstanding in the United States.^[62] In 2019, Reuters reported that faulty redactions in court documents revealed allegations from plaintiffs that Merck had known of persistent side effects in their original clinical trials but chose not to disclose them in warning labels.^[62]

Overdose

Finasteride has been studied in humans at single doses of up to 400 mg and at continuous dosages of up to 80 mg/day for three months, without adverse effects observed.^[4][3][63] There is no specific recommended antidote for finasteride overdose.^[4][3]

Interactions

No significant drug interactions have been observed between finasteride and a limited selection of medications.^[64]

Pharmacology

Pharmacodynamics

Finasteride is a 5α-reductase inhibitor.^[4][5] It is specifically a selective inhibitor of the type II and III isoforms of the enzyme.^[5][65][66] By inhibiting these two isozymes of 5α-reductase, finasteride reduces the formation of the potent androgen dihydrotestosterone (DHT) from its precursor testosterone in certain tissues in the body such as the prostate gland, skin, and hair follicles.^[5][67] As such, finasteride is a type of antiandrogen, or more specifically, an androgen synthesis inhibitor.^[68][69] However, some authors do not define finasteride as an "antiandrogen," a term which can refer more specifically to antagonists of the androgen receptor.^[70]

Finasteride results in a decrease of circulating DHT levels by about 65–70% with an oral dosage of 5 mg/day and of DHT levels in the prostate gland by up to 80–90% with an oral dosage of 1 or 5 mg/day.^[65][71][72] In parallel, circulating levels of testosterone increase by approximately 10%, while local concentrations of testosterone in the prostate gland increase by about 7-fold and local testosterone levels in hair follicles increase by around 27–53%.^[73][74] An oral dosage of finasteride of only 0.2 mg/day has been found to achieve near-maximal suppression of DHT levels (68.6% for 0.2 mg/day relative to 72.2% for 5 mg/day).^[74][75] Finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the 5α-reductase type I isoenzyme, with more than 100-fold less inhibitory potency for type I as compared to type II (IC₅₀Tooltip Half-maximal inhibitory concentration = 313 nM and 11 nM, respectively).^[4][5] This is in contrast to inhibitors of all three isoenzymes of 5α-reductase like dutasteride, which can reduce DHT levels in the entire body by more than 99%.^[65] In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit 5β-reductase (AKR1D1).^[76] However, its affinity for the enzyme is substantially less than for 5α-reductase (an order of magnitude less than for 5α-reductase type I) and hence is unlikely to be of clinical significance.^[76]

As of 2012, the tissues in which the different isozymes of 5α-reductase are expressed are not fully clear.^[67] This is because different investigators have obtained varying results with different reagents, methods, and tissues examined.^[67] However, the different isozymes of 5α-reductase appear to be widely expressed, with notable tissues including the prostate gland, seminal vesicles, testes, epididymides, skin, hair follicles, liver, kidneys, and brain, among others.^[67]

By inhibiting 5α-reductase and thus preventing DHT production, finasteride reduces androgen signaling in tissues like the prostate gland and the scalp. In the prostate, this reduces prostate volume, which improves BPH and reduces risk of prostate cancer. Finasteride reduces prostate volume by 20 to 30% in men with benign prostatic hyperplasia.^[77] Inhibition of 5α-reductase also reduces epididymal weight, and decreases motility and normal morphology of spermatozoa in the epididymis.^[78]

Neurosteroids like 3α-androstanediol (derived from DHT) and allopregnanolone (derived from progesterone) activate the GABA_A receptor in the brain; because finasteride prevents the formation of neurosteroids, it functions as a neurosteroidogenesis inhibitor and may contribute to a reduction of GABA_A activity. Reduction of GABA_A receptor activation by these neurosteroids has been implicated in depression, anxiety, and sexual dysfunction.^[79][80][81]

In accordance with finasteride being a potent 5α-reductase inhibitor but a weak inhibitor of 5β-reductase, the medication decreases circulating levels of 5α-reduced steroids like allopregnanolone but does not reduce concentrations of 5β-reduced steroids like pregnanolone.^[82][83][84] Pregnanolone acts as a potent GABA_A receptor positive allosteric modulator similarly to allopregnanolone.^[85]

Pharmacokinetics

The mean oral bioavailability of finasteride is approximately 65%.^[5] The absorption of finasteride is not affected by food.^[4][3] At steady-state with 1 mg/day finasteride, mean peak concentrations of finasteride were 9.2 ng/mL (25 nmol/L).^[4] Conversely, following a single 5 mg dose of finasteride, mean peak levels of finasteride were 37 ng/mL (99 nmol/L), and plasma concentrations increased by 47–54% following 2.5 weeks of continued daily administration.^[3] The volume of distribution of finasteride is 76 L.^[5] Its plasma protein binding is 90%.^[5] The drug has been found to cross the blood–brain barrier, whereas levels in semen were found to be undetectable.^[5]

Finasteride is extensively metabolized in the liver, first by hydroxylation via CYP3A4 and then by aldehyde dehydrogenase.^[5] It has two major metabolites, which are the tert-butyl side chain monohydroxylated and monocarboxylic acid metabolites.^[5] These metabolites show approximately 20% of the inhibitory activity of finasteride on 5α-reductase.^[5] Hence, the metabolites of finasteride are not particularly active.^[5] The drug has a terminal half-life of 5 to 6 hours in adult men (18–60 years of age) and a terminal half-life of 8 hours or more in elderly men (more than 70 years of age).^[5] It is eliminated as its metabolites 57% in the feces and 40% in the urine.^[5]

Chemistry

See also: List of 5α-reductase inhibitors

Finasteride, also known as 17β-(N-tert-butylcarbamoyl)-4-aza-5α-androst-1-en-3-one, is a synthetic androstane steroid and 4-azasteroid.^[64][86] It is an analogue of androgen steroid hormones like testosterone and DHT.^[64] As an unconjugated steroid, finasteride is a highly lipophilic compound.^[64][87]

History

In 1942, James Hamilton observed that prepubertal castration prevents the later development of male pattern baldness in mature men.^[88] In 1974, Julianne Imperato-McGinley of Cornell Medical College in New York attended a conference on birth defects. She reported on a group of intersex children in the Caribbean who appeared sexually ambiguous at birth, and were initially raised as girls, but then grew external male genitalia and other masculine characteristic after onset of puberty. These children, despite being raised as girls until puberty, were generally heterosexual, and were termed "Guevedoces" by their local community, which means "penis at twelve" in Spanish.^[89] Her research group found these children shared a genetic mutation, causing deficiency of the 5α-reductase enzyme and male hormone dihydrotestosterone (DHT), which was found to have been the etiology behind abnormalities in male sexual development. Upon maturation, these individuals were observed to have smaller prostates which were underdeveloped, and were also observed to lack incidence of male pattern baldness.^[90][91]

In 1975, copies of Imperato-McGinley's presentation were seen by P. Roy Vagelos, who was then serving as Merck's basic-research chief. He was intrigued by the notion that decreased levels of DHT led to the development of smaller prostates. Dr. Vagelos then sought to create a drug which could mimic the condition found in these children to treat older men who had benign prostatic hyperplasia.^[92]

Finasteride was developed by Merck under the code name MK-906.^[64] A team led by chemist Gary Rasmusson and biologist Jerry Brooks developed potential 5α-reductase inhibitors based on transition state inhibitors, using an iterative process of molecular design, testing, and redesign.^[93] In 1992, finasteride (5 mg) was approved by the U.S. Food and Drug Administration (FDA) for treatment of BPH, which Merck marketed under the brand name Proscar. Rasmusson and Brooks were awarded IPO's "Inventor of the Year" award in 1993 for their work on finasteride.^[94] In 1997, Merck was successful in obtaining FDA approval for a second indication of finasteride (1 mg) for treatment of male pattern hair loss, which was marketed under the brand name Propecia.^[95] It was the first 5α-reductase inhibitor to be introduced and was followed by dutasteride in 2001.^[96] The first study of finasteride in the treatment of hirsutism in women was published in 1994.^[97]

Society and culture

Generic names

Finasteride is the generic name of the drug and its INNTooltip International Nonproprietary Name, USANTooltip United States Adopted Name, BANTooltip British Approved Name, and JANTooltip Japanese Accepted Name, while finastéride is its DCFTooltip Dénomination Commune Française.^{[98][99][100][101]} It is also known by its former developmental code names MK-906, YM-152, and L-652,931.^{[98][99][100][101]}

Brand names

Finasteride is marketed primarily under the brand names Propecia, for pattern hair loss, and Proscar, for BPH, both of which are products of Merck & Co.^[101] There is 1 mg of finasteride in Propecia and 5 mg in Proscar. Merck's patent on finasteride for the treatment of BPH expired in June 2006.^[102] Merck was awarded a separate patent for the use of finasteride to treat pattern hair loss and it expired in November 2013.^[103] Finasteride is also marketed under a variety of other brand names throughout the world.^[101]

Athletics

From 2005 to 2009, the World Anti-Doping Agency banned finasteride because it was discovered that the drug could be used to mask steroid abuse.^[104] It was removed from the list effective 1 January 2009, after improvements in testing methods made the ban unnecessary.^[105] Athletes who used finasteride and were banned from international competition include skeleton racer Zach Lund, bobsledder Sebastien Gattuso, footballer Romário, and ice hockey goaltender José Théodore.^[105][106]

Miscellaneous

The U.S. Food and Drug Administration advises that donation of blood or plasma be deferred for at least one month after taking the last dose of finasteride.^[107] The UK also has a one-month deferral period.^[108]

Research

Preliminary research suggests that topical finasteride may be effective in the treatment of pattern hair loss.^[109][110] Topical finasteride, like the oral preparation, reduces serum DHT.^[110][109]

DHT may be involved in the cause of acne, and 5α-reductase inhibitors might be effective in the treatment of the condition.^[111][112] A small retrospective study reported that finasteride was effective in the treatment of acne in women with normal testosterone levels.^[113][112] A randomized controlled trial found that finasteride was less effective than flutamide or an ethinylestradiol/cyproterone acetate birth control pill in the treatment of acne in women with high androgen levels.^[113]

Androgens and estrogens may be involved in the cause of hidradenitis suppurativa (acne inversa).^[114][115] Two case series have reported that finasteride is effective in the treatment of hidradenitis suppurativa in girls and women.^[113]

Finasteride and other antiandrogens might be useful in the treatment of obsessive–compulsive disorder, but more research is needed.^[116]

References

1. "Propecia 1 mg Film-Coated Tablets - Summary of Product Characteristics (SmPC)". (emc). 27 July 2020. Retrieved 29 September 2020.
2. "Proscar 5mg film-coated Tablets - Summary of Product Characteristics (SmPC)". (emc). 10 July 2020. Retrieved 29 September 2020.
3. "Proscar- finasteride tablet, film coated". DailyMed. 15 November 2019. Retrieved 16 September 2020.
4. "Propecia- finasteride tablet, film coated". DailyMed. 15 November 2019. Retrieved 16 September 2020.
5. Lemke TL, Williams DA (2008). Foye's Principles of Medicinal Chemistry (6th ed.). Lippincott Williams & Wilkins. pp. 1286–. ISBN 978-0-7817-6879-5.
6. "Finasteride Monograph for Professionals". Drugs.com. American Society of Health-System Pharmacists. Retrieved 5 March 2019.
7. Blume-Peytavi U, Whiting DA, Trüeb RM (26 June 2008). Hair Growth and Disorders. Springer Science & Business Media. p. 369. ISBN 978-3-540-46911-7.
8. Knezevich EL, Viereck LK, Drincic AT (January 2012). "Medical management of adult transsexual persons". Pharmacotherapy. 32 (1): 54–66. doi:10.1002/PHAR.1006. PMID 22392828. S2CID 12853220.
9. Piraccini BM, Blume-Peytavi U, Scarci F, Jansat JM, Falqués M, Otero R, et al. (February 2022). "Efficacy and safety of topical finasteride spray solution for male androgenetic alopecia: a phase III, randomized, controlled clinical trial". Journal of the European Academy of Dermatology and Venereology. 36 (2): 286–294. doi:10.1111/jdv.17738. PMC 9297965. PMID 34634163.
10. Ferri FF (2014). Ferri's Clinical Advisor 2015 E-Book: 5 Books in 1. Elsevier Health Sciences. p. 580. ISBN 9780323084307.
11. Samba Reddy D, Ramanathan G (September 2012). "Finasteride inhibits the disease-modifying activity of progesterone in the hippocampus kindling model of epileptogenesis". Epilepsy & Behavior. 25 (1): 92–7. doi:10.1016/j.yebeh.2012.05.024. PMC 3444667. PMID 22835430.
12. Tacklind J, Fink HA, Macdonald R, Rutks I, Wilt TJ (October 2010). "Finasteride for benign prostatic hyperplasia". The Cochrane Database of Systematic Reviews. 2015 (10): CD006015. doi:10.1002/14651858.CD006015.pub3. PMC 8908761. PMID 20927745.
13. Zakhem GA, Goldberg JE, Motosko CC, Cohen BE, Ho RS (July 2019). "Sexual dysfunction in men taking systemic dermatologic medication: A systematic review". Journal of the American Academy of Dermatology. 81 (1): 163–172. doi:10.1016/j.jaad.2019.03.043. PMID 30905792. S2CID 85497115.
14. Varothai S, Bergfeld WF (July 2014). "Androgenetic alopecia: an evidence-based treatment update". American Journal of Clinical Dermatology. 15 (3): 217–30. doi:10.1007/s40257-014-0077-5. PMID 24848508. S2CID 31245042.
15. Zakhem GA, Goldberg JE, Motosko CC, Cohen BE, Ho RS (July 2019). "Sexual dysfunction in men taking systemic dermatologic medication: A systematic review". Journal of the American Academy of Dermatology. 81 (1): 163–172. doi:10.1016/j.jaad.2019.03.043. PMID 30905792. S2CID 85497115. In studies addressing reversibility, most of these patients have resolution of sexual adverse effects after discontinuation of finasteride, and many have improvement of adverse effects over time with continued finasteride use. However, some studies describe a subset of patients with persistent adverse effects after discontinuation... Level 1 evidence evaluating sexual dysfunction as a primary outcome was available for finasteride.
16. Traish AM (January 2020). "Post-finasteride syndrome: a surmountable challenge for clinicians". Fertility and Sterility. 113 (1): 21–50. doi:10.1016/j.fertnstert.2019.11.030. PMID 32033719. S2CID 211064052.
17. Fischer J, Ganellin CR (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 483. ISBN 9783527607495.
18. Sataloff RT, Sclafani AP (30 November 2015). Sataloff's Comprehensive Textbook of Otolaryngology: Head & Neck Surgery: Facial Plastic and Reconstructive Surgery. JP Medical Ltd. pp. 400–. ISBN 978-93-5152-459-5.
19. "The Top 300 of 2021". ClinCalc. from the original on 15 January 2024. Retrieved 14 January 2024.
20. "Finasteride - Drug Usage Statistics". ClinCalc. Retrieved 14 January 2024.
21. Smith AB, Carson CC (June 2009). "Finasteride in the treatment of patients with benign prostatic hyperplasia: a review". Therapeutics and Clinical Risk Management. 5 (3): 535–45. doi:10.2147/tcrm.s6195. PMC 2710385. PMID 19707263.
22. "Benign prostate enlargement". nhs.uk. 20 October 2017. Retrieved 20 October 2020.
23. Corona G, Tirabassi G, Santi D, Maseroli E, Gacci M, Dicuio M, et al. (July 2017). "Sexual dysfunction in subjects treated with inhibitors of 5α-reductase for benign prostatic hyperplasia: a comprehensive review and meta-analysis". Andrology. 5 (4): 671–678. doi:10.1111/andr.12353. hdl:11380/1132897. PMID 28453908. S2CID 3577324.
24. Kanti V, Messenger A, Dobos G, Reygagne P, Finner A, Blumeyer A, Trakatelli M, Tosti A, Del Marmol V, Piraccini BM, Nast A, Blume-Peytavi U (January 2018). "Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men - short version". Journal of the European Academy of Dermatology and Venereology. 32 (1): 11–22. doi:10.1111/jdv.14624. PMID 29178529.
25. Adil A, Godwin M (July 2017). "The effectiveness of treatments for androgenetic alopecia: A systematic review and meta-analysis". Journal of the American Academy of Dermatology. 77 (1): 136–141.e5. doi:10.1016/j.jaad.2017.02.054. PMID 28396101. S2CID 46036459.
26. Habif TP (23 April 2015). Clinical Dermatology. Elsevier Health Sciences. pp. 934–. ISBN 978-0-323-26607-9.
27. Yim E, Nole KL, Tosti A (December 2014). "5α-Reductase inhibitors in androgenetic alopecia". Current Opinion in Endocrinology, Diabetes and Obesity. 21 (6): 493–8. doi:10.1097/MED.0000000000000112. PMID 25268732. S2CID 30008068.
28. Gupta AK, Charrette A (April 2014). "The efficacy and safety of 5α-reductase inhibitors in androgenetic alopecia: a network meta-analysis and benefit-risk assessment of finasteride and dutasteride". The Journal of Dermatological Treatment. 25 (2): 156–61. doi:10.3109/09546634.2013.813011. PMID 23768246. S2CID 24833568.
29. Levy LL, Emer JJ (August 2013). "Female pattern alopecia: current perspectives". International Journal of Women's Health. 5: 541–56. doi:10.2147/IJWH.S49337. PMC 3769411. PMID 24039457.
30. Dhurat R, Sharma A, Rudnicka L, Kroumpouzos G, Kassir M, Galadari H, Wollina U, Lotti T, Golubovic M, Binic I, Grabbe S, Goldust M (May 2020). "5-Alpha reductase inhibitors in androgenetic alopecia: Shifting paradigms, current concepts, comparative efficacy, and safety". Dermatol Ther. 33 (3): e13379. doi:10.1111/dth.13379. PMID 32279398. S2CID 215748750.
31. Zhou Z, Song S, Gao Z, Wu J, Ma J, Cui Y (2019). "The efficacy and safety of dutasteride compared with finasteride in treating men with androgenetic alopecia: a systematic review and meta-analysis". Clin Interv Aging. 14: 399–406. doi:10.2147/CIA.S192435. PMC 6388756. PMID 30863034.
32. "Finasteride for Prostate Cancer Prevention". National Cancer Institute. 28 August 2013. Retrieved 8 February 2020.
33. Wilt TJ, Macdonald R, Hagerty K, Schellhammer P, Tacklind J, Somerfield MR, Kramer BS (2010). "5-α-Reductase inhibitors for prostate cancer chemoprevention: an updated Cochrane systematic review". BJU Int. 106 (10): 1444–51. doi:10.1111/j.1464-410X.2010.09714.x. PMID 20977593. S2CID 22178061.
34. Unger JM, Hershman DL, Till C, Tangen CM, Barlow WE, Ramsey SD, Goodman PJ, Thompson IM (March 2018). "Using Medicare Claims to Examine Long-term Prostate Cancer Risk of Finasteride in the Prostate Cancer Prevention Trial". Journal of the National Cancer Institute. 110 (11): 1208–1215. doi:10.1093/jnci/djy035. PMC 6235685. PMID 29534197.
35. Hirshburg JM, Kelsey PA, Therrien CA, Gavino AC, Reichenberg JS (2016). "Adverse Effects and Safety of 5-alpha Reductase Inhibitors (Finasteride, Dutasteride): A Systematic Review". J Clin Aesthet Dermatol. 9 (7): 56–62. PMC 5023004. PMID 27672412.
36. Trüeb RM (June 2017). "Discriminating in favour of or against men with increased risk of finasteride-related side effects?". Experimental Dermatology. 26 (6): 527–528. doi:10.1111/exd.13155. PMID 27489125. S2CID 36236057. [...] caution is recommended while prescribing oral finasteride to male-to-female transsexuals, as the drug has been associated with inducing depression, anxiety and suicidal ideation, symptoms that are particularly common in patients with gender dysphoria, who are already at a high risk.[9]
37. Patisaul HB, Belcher SM (18 May 2017). Receptor and Enzyme Mechanisms as Targets for Endocrine Disruptors. Vol. 1. Oxford University Press. p. 127. doi:10.1093/acprof:oso/9780199935734.003.0005. ISBN 9780190678524.
38. "PROPECIA Prescribing Information" (PDF). US Food & Drug Administration / Merck & Co., Inc. Retrieved 30 January 2020.
39. "PROSCAR Prescribing Information" (PDF). US Food & Drug Administration / Merck & Co., Inc. Retrieved 30 January 2020.
40. "Deferral of Blood and Plasma donors – Medications". FDA. 28 July 1993. Retrieved 30 January 2020.
41. FDA. Posted 9 June 2011. 5-alpha reductase inhibitors (5-ARIs): Label Change – Increased Risk of Prostate Cancer
42. Walsh PC (April 2010). "Chemoprevention of prostate cancer". The New England Journal of Medicine. 362 (13): 1237–8. doi:10.1056/NEJMe1001045. PMID 20357287.
43. Medicines and Healthcare products Regulatory Agency Drug Safety Update. December 2009 Finasteride: potential risk of male breast cancer
44. Wang J, Zhao S, Luo L, Li E, Li X, Zhao Z (2018). "5-alpha Reductase Inhibitors and risk of male breast cancer: a systematic review and meta-analysis". Int Braz J Urol. 44 (5): 865–873. doi:10.1590/S1677-5538.IBJU.2017.0531. PMC 6237523. PMID 29697934.
45. Narula HS, Carlson HE (August 2014). "Gynaecomastia-pathophysiology, diagnosis and treatment". Nat Rev Endocrinol. 10 (11): 684–698. doi:10.1038/nrendo.2014.139. PMID 25112235. S2CID 40159424.
46. Deepinder F, Braunstein GD (2012). "Drug-induced gynecomastia: an evidence-based review". Expert Opinion on Drug Safety. 11 (5): 779–795. doi:10.1517/14740338.2012.712109. PMID 22862307. S2CID 22938364.
47. Chung EY, Ruospo M, Natale P, Bolignano D, Navaneethan SD, Palmer SC, Strippoli GF (October 2020). "Aldosterone antagonists in addition to renin angiotensin system antagonists for preventing the progression of chronic kidney disease". The Cochrane Database of Systematic Reviews. 2020 (10): CD007004. doi:10.1002/14651858.CD007004.pub4. PMC 8094274. PMID 33107592.
48. Aiman U, Haseeen MA, Rahman SZ (December 2009). "Gynecomastia: An ADR due to drug interaction". Indian Journal of Pharmacology. 41 (6): 286–7. doi:10.4103/0253-7613.59929. PMC 2846505. PMID 20407562.
49. Trost L, Saitz TR, Hellstrom WJ (2013). "Side Effects of 5-Alpha Reductase Inhibitors: A Comprehensive Review". Sex Med Rev. 1 (1): 24–41. doi:10.1002/smrj.3. PMID 27784557.
50. Locci A, Pinna G (2017). "Neurosteroid biosynthesis downregulation and changes in GABAA receptor subunit composition: A biomarker axis in stress-induced cognitive and emotional impairment". Br. J. Pharmacol. 174 (19): 3226–3241. doi:10.1111/bph.13843. PMC 5595768. PMID 28456011.
51. Lee S, Lee YB, Choe SJ, Lee WS (2019). "Adverse Sexual Effects of Treatment with Finasteride or Dutasteride for Male Androgenetic Alopecia: A Systematic Review and Meta-analysis". Acta Derm Venereol. 99 (1): 12–17. doi:10.2340/00015555-3035. PMID 30206635.
52. Gur S, Kadowitz PJ, Hellstrom WJ (January 2013). "Effects of 5-alpha reductase inhibitors on erectile function, sexual desire and ejaculation". Expert Opinion on Drug Safety. 12 (1): 81–90. doi:10.1517/14740338.2013.742885. PMID 23173718. S2CID 11624116.
53. FDA (11 April 2012). "Questions and Answers: Finasteride Label Changes". US FDA. Retrieved 26 October 2014.
54. Kiguradze T, Temps WH, Yarnold PR, Cashy J, Brannigan RE, Nardone B, et al. (9 March 2017). "Persistent erectile dysfunction in men exposed to the 5α-reductase inhibitors, finasteride, or dutasteride". PeerJ. 5: e3020. doi:10.7717/peerj.3020. PMC 5346286. PMID 28289563.
55. Traish AM (January 2020). "Post-finasteride syndrome: a surmountable challenge for clinicians". Fertility and Sterility. 113 (1): 21–50. doi:10.1016/j.fertnstert.2019.11.030. PMID 32033719. S2CID 211064052.
56. Margo J (26 September 2012). . Australian Financial Review. Archived from the original on 14 November 2012.
57. Maksym RB, Kajdy A, Rabijewski M (December 2019). "Post-finasteride syndrome - does it really exist?". The Aging Male. 22 (4): 250–259. doi:10.1080/13685538.2018.1548589. PMID 30651009. S2CID 58569946.
58. Pompili M, Magistri C, Maddalena S, Mellini C, Persechino S, Baldessarini RJ (1 May 2021). "Risk of Depression Associated With Finasteride Treatment". Journal of Clinical Psychopharmacology. 41 (3): 304–309. doi:10.1097/JCP.0000000000001379. PMID 33814544. S2CID 233028103.
59. Gray SL, Semla TP (August 2019). "Post-finasteride syndrome". BMJ. 366: l5047. doi:10.1136/bmj.l5047. PMID 31399423. S2CID 199518161.
60. Gray SL, Semla TP (August 2019). "Post-finasteride syndrome". BMJ. 366: l5047. doi:10.1136/bmj.l5047. PMID 31399423. S2CID 199518161.
61. Marchalik D (4 February 2017). "Watch for these potential side effects in drug Trump reportedly takes for hair loss". Miami Herald. Retrieved 9 December 2018.
62. "U.S. court let Merck hide secrets about popular drug's risks". Reuters. Retrieved 25 March 2021. these legal briefs filed by plaintiffs' lawyers allege that in revisions to the drug's original 1997 label, Merck understated the number of men who experienced sexual symptoms in clinical trials, and how long those symptoms lasted.
63. Frye SV (2006). "Discovery and clinical development of dutasteride, a potent dual 5alpha-reductase inhibitor". Curr Top Med Chem. 6 (5): 405–21. doi:10.2174/156802606776743101. PMID 16719800.
64. Sudduth SL, Koronkowski MJ (1993). "Finasteride: the first 5α-reductase inhibitor". Pharmacotherapy. 13 (4): 309–25, discussion 325–9. doi:10.1002/j.1875-9114.1993.tb02739.x. PMID 7689728. S2CID 71103672.
65. Yamana K, Labrie F, Luu-The V (August 2010). "Human type 3 5α-reductase is expressed in peripheral tissues at higher levels than types 1 and 2 and its activity is potently inhibited by finasteride and dutasteride". Hormone Molecular Biology and Clinical Investigation. 2 (3): 293–9. doi:10.1515/hmbci.2010.035. PMID 25961201. S2CID 28841145.
66. Aggarwal S, Thareja S, Verma A, Bhardwaj TR, Kumar M (February 2010). "An overview on 5alpha-reductase inhibitors". Steroids. 75 (2): 109–53. doi:10.1016/j.steroids.2009.10.005. PMID 19879888. S2CID 44363501.
67. Azzouni F, Godoy A, Li Y, Mohler J (2012). "The 5 alpha-reductase isozyme family: a review of basic biology and their role in human diseases". Adv Urol. 2012: 1–18. doi:10.1155/2012/530121. PMC 3253436. PMID 22235201.
68. Preedy VR (2012). Handbook of Hair in Health and Disease. Springer Science & Business Media. pp. 89–. ISBN 978-90-8686-728-8.
69. Wu JJ (18 October 2012). Comprehensive Dermatologic Drug Therapy E-Book. Elsevier Health Sciences. pp. 361–. ISBN 978-1-4557-3801-4.
70. Clapauch R, Weiss RV, Rech CM (2017). "Testosterone and Women". Testosterone. Springer. pp. 319–351. doi:10.1007/978-3-319-46086-4_17. ISBN 978-3-319-46084-0. Finasteride is not actually an antiandrogen but a 5α-reductase inhibitor.
71. Bartsch G, Rittmaster RS, Klocker H (April 2000). "Dihydrotestosterone and the concept of 5alpha-reductase inhibition in human benign prostatic hyperplasia". European Urology. 37 (4): 367–80. doi:10.1159/000020181. PMID 10765065. S2CID 25793400.
72. Kim EH, Brockman JA, Andriole GL (January 2018). "The use of 5-alpha reductase inhibitors in the treatment of benign prostatic hyperplasia". Asian Journal of Urology. 5 (1): 28–32. doi:10.1016/j.ajur.2017.11.005. PMC 5780290. PMID 29379733.
73. Rittmaster RS (January 1994). "Finasteride". N. Engl. J. Med. 330 (2): 120–5. doi:10.1056/NEJM199401133300208. PMID 7505051.
74. Libecco JF, Bergfeld WF (April 2004). "Finasteride in the treatment of alopecia". Expert Opin Pharmacother. 5 (4): 933–40. doi:10.1517/14656566.5.4.933. PMID 15102575. S2CID 24296644.
75. Shapiro J, Kaufman KD (June 2003). "Use of finasteride in the treatment of men with androgenetic alopecia (male pattern hair loss)". J. Investig. Dermatol. Symp. Proc. 8 (1): 20–3. doi:10.1046/j.1523-1747.2003.12167.x. PMID 12894990.
76. Drury JE, Di Costanzo L, Penning TM, Christianson DW (July 2009). "Inhibition of human steroid 5beta-reductase (AKR1D1) by finasteride and structure of the enzyme-inhibitor complex". The Journal of Biological Chemistry. 284 (30): 19786–90. doi:10.1074/jbc.C109.016931. PMC 2740403. PMID 19515843.
77. Bostwick DG, Cheng L (24 January 2014). Urologic Surgical Pathology E-Book. Elsevier Health Sciences. pp. 402–. ISBN 978-0-323-08619-6.
78. Robaire B, Henderson NA (May 2006). "Actions of 5alpha-reductase inhibitors on the epididymis". Molecular and Cellular Endocrinology. 250 (1–2): 190–5. doi:10.1016/j.mce.2005.12.044. PMID 16476520. S2CID 53464391.
79. Finn DA, Beadles-Bohling AS, Beckley EH, Ford MM, Gililland KR, Gorin-Meyer RE, Wiren KM (2006). "A new look at the 5alpha-reductase inhibitor finasteride". CNS Drug Reviews. 12 (1): 53–76. doi:10.1111/j.1527-3458.2006.00053.x. PMC 6741762. PMID 16834758.
80. Römer B, Gass P (December 2010). "Finasteride-induced depression: new insights into possible pathomechanisms". Journal of Cosmetic Dermatology. 9 (4): 331–2. doi:10.1111/j.1473-2165.2010.00533.x. PMID 21122055. S2CID 24328589.
81. Gunn BG, Brown AR, Lambert JJ, Belelli D (2011). "Neurosteroids and GABA(A) Receptor Interactions: A Focus on Stress". Frontiers in Neuroscience. 5: 131. doi:10.3389/fnins.2011.00131. PMC 3230140. PMID 22164129.
82. Traish AM, Hassani J, Guay AT, Zitzmann M, Hansen ML (March 2011). "Adverse side effects of 5α-reductase inhibitors therapy: persistent diminished libido and erectile dysfunction and depression in a subset of patients". J Sex Med. 8 (3): 872–84. doi:10.1111/j.1743-6109.2010.02157.x. PMID 21176115.
83. Dusková M, Hill M, Hanus M, Matousková M, Stárka L (2009). "Finasteride treatment and neuroactive steroid formation". Prague Med Rep. 110 (3): 222–30. PMID 19655698.
84. Dušková M, Hill M, Stárka L (January 2010). "The influence of low dose finasteride, a type II 5α-reductase inhibitor, on circulating neuroactive steroids". Horm Mol Biol Clin Investig. 1 (2): 95–102. doi:10.1515/HMBCI.2010.010. PMID 25961975. S2CID 28578077.
85. Reddy DS (2003). "Pharmacology of endogenous neuroactive steroids". Crit Rev Neurobiol. 15 (3–4): 197–234. doi:10.1615/critrevneurobiol.v15.i34.20. PMID 15248811.
86. Tian G, Stuart JD, Moss ML, Domanico PL, Bramson HN, Patel IR, Kadwell SH, Overton LK, Kost TA, Mook RA (1994). "17 beta-(N-tert-butylcarbamoyl)-4-aza-5 alpha-androstan-1-en-3-one is an active site-directed slow time-dependent inhibitor of human steroid 5 alpha-reductase 1". Biochemistry. 33 (8): 2291–6. doi:10.1021/bi00174a041. PMID 8117686.
87. Azeem A, Khan ZI, Aqil M, Ahmad FJ, Khar RK, Talegaonkar S (May 2009). "Microemulsions as a surrogate carrier for dermal drug delivery". Drug Development and Industrial Pharmacy. 35 (5): 525–47. doi:10.1080/03639040802448646. PMID 19016057. S2CID 205563538.
88. Hamilton J (1942). "Male hormone stimulation is prerequisite and an incitant in common baldness". American Journal of Anatomy. 71 (3): 451–480. doi:10.1002/aja.1000710306.
89. "The extraordinary case of the Guevedoces". BBC News. 20 September 2015. Retrieved 3 September 2018.
90. Imperato-McGinley J, Guerrero L, Gautier T, Peterson RE (December 1974). "Steroid 5alpha-reductase deficiency in man: an inherited form of male pseudohermaphroditism". Science. 186 (4170): 1213–5. Bibcode:1974Sci...186.1213I. doi:10.1126/science.186.4170.1213. PMID 4432067. S2CID 36427689.
91. Isfort AH, Emerick JE, Paz RA (11 November 2016). "5-Alpha-Reductase Deficiency". WebMD. News & Perspective Drugs & Diseases CME & Education Academy Consult, Drugs & Diseases > Pediatrics: General Medicine.
92. Freudenheim M (16 February 1992). "Keeping the Pipeline Filled at Merck". The New York Times.
93. Cordes EH (2014). Hallelujah Moments: Tales of Drug Discovery. Oxford University Press. ISBN 9780199337149.
94. "Past Inventor of the Year Award Winners". ipoef.org. Intellectual Property Owners Education Foundation. Retrieved 21 June 2020.
95. Burger A, Abraham DJ (20 February 2003). Burger's Medicinal Chemistry and Drug Discovery, Autocoids, Diagnostics, and Drugs from New Biology. Wiley. p. 439. ISBN 978-0-471-37030-7.
96. Doherty AM (2003). Annual Reports in Medicinal Chemistry. Academic Press. pp. 353–. ISBN 978-0-12-040538-1.
97. Diamanti-Kandarakis E, Tolis G, Duleba AJ (1995). "Androgens and therapeutic aspects of antiandrogens in women". J. Soc. Gynecol. Investig. 2 (4): 577–92. doi:10.1177/107155769500200401. PMID 9420861. S2CID 32242838.
98. Index Nominum 2000: International Drug Directory. Taylor & Francis. 2000. p. 443. ISBN 978-3-88763-075-1.
99. Morton IK, Hall JM (6 December 2012). Concise Dictionary of Pharmacological Agents: Properties and Synonyms. Springer Science & Business Media. pp. 121–. ISBN 978-94-011-4439-1.
100. Bycroft BW, Payne DJ (9 August 2013). Dictionary of Antibiotics and Related Substances: with CD-ROM, Second Edition. CRC Press. pp. 816–. ISBN 978-1-4822-8215-3.
101. "Finasteride".
102. . RxNews. Prescription Solutions. Archived from the original on 21 March 2008.
103. FDA. "Patent Expiration for Propecia". Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations.
104. Sandomir R (19 January 2006). "Skin Deep; Fighting Baldness, and Now an Olympic Ban". The New York Times. Retrieved 2 May 2010.
105. Staff (28 October 2008). "WADA removes Finasteride from ban list". The Australian.
106. Staff (9 October 2008). . Sydney Morning Herald. Archived from the original on 25 September 2015. Retrieved 25 October 2014.
107. "Deferral of Blood and Plasma donors – Medications" (PDF). FDA. 28 July 1993. Retrieved 4 February 2017.
108. "Anti-Androgens - Joint United Kingdom Blood Transfusion and Tissue Transplantation Services Professional Advisory Committee". www.transfusionguidelines.org. 1 June 2007. Retrieved 13 May 2020.
109. Lee SW, Juhasz M, Mobasher P, Ekelem C, Mesinkovska NA (April 2018). "A Systematic Review of Topical Finasteride in the Treatment of Androgenetic Alopecia in Men and Women". Journal of Drugs in Dermatology. 17 (4): 457–463. PMC 6609098. PMID 29601622.
110. Marks DH, Prasad S, De Souza B, Burns LJ, Senna MM (April 2020). "Topical Antiandrogen Therapies for Androgenetic Alopecia and Acne Vulgaris". American Journal of Clinical Dermatology. 21 (2): 245–254. doi:10.1007/s40257-019-00493-z. PMID 31832993. S2CID 209331373.
111. Danby FW (27 January 2015). Acne: Causes and Practical Management. John Wiley & Sons. pp. 147–. ISBN 978-1-118-23277-4.
112. Marchetti PM, Barth JH (March 2013). "Clinical biochemistry of dihydrotestosterone". Ann. Clin. Biochem. 50 (Pt 2): 95–107. doi:10.1258/acb.2012.012159. PMID 23431485. S2CID 8325257.
113. Hu AC, Chapman LW, Mesinkovska NA (January 2019). "The efficacy and use of finasteride in women: a systematic review". Int. J. Dermatol. 58 (7): 759–776. doi:10.1111/ijd.14370. PMID 30604525. S2CID 58555908.
114. Alikhan A, Lynch PJ, Eisen DB (April 2009). "Hidradenitis suppurativa: a comprehensive review". J. Am. Acad. Dermatol. 60 (4): 539–61, quiz 562–3. doi:10.1016/j.jaad.2008.11.911. PMID 19293006.
115. Riis PT, Ring HC, Themstrup L, Jemec GB (December 2016). "The Role of Androgens and Estrogens in Hidradenitis Suppurativa - A Systematic Review". Acta Dermatovenerol Croat. 24 (4): 239–249. PMID 28128074.
116. Nomani H, Mohammadpour AH, Moallem SM, YazdanAbad MJ, Barreto GE, Sahebkar A (December 2019). "Anti-androgen drugs in the treatment of obsessive-compulsive disorder: a systematic review". Curr Med Chem. 27 (40): 6825–6836. doi:10.2174/0929867326666191209142209. PMID 31814547. S2CID 208956450.