Hubbry Logo
DutasterideDutasterideMain
Open search
Dutasteride
Community hub
Dutasteride
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Dutasteride
Dutasteride
Dutasteride
View on Wikipedia
from Wikipedia

Dutasteride
Clinical data
Pronunciation/duˈtæstəˌraɪd/
doo-TA-stə-RYDE
Trade namesAvodart, others
Other namesGG-745; GI-198745; GI-198745X; N-[2,5-Bis(trifluoromethyl)phenyl]-3-oxo-4-aza-5α-androst-1-ene-17β-carboxamide
AHFS/Drugs.comMonograph
MedlinePlusa603001
License data
Pregnancy
category
  • Not to be used during pregnancy
Routes of
administration		By mouth
Drug class5α-Reductase inhibitor
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability60%[1]
Protein binding99%[1]
MetabolismLiver (CYP3A4)[1]
Metabolites• 4'-Hydroxydutasteride[1]
• 6'-Hydroxydutasteride[1]
• 1,2-Dihydrodutasteride[1]
(All three active)[1]
Elimination half-life4–5 weeks[2][3]
ExcretionFeces: 40% (metabolites)[1]
Urine: 5% (unchanged)[1]
Identifiers
  • (1S,3aS,3bS,5aR,9aR,9bS,11aS)-N-[2,5-bis(trifluoromethyl)phenyl]-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
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.166.372 Edit this at Wikidata
Chemical and physical data
FormulaC27H30F6N2O2
Molar mass528.539 g·mol−1
3D model (JSmol)
Density1.346 g/cm3 at 294 K (calculated)[4]
  • FC(F)(F)c1cc(c(cc1)C(F)(F)F)NC(=O)[C@@H]3[C@]2(CC[C@H]4[C@H]([C@@H]2CC3)CC[C@H]5NC(=O)\C=C/[C@]45C)C
  • InChI=1S/C27H30F6N2O2/c1-24-11-9-17-15(4-8-21-25(17,2)12-10-22(36)35-21)16(24)6-7-19(24)23(37)34-20-13-14(26(28,29)30)3-5-18(20)27(31,32)33/h3,5,10,12-13,15-17,19,21H,4,6-9,11H2,1-2H3,(H,34,37)(H,35,36)/t15-,16-,17-,19+,21+,24-,25+/m0/s1 checkY
  • Key:JWJOTENAMICLJG-QWBYCMEYSA-N checkY
  (verify)

Dutasteride, sold under the brand name Avodart among others, is a medication primarily used to treat the symptoms of a benign prostatic hyperplasia (BPH), an enlarged prostate not associated with cancer. A few months may be required before benefits occur.[5] It is also used for scalp hair loss in men and as a part of hormone therapy in transgender women.[6][7] It is usually taken by mouth.[8][9][5]

The most commonly reported side effects of dutasteride, although rare, include sexual dysfunction and depression.[10] In the largest available study of 6,729 men with BPH, 9% experienced erectile dysfunction (compared to 5.7% treated with a placebo), 3.3% experienced decreased sex drive (vs 1.6% of placebo), and 1.9% had enlarged breasts (vs 1% of placebo).[11][12] Exposure during pregnancy is specifically contraindicated because antiandrogens such as dutasteride have been shown to interfere with the sexual development of male fetuses.[3][8]

Dutasteride was patented in 1993 by Glaxo Wellcome (later known as GSK after additional mergers) and was approved for medical use in 2001.[13][8] In the United States and elsewhere, it is available as a generic medication.[5] In 2023, it was the 236th most commonly prescribed medication in the US with more than 1 million prescriptions.[14]

Medical uses

[edit]

Benign prostatic hyperplasia and prostate cancer

[edit]

Dutasteride is used for treating BPH, colloquially known as an "enlarged prostate".[9][15] It is approved by the Food and Drug Administration (FDA) in the U.S. for this indication.[16] A 2010 Cochrane review found a 25–26% reduction in the risk of developing prostate cancer with 5α-reductase inhibitor chemoprevention.[17]

Scalp hair loss and excessive hair growth

[edit]

Dutasteride is approved for the treatment of male androgenetic alopecia in South Korea and Japan at a dosage of 0.5 mg per day.[6][18] Several studies have found it to induce hair regrowth in men more rapidly and to a greater extent than even the highest approved dosage of finasteride.[6][19][20][21] The superior effectiveness of dutasteride relative to finasteride for this indication is because the inhibition of 5α-reductase and consequent reduction of dihydrotestosterone (DHT) production within the hair follicles is more complete with dutasteride. Dutasteride is also used off-label in the treatment of female pattern hair loss.[22][23]

Other 5α-reductase inhibitors such as finasteride (a type 2 inhibitor) have been used off-label to treat excessive hair growth in women with hirsutism.[3][24] Since dutasteride is an inhibitor of both type 1 and 2 5α-reductases, it could theoretically be a more effective therapy for hirsutism. However, dutasteride is not recommended for this indication due to a lack of supportive clinical evidence and a substantial risk of birth defects in female patients who inadvertently become pregnant.[24][25]

Available forms

[edit]

Dutasteride is provided in the form of soft, oil-filled gelatin capsules containing 0.5 mg dutasteride each.[26]

Contraindications

[edit]

Women who are or who may become pregnant should not handle the drug. Dutasteride can cause birth defects in male fetuses, specifically ambiguous genitalia and undermasculinization.[26][27] This is due to its antiandrogenic effects similar to what is seen in 5α-reductase deficiency.[27] For the same reason, women who are currently pregnant should never take dutasteride.[26] People taking dutasteride should not donate blood to prevent birth defects if a pregnant woman receives blood and should also not donate blood for at least 6 months after the cessation of treatment due to the drug's long elimination half-life.[26]

Children and people with known significant hypersensitivity (e.g., serious skin reactions, angioedema) to dutasteride should not take it.[26]

Adverse effects

[edit]

Dutasteride has overall been found to be well tolerated in studies of both men and women, producing minimal side effects.[28] Adverse effects include headache and gastrointestinal discomfort.[28] Isolated reports of menstrual changes, acne, and dizziness also exist.[28] A small risk of sexual side effects has been documented in men taking the drug during the first few months of therapy.[28][29]

The FDA added a black-box warning to dutasteride in 2011 describing an increased risk of high-grade prostate cancer in those who take the drug.[30] No direct mechanistic link between 5α-reductase inhibitors and prostate cancer has been established.[31] This is not due to a direct link between dutasteride or other 5α-reductase inhibitors and cancer per se, but rather that those who take 5α-reductase inhibitors may have a decrease in prostate-specific antigen (PSA) levels, and therefore increases in PSA (which are an indicator of possible cancer) may be masked in those who take the drug.[32] This is thought to delay cancer diagnosis so that patients taking 5α-reductase inhibitors present with a higher-grade tumor at the time of diagnosis. The American Urological Association advises that increased risk for patients taking these drugs leads to higher prostate cancer-specific and all-cause mortality.[31] The AUA also advises that this affect can be alleviated with more frequent screening and lower PSA cutoffs for diagnostic biopsies in men taking dutasteride or other 5α-reductase inhibitors.[31] Dutasteride is known to reduce the growth and prevalence of benign prostate tumors.[33] A 2018 meta-analysis found no higher risk of breast cancer with 5α-reductase inhibitors.[34]

Sexual and mood side effects, such as erectile dysfunction,[35] loss of libido,[10] depression,[36] and reduced semen volume occur in as many as 4.8% of patients taking 5α-reductase inhibitors including dutasteride.[37][10] In affected men, semen volume is decreased an average of 30%,[38] with a smaller subgroup of patients also experiencing a decrease of sperm motility of 6 to 12%.[39][40] Sperm shape and function are unaffected and the impact on male fertility is unknown.[41] These negative effects reverse by 3–4 months after discontinuation of the drug.[41][40][31]

In a study of 6,729 men with benign prostatic hyperplasia (BPH, a condition where the prostate grows unassociated with cancer), 9% had erectile dysfunction (compared to 5.7% treated with a placebo), 3.3% experienced decreased sex drive (vs 1.6% of placebo), and 1.9% had enlarged breasts (vs 1% of placebo).[35][12] These effects were noted to resolve over time, with many fewer men reporting any adverse effects by the end of the 4-year study.[12][35] The rate of discontinuation of the drug due to adverse effects was less than 5%.[12]

A subset of men affected by sexual and mood side effects report persistent loss of libido,[35] depression,[28] and erectile dysfunction for several years after discontinuing treatment.[10] This remains a highly contested topic in the academic literature due to disagreements about whether the nocebo effect may play a role,[42][43][44] whether self-report questionnaires are reliable for this data,[31] and whether enough objective evidence exists to conclude these effects are persistent after discontinuation of the drug.[31][45][46] The Post-Finasteride Syndrome Foundation (PFSF) was created with a medical advisory board to study the topic (finasteride is a similar 5α-reductase inhibitor)[47] and lawsuits alleging harm from the drug are ongoing.[48] Concerns from the PFSF and other patient advocates led the FDA to add a black-box warning to Finasteride for possible risks of suicide in June 2022.[31][49] Some experts have questioned the basis of the black-box warning, given that it relies on anecdotal patient-reported outcomes rather than prospective trials.[31]

Overdose

[edit]

No specific antidote for overdose of dutasteride is known, since the drug is extremely safe and well tolerated. Research studies show that even at 100 times the normal dose, dutasteride is not lethal.[50] Treatment of dutasteride overdose should be based on symptoms and should be with supportive therapies.[50] The long elimination half-life of dutasteride should be taken into consideration in the event of an overdose of the medication.[50] Dutasteride has been used in clinical studies at doses of up to 40 mg/day for a week (80 times the therapeutic dosage) and 5 mg/day for 6 months (10 times the therapeutic dosage) with no significant safety concerns or additional side effects.[50]

Current investigations

[edit]

Dutasteride has been studied in combination with bicalutamide in the treatment of prostate cancer.[51][52][53]

Ongoing clinical trials are investigating whether dutasteride may be an effective treatment for premenstrual dysphoric disorder (PMDD), because dutasteride may inhibit the conversion of progesterone to allopregnanolone, a neurosteroid metabolite, which may be responsible for some of the debilitating symptoms of PMDD.[54][55]

Pharmacology

[edit]

Pharmacodynamics

[edit]

Dutasteride belongs to a class of drugs called 5α-reductase inhibitors, which block the action of the 5α-reductase enzymes that convert testosterone into DHT.[56] It inhibits all three forms of 5α-reductase, and can decrease DHT levels in the blood by up to 98%.[1][57][58] Specifically it is a competitive, mechanism-based (irreversible) inhibitor of all three isoforms of 5α-reductase, types I, II, and III (IC50Tooltip Half-maximal inhibitory concentration values are 3.9 nM for type I and 1.8 nM for type II).[1][57][59][60] This is in contrast to finasteride, which is similarly an irreversible inhibitor of 5α-reductase but only inhibits the type II and III isoenzymes.[60][61][57] As a result of this difference, dutasteride is able to achieve a reduction in circulating DHT levels of up to 98%, whereas finasteride is able to achieve a reduction of only 65 to 70%.[58][2][56][62] In spite of the differential reduction in circulating DHT levels, the two drugs decrease levels of DHT to a similar extent of approximately 85 to 90% in the prostate gland,[62] where the type II isoform predominates.[59]

Since 5α-reductases degrade testosterone to DHT, the inhibition of these enzymes could theoretically cause an increase in testosterone. A 2018 review found that initiation of 5α-reductase inhibitors did not result in a consistent increase in testosterone levels.[63] Among the studies analyzed, there was no statistically significant change in testosterone levels from 5α-reductase inhibitors overall, though men with lower baseline testosterone levels did show an increase.[63]

In addition to inhibition of DHT production, 5α-reductase inhibitors such as dutasteride are also neurosteroidogenesis inhibitors, preventing the 5α-reductase-mediated biosynthesis of various neurosteroids, including allopregnanolone (from progesterone), THDOCTooltip tetrahydrodeoxycorticosterone (from deoxycorticosterone), and 3α-androstanediol (from testosterone).[37] These neurosteroids are potent positive allosteric modulators of the GABAA receptor and have shown antidepressant, anxiolytic, and pro-sexual effects in animal research.[37][64][65] For this reason, decreased neurosteroid production is one hypothesized mechanism for sexual dysfunction and depression associated with 5α-reductase inhibitors such as dutasteride.[37]

Pharmacokinetics

[edit]

The oral bioavailability of dutasteride is about 60%.[1] Consumption with food does not adversely affect its absorption.[1] Peak plasma levels occur 2 to 3 hours after administration.[1] Dutasteride is present in semen at levels up to 3 ng/ml, with no significant effects on DHT levels of sexual partners.[1] The drug is extensively metabolized in the liver by CYP3A4.[1] It has three major metabolites: 6'-hydroxydutasteride, 4'-hydroxydutasteride, and 1,2-dihydrodutasteride. The former two are formed by CYP3A4, while the latter is not.[1] All three metabolites are active; 6'-hydroxydutasteride has similar 5α-reductase inhibitor potency as dutasteride, while the other two are less potent.[1] Dutasteride has an extremely long terminal or elimination half-life of about 4 to 5 weeks.[2][3] Its elimination half-life is increased in the elderly (170 hours for men aged 20–49 years, 300 hours for men aged >70 years).[1] No dosage adjustment is necessary in the elderly nor in patients with renal impairment.[1] Because of its long elimination half-life, dutasteride requires 5 to 6 months to reach steady-state concentrations.[59] It also remains in the body for a long time after discontinuation and can be detected up to 4 to 6 months.[1][2] In contrast to dutasteride, finasteride has a short terminal half-life of only 5 to 8 hours.[3][1] Dutasteride is eliminated mainly in the feces (40%) as metabolites.[1] A smaller portion (5%) is eliminated unchanged in the urine.[1]

Chemistry

[edit]
See also: List of 5α-reductase inhibitors

Dutasteride, also known as N-[2,5-bis(trifluoromethyl)phenyl]-3-oxo-4-aza-5α-androst-1-ene-17β-carboxamide, is a synthetic androstane steroid and a 4-azasteroid.[66][67] It is an analogue of finasteride in which the tert-butyl amide moiety has been replaced with a 2,5-bis(trifluoromethyl)phenyl group.[67]

History

[edit]

Dutasteride was patented in 1996 and was first described in the scientific literature in 1997.[68][69] It was approved by the FDA for the treatment of BPH in November 2001, and was introduced on the United States market the following year under the brand name Avodart.[69] Dutasteride has subsequently been introduced in many other countries, including throughout Europe and South America.[69] The patent protection of dutasteride expired in November 2015, so the drug has since become available in the United States in a variety of low-cost generic formulations.[68]

It was approved for the treatment of scalp hair loss in South Korea in 2009 and in Japan in 2015.[70] It has not been approved for this indication in the United States,[6][18] though it is often used off-label both orally and topically.[22][71]

Society and culture

[edit]
Avodart (dutasteride) 500 μg soft capsules

Generic names

[edit]

Dutasteride is the generic name of the drug Avodart and its international nonproprietary name, United States Adopted Name, British Approved Name, and Japanese Accepted Name.[72]

Brand names

[edit]

Dutasteride is sold primarily under the brand name Avodart, but also in combination with tamsulosin under the brand names Combodart, Duodart, and Jalyn.[72] Dutasteride is also available in India in combination with alfuzosin under the brand names Alfusin-D and Dutalfa.[72]

Availability

[edit]

Dutasteride is available widely throughout the world, including in the United States, Canada, the United Kingdom, Ireland, Europe, Australia, South Africa, Latin America, Asia, and elsewhere.[72] It is available as a generic medication in many countries, including the United States.[68]

References

[edit]

Further reading

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Dutasteride

View on Grokipedia
from Grokipedia

Dutasteride is a synthetic 4-azasteroid compound that acts as a dual inhibitor of both type I and type II enzymes, potently suppressing the conversion of testosterone to the more androgenic (DHT). Developed by GlaxoSmithKline and approved by the U.S. in 2001 for the treatment of symptomatic (BPH) in men with an enlarged , it is marketed under the brand name Avodart in oral capsule form (0.5 mg). By reducing serum DHT levels by over 90%, dutasteride shrinks volume, alleviates , and lowers the risk of acute and BPH-related surgery. Clinical trials have demonstrated dutasteride's superior efficacy over in improving BPH symptoms and levels, with alongside alpha-blockers like tamsulosin providing additive benefits. for androgenetic alopecia has shown promising results, with dutasteride outperforming —a type II-selective inhibitor—in promoting hair regrowth due to its more comprehensive DHT suppression (up to 98% versus 71%). However, the Reduction by Dutasteride of Events (REDUCE) trial revealed that while dutasteride reduced overall incidence by 22.8%, it was associated with a higher detection rate of high-grade (Gleason 8-10) tumors, sparking debate over potential carcinogenic risks versus detection artifacts. Common adverse effects include such as (up to 7-15% incidence), decreased , and ejaculatory disorders, which are generally reversible upon discontinuation but have raised concerns about persistent effects in some users. Empirical data from long-term studies indicate these risks are dose-dependent and more pronounced than with , underscoring the need for informed patient consent regarding hormonal modulation's broader physiological impacts. Despite its efficacy, dutasteride's in women—particularly those pregnant or of childbearing potential—stems from risks of fetal genital abnormalities due to DHT's role in male .

Clinical Applications

Benign Prostatic Hyperplasia

Dutasteride, administered at a dose of 0.5 mg once daily, is approved by the U.S. (FDA) for the treatment of symptomatic (BPH) in men with an enlarged , with approval granted in November 2001. It is indicated to improve symptoms, reduce the risk of acute (AUR), and decrease the need for BPH-related surgery. In clinical practice, it is often used as monotherapy for patients with moderate to severe symptoms and prostate volumes greater than 30 mL, or in combination with such as tamsulosin for enhanced symptom relief. Phase III trials, including a 2-year study involving over 4,000 men, demonstrated that dutasteride significantly reduces volume by approximately 25% at 12 months and 27% at 24 months, compared to . This reduction correlates with improvements in (LUTS), as measured by the International Prostate Symptom Score (IPSS), with mean decreases of 4.7 to 6.2 points over 2 years versus 2.7 to 3.4 points with . Maximum urinary flow rate (Qmax) also improves, increasing by 1.6 to 2.2 mL/s from baseline, exceeding gains of 0.5 to 1.0 mL/s. Long-term data from a 4-year extension confirm sustained efficacy, with continued volume shrinkage and symptom control without tachyphylaxis. The (Combination of Avodart and Tamsulosin) trial, a 4-year randomized study of 4,844 men with moderate to severe BPH, showed that dutasteride plus tamsulosin superior to either monotherapy in reducing clinical progression risk by 44.1% relative to tamsulosin alone and 31.2% relative to dutasteride monotherapy. yielded greater IPSS reductions (mean -6.3 points at 48 months vs. -4.3 for tamsulosin and -5.3 for dutasteride) and lowered AUR or invasive surgery incidence to 4.2% versus 10.7% for tamsulosin and 7.0% for dutasteride. Dutasteride monotherapy reduced AUR risk by 57% and surgery risk by 48% compared to in pooled analyses. Compared to , another 5-alpha reductase inhibitor selective for type 2 isoenzyme, dutasteride achieves greater serum suppression (over 90% vs. 70%) and modestly larger volume reductions (25% vs. 18% at 12 months). Head-to-head trials, such as the Enlarged Prostate International Comparator Study (EPICS), found similar overall efficacy in symptom improvement and after 12 months, though dutasteride showed superior gains in meta-analyses (mean difference 1.11 mL/s). Dutasteride users exhibited a lower for BPH-related (0.75) in observational cohorts. Both agents reduce progression risk comparably, with odds ratios around 0.47 for dutasteride versus .

Androgenetic Alopecia

Dutasteride, a dual inhibitor of type I and type II enzymes, at 0.5 mg/day reduces (DHT) levels by 90-95%, more profoundly than . According to Olsen et al. (2006), 5 mg finasteride reduces serum DHT by 73% and scalp DHT by 41%, while 0.5 mg dutasteride reduces serum DHT by 92% and scalp DHT by 51%, and 2.5 mg dutasteride reduces serum DHT by 96% and scalp DHT by 79%. Dallob et al. (1994) reported approximately 40% scalp DHT reduction with 5 mg finasteride. This superior suppression, compared to approximately 70% serum DHT reduction with finasteride, targets the primary hormonal driver of androgenetic alopecia (AGA) in genetically susceptible scalp follicles. AGA, characterized by progressive of hair follicles due to DHT-mediated shortening of the anagen phase, affects up to 50% of men by age 50 and leads to visible in patterned areas such as the vertex and frontal scalp. While not approved by the FDA for AGA treatment—where and topical hold approval—dutasteride is prescribed off-label but widely used, particularly in regions like and , and primarily for men with stubborn or treatment-resistant AGA, based on evidence of superior DHT suppression and hair preservation. For off-label use in adult males, the typical dosage is 0.5 mg orally once daily; the capsule should be swallowed whole without chewing or opening, as the contents may irritate the mouth or throat, and it can be taken with or without food. In some countries such as Japan or Korea, treatment may start at 0.1 mg daily and increase to 0.5 mg if needed. Treatment requires long-term use, with visible effects often after 3-6 months; discontinuation may lead to relapse, though effects fade more slowly than with finasteride due to dutasteride's longer half-life. Clinical trials demonstrate dutasteride's in increasing count and thickness. In a phase II randomized, placebo-controlled study of 416 men with AGA, oral dutasteride at doses of 0.05 mg, 0.1 mg, 0.5 mg, and 2.5 mg daily increased target area count in a dose-dependent manner over 24 weeks, with the 2.5 mg dose outperforming 1 mg by 109 hairs/cm² at week 24 versus placebo's decline. A subsequent randomized trial in 153 Korean men found 0.5 mg dutasteride superior to 1 mg after 24 weeks, yielding greater improvements in total count (mean +96.0 vs. +72.2 hairs) and investigator-assessed global photography scores. Long-term data from a 4-year of 576 men showed dutasteride maintained superior over , with 83.3% of dutasteride users exhibiting improved or stable growth versus 73.7% on , alongside sustained increases in density. Systematic reviews confirm dutasteride's generally superior over finasteride for androgenetic alopecia, including aggressive and diffuse forms, with meta-analyses showing greater hair count increases and DHT suppression compared to finasteride; however, individual non-response occurs at rates similar to finasteride (approximately 10-20%), and combination therapies are often recommended for aggressive cases. A of randomized controlled trials reported dutasteride significantly outperformed in regrowth parameters, including mean change in total count (weighted mean difference +23.58 hairs) and vertex count, across studies involving over 1,000 participants. Intermittent dosing regimens, such as twice- or thrice-weekly 0.5 mg, have shown comparable or superior results to daily in pilot randomized trials, with thrice-weekly achieving moderate-to-marked improvement in 35% of men versus 21% on daily after 24 weeks, potentially mitigating cumulative exposure. Emerging topical formulations, tested in phase II trials, reduced scalp DHT by 50-70% with minimal systemic absorption, yielding dose-dependent count gains (e.g., +19.1 hairs/cm² at 0.05% w/v over 24 weeks) superior to vehicle placebo. Intralesional mesotherapy with dutasteride, an off-label delivery method involving microinjections into the scalp, has shown promising but heterogeneous evidence in clinical studies, with overall improvements in hair density, count, and thickness reported in approximately 60-80% of cases and greater benefits in combination therapies; however, results vary, and larger placebo-controlled trials are needed to confirm efficacy. Safety profiles in AGA trials mirror those from benign prostatic hyperplasia studies, with primarily sexual adverse effects reported at rates similar to finasteride but potentially more frequent or pronounced. Common side effects include decreased (3-6%), (4-8%), and ejaculation disorders (1-2%), occurring in 5-15% of users overall, often resolving upon discontinuation; affects <1%. Long-term use up to 4 years showed no increased incidence of serious events like prostate cancer or depression beyond baseline risks, though persistent sexual dysfunction has been anecdotally reported post-cessation in subsets, warranting informed consent. Dutasteride is contraindicated in women of childbearing potential due to teratogenic risks from fetal DHT inhibition, with limited evidence in female AGA showing modest benefits but higher caution. Monitoring PSA levels is advised for men over 50, as dutasteride halves PSA values, potentially masking prostate issues.

Prostate Cancer Chemoprevention

Dutasteride, a dual 5α-reductase inhibitor, has been evaluated for prostate cancer chemoprevention due to its suppression of dihydrotestosterone (DHT), a hormone implicated in prostate carcinogenesis. In preclinical models, dutasteride reduces prostate epithelial proliferation and lowers intraprostatic DHT levels by over 90%, potentially halting early neoplastic changes. Clinical interest stemmed from the Prostate Cancer Prevention Trial (PCPT) with finasteride, which demonstrated a 25% relative risk reduction in overall prostate cancer incidence over 7 years, prompting similar investigations with dutasteride. The primary evidence comes from the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial, a multicenter, randomized, double-blind, placebo-controlled study involving 8,231 men aged 50-75 with serum prostate-specific antigen (PSA) levels of 2.5-10.0 ng/mL and a negative baseline prostate biopsy. Participants received dutasteride 0.5 mg daily or placebo for 4 years, with protocol-mandated biopsies at 2 and 4 years regardless of PSA. The trial reported a 22.8% relative reduction in prostate cancer prevalence (19.9% in the dutasteride group vs. 25.1% in placebo; absolute risk reduction 5.1%; hazard ratio 0.77, 95% CI 0.70-0.85). This effect was primarily driven by fewer low-grade (Gleason score ≤6) tumors, with no significant difference in intermediate-grade (Gleason 7) cancers. However, high-grade (Gleason 8-10) cancers occurred more frequently in the dutasteride arm (1.0% vs. 0.5%; relative risk 1.83, 95% CI 1.01-3.32), raising concerns about potential promotion of aggressive disease. Explanations for the high-grade signal include ascertainment bias from dutasteride-induced prostate volume shrinkage (approximately 25% reduction) and PSA lowering (about 50%), which may enhance biopsy sensitivity for aggressive lesions while masking indolent ones. Long-term follow-up from REDUCE, extending to 10 years post-treatment, found no sustained excess of high-grade cancers and suggested a persistent chemopreventive benefit, with overall prostate cancer risk remaining lower in the dutasteride group. Observational data from large cohorts indicate that 5α-reductase inhibitors like dutasteride are associated with reduced prostate cancer-specific mortality (hazard ratio 0.73-0.84 in meta-analyses), though confounding by indication (e.g., use in men with larger prostates) limits causal inference. Despite these findings, regulatory and guideline bodies have not endorsed dutasteride for routine chemoprevention. The U.S. Food and Drug Administration declined approval in 2011, citing unfavorable risk-benefit due to high-grade concerns, and updated labels to warn of increased detection of Gleason score 8-10 tumors. The National Comprehensive Cancer Network and American Urological Association guidelines (as of 2024) do not recommend 5α-reductase inhibitors for primary prevention in average-risk men, emphasizing shared decision-making for high-risk individuals (e.g., family history, elevated PSA) where benefits may outweigh risks of sexual side effects and potential undetected aggressive cancers. Evidence remains inadequate to confirm mortality benefits, with ongoing trials like REDEEM exploring shorter-term use in low-risk cohorts post-biopsy.

Hirsutism and Other Uses

Dutasteride has been explored off-label for the treatment of hirsutism, a condition characterized by excessive terminal hair growth in women due to elevated androgen activity, primarily through its inhibition of both type 1 and type 2 5α-reductase enzymes, which substantially reduces dihydrotestosterone (DHT) levels implicated in hair follicle stimulation. Unlike finasteride, which selectively targets type 2 5α-reductase and has shown efficacy in reducing hirsutism scores in randomized trials (e.g., a 12-month study demonstrating significant decreases in Ferriman-Gallwey scores), direct clinical evidence for dutasteride remains preliminary and largely mechanistic. Small-scale observations and extrapolations from its superior DHT suppression (up to 90-95% serum reduction versus 70% with finasteride) suggest potential benefits in lowering hair growth rates, but no large randomized controlled trials confirm its superiority or long-term safety in this context, with risks including teratogenicity necessitating contraception in women of childbearing age. In dermatology, dutasteride is also investigated for acne vulgaris, particularly in males with coexisting androgenetic alopecia, where DHT contributes to sebaceous gland hyperactivity and comedogenesis. A clinical trial evaluating 0.5 mg daily dutasteride in such patients reported significant reductions in acne lesion counts and severity after 24 weeks, attributed to profound DHT inhibition, positioning it as a potential adjunctive therapy despite lacking FDA approval for this indication. Evidence for other dermatologic applications, such as seborrhea or hidradenitis suppurativa, is anecdotal and unsupported by robust trials, underscoring the need for further research to establish efficacy beyond its established roles. Overall, these uses highlight dutasteride's broader anti-androgenic potential but are constrained by limited high-quality data and pregnancy contraindications.

Off-Label Use in Transgender Hormone Therapy

Dutasteride, a dual inhibitor of type 1 and type 2 5α-reductase enzymes, is used off-label in hormone therapy for transgender women to suppress dihydrotestosterone (DHT) levels, a more potent androgen than testosterone that contributes to masculinizing traits such as body and facial hair growth, scalp hair loss, and prostate enlargement. By reducing DHT by over 90% at standard doses of 0.5 mg daily, it complements estrogen therapy and primary antiandrogens like spironolactone, potentially enhancing feminization without broadly blocking testosterone receptor activity. This selective mechanism contrasts with non-specific blockers, preserving some testosterone for estrogen conversion via aromatase, though clinical outcomes depend on individual androgen sensitivity and concurrent therapies. Evidence for efficacy remains limited to small studies, case series, and expert guidelines, primarily focused on androgenetic alopecia (AGA) rather than broad feminization. In transgender women on feminizing regimens, dutasteride has shown utility in stabilizing or improving scalp hair density, with one review recommending it as a second-line option alongside topical for those experiencing hormone-related hair thinning. Adjunctive use may also reduce hirsutism by targeting DHT-dependent follicle activity, though randomized trials are absent, and benefits are inferred from its established role in cisgender men for similar DHT-mediated conditions. Guidelines from institutions like UCSF list dutasteride at 0.5 mg daily as an antiandrogen alternative, but emphasize monitoring for additive effects with , as DHT suppression does not fully mitigate testosterone's peripheral actions. Safety profiles in this context mirror general use, with risks including decreased libido, erectile dysfunction, and gynecomastia, potentially exacerbated by estrogen co-administration; long-term data specific to transgender populations are scarce, with no large-scale studies assessing prostate health or fertility impacts post-suppression. Contraindications include pregnancy exposure risks due to teratogenicity, necessitating contraception in fertile individuals, and baseline PSA screening for prostate monitoring. While peer-reviewed sources support its mechanistic rationale, the lack of robust, prospective trials underscores its experimental status, with clinicians weighing it against proven alternatives amid variable patient responses.

Pharmacology

Pharmacodynamics

Dutasteride acts as a potent, competitive inhibitor of both type I and type II 5α-reductase isoenzymes, enzymes that catalyze the NADPH-dependent conversion of testosterone to dihydrotestosterone (DHT), a more potent androgen responsible for androgen-dependent tissue growth and function. By forming a stable, slowly reversible enzyme-inhibitor complex, dutasteride effectively blocks this reduction step, leading to marked suppression of DHT synthesis across tissues where the isoenzymes are expressed. Type II 5α-reductase predominates in the prostate, seminal vesicles, and hair follicles, while type I is more abundant in skin, liver, and sebaceous glands, enabling dutasteride's broader DHT reduction compared to selective type II inhibitors. In clinical studies with 0.5 mg daily dosing in men, dutasteride reduces serum DHT concentrations by over 90%, with median decreases of 94% after 1 year and 93% after 2 years of treatment. Intraprostatic DHT levels fall by approximately 94%, alongside near-complete suppression (up to 94%) in seminal fluid, contributing to reduced prostate volume and improved urinary symptoms in benign prostatic hyperplasia. These effects persist due to dutasteride's long terminal half-life of about 5 weeks, allowing steady-state inhibition with once-daily administration. The inhibition indirectly elevates serum testosterone levels by 15% to 25%, typically remaining within normal ranges, without clinically meaningful changes in , sex hormone-binding globulin, luteinizing hormone, follicle-stimulating hormone, or adrenal steroids like . Dutasteride exhibits high selectivity, showing no significant binding to or inhibition of other steroidogenic enzymes such as 17α-hydroxylase or 17,20-lyase at therapeutic doses. This profile underlies its efficacy in androgen-driven conditions while minimizing off-target hormonal disruptions.

Pharmacokinetics

Dutasteride is administered orally as soft gelatin capsules, with peak serum concentrations (Tmax) reached within 2 to 3 hours following a single 0.5 mg dose. Absolute is approximately 60%, ranging from 40% to 94% across individuals. Ingestion with food decreases maximum serum concentrations by 10% to 15%, though this effect lacks and does not alter overall bioavailability. The drug exhibits extensive distribution, with a of 300 to 500 L, indicating broad tissue penetration. Dutasteride is highly bound to plasma proteins, with 99.0% binding to and 96.6% to alpha-1 acid glycoprotein. At after 12 months of dosing, concentrations in average 3.4 ng/mL (range: 0.4 to 14 ng/mL), representing about 11.5% of corresponding serum levels.
ParameterValue
Half-life (steady state)~5 weeks
Steady-state achievement3–6 months (65% at 1 month, ~90% at 3 months)
Clearance~0.6 L/hour
Dutasteride undergoes extensive hepatic metabolism primarily via enzymes and , yielding metabolites such as 4’-hydroxydutasteride and 6-hydroxydutasteride, some of which retain inhibitory activity comparable to the parent compound. Elimination occurs mainly through , with approximately 40% as metabolites and 5% as unchanged drug; urinary accounts for less than 1% unchanged dutasteride. The terminal elimination at steady state is approximately 5 weeks, with serum concentrations remaining detectable (>0.1 ng/mL) for 4 to 6 months after discontinuation. Steady-state serum concentrations average 40 ng/mL after one year of daily 0.5 mg dosing.

Safety Profile

Contraindications and Precautions

Dutasteride is contraindicated in women who are pregnant due to the risk of causing birth defects in fetuses, as it inhibits the conversion of testosterone to (DHT), a essential for normal external genitalia development. It is also contraindicated in women of childbearing potential and pediatric patients, for whom safety and efficacy have not been established. Hypersensitivity to dutasteride or to , another , represents an absolute , with potential for reactions such as . Pregnant women or those who may become pregnant must avoid handling dutasteride capsules, as absorption through the skin could occur, leading to systemic exposure and fetal risk; capsules should be swallowed whole without chewing or opening to prevent content leakage and mucosal irritation. Men treated with dutasteride should refrain from blood donation for at least six months after the last dose to minimize the theoretical risk of fetal exposure via transfusion to pregnant recipients. Precautions include monitoring for , as dutasteride reduces serum (PSA) levels by approximately 50% within six months of initiation, potentially masking early detection; a new PSA baseline should be established after six months, with subsequent values approximately doubled for interpretation. Clinical trials, including the Reduction by Dutasteride of Events (REDUCE) study, have shown an increased incidence of high-grade (Gleason score 8-10) s in dutasteride-treated patients compared to , prompting FDA warnings about this association despite overall risk reduction. Hepatic impairment warrants caution, as dutasteride undergoes extensive hepatic metabolism via and enzymes with negligible renal clearance; while no specific dose adjustment is recommended, patients with moderate to severe should be closely monitored for adverse effects due to potential accumulation. Concomitant use with potent CYP3A4 inhibitors (e.g., , ) can substantially elevate dutasteride exposure—up to 4.3-fold with steady-state —necessitating consideration of dose reduction or alternative therapy in such cases. Prior to starting therapy, clinicians should exclude other urologic conditions mimicking symptoms, such as or . has been reported in patients undergoing or surgery, particularly those with a history of α1-blocker use, though dutasteride itself does not directly cause this; surgical teams should be informed of exposure.

Common Adverse Effects

In clinical trials for benign prostatic hyperplasia (BPH), the most frequently reported adverse effects of dutasteride monotherapy, occurring at rates greater than 1% and exceeding , were sexual in nature, including impotence (4.7% versus 1.7% on ), decreased (3.0% versus 1.4%), and ejaculation disorders such as reduced volume (1.4% versus 0.5%). While these ejaculatory disorders are associated with dutasteride use, symptoms such as ejaculation discomfort or post-ejaculation issues may arise from alternative causes including infections, stress, or pelvic floor dysfunction, and professional medical evaluation is recommended to confirm the etiology. These effects were primarily observed during the first 6 months of treatment, with incidence rates declining thereafter and stabilizing at levels similar to by 2-4 years of follow-up in long-term studies involving up to 4,325 patients. Breast disorders, encompassing tenderness, enlargement, and , occurred in 0.5% of dutasteride-treated patients compared to 0.2% on , with higher rates (up to 1.1%) noted in extended therapy beyond 4 years. Other less prevalent but notable effects included (1.1% versus 0.6%) and , though these did not consistently exceed rates across trials. Discontinuation due to adverse effects was low, at approximately 4-6% for sexual side effects, with impotence being the leading cause (1-1.5%).
Adverse EffectDutasteride IncidencePlacebo IncidenceSource
Impotence4.7%1.7%FDA Label (Phase III Trials, n>4,300)
Decreased 3.0%1.4%FDA Label (Phase III Trials, n>4,300)
Disorders1.4%0.5%FDA Label (Phase III Trials, n>4,300)
Breast Disorders0.5%0.2%FDA Label (Phase III Trials, n>4,300)
These profiles align with dutasteride's mechanism as a dual 5α-reductase inhibitor, reducing levels and thereby influencing androgen-dependent functions, though individual variability exists and not all patients experience effects. In smaller studies for androgenetic alopecia, similar sexual adverse effects were reported at rates of 0.3-12% for impotence, 0.3-7.6% for decreased , and 0.3-11% for ejaculation issues, consistent with BPH data but derived from less extensive cohorts.

Serious and Long-Term Risks

Dutasteride, a dual 5-alpha-reductase inhibitor, has been associated with an increased detection of high-grade prostate cancers in clinical trials, prompting regulatory warnings despite an overall reduction in prostate cancer incidence. In the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial, involving 8,231 men at increased risk for prostate cancer, dutasteride reduced the overall risk of biopsy-detectable prostate cancer by 23% over four years compared to placebo. However, it was linked to a higher incidence of Gleason score 8-10 tumors (1.5% vs. 0.5% in placebo), raising concerns about promoting aggressive disease, though long-term follow-up data suggested no overall survival detriment. The U.S. Food and Drug Administration has issued a safety communication stating that 5-alpha-reductase inhibitors like dutasteride may increase the risk of high-grade prostate cancer, advising against their use for chemoprevention in the general population. Persistent sexual dysfunction represents a significant long-term risk, with reports of symptoms enduring beyond treatment cessation. Clinical data indicate dutasteride causes , decreased , and ejaculation disorders in up to 10-20% of users during , with animal models and human case series demonstrating reduced erectile responses persisting after short-term exposure (e.g., 4-8 weeks). A retrospective analysis found men with longer exposure to dutasteride or had elevated odds of persistent , with risks increasing by 4.9-fold for exposures over 205 days. These effects stem from profound DHT suppression (over 90%), potentially altering pathways and penile tissue integrity, though causality remains debated due to reliance on self-reports and potential influences in some studies. Mental health risks, including depression and suicidality, have emerged as concerns in post-marketing surveillance and pharmacoepidemiologic studies. Dutasteride use correlates with elevated risks of depressive symptoms, , and , particularly in the first months of treatment, mirroring patterns observed with . A 2022 reported 5-alpha-reductase inhibitors associated with a 1.5-2.0-fold increased of depression and suicide attempts among older men with . The has mandated warnings for dutasteride regarding potential suicidal thoughts, based on disproportionality signals in databases, though confounding by underlying conditions like disease complicates attribution. disruption (e.g., reduced ) provides a mechanistic , but prospective randomized data are lacking. Other long-term risks include metabolic perturbations and endocrine alterations. Extended dutasteride therapy (up to four years) has been linked to worsening erectile function, declining serum testosterone levels, and elevations in fasting glucose and HbA1c, potentially exacerbating and risk. Reviews hypothesize associations with , , and renal impairment due to DHT's role in tissue maintenance, though these derive from observational data prone to bias. and breast tenderness occur in 1-2% of users, with rare reports of prompting monitoring recommendations. Bone density reductions may heighten risk, as evidenced by increased diagnoses in users and analogous DHT inhibition effects.

Overdose

No specific human data on dutasteride overdose exist, as reported cases are rare and typically involve no severe outcomes due to the drug's wide and slow absorption profile. Treatment remains supportive and symptomatic, with no established available. Clinicians should monitor for potential exacerbation of known adverse effects, such as , , or hormonal imbalances from inhibited activity, though manifestations are not well-documented. Given dutasteride's large (approximately 300-500 L), or is unlikely to enhance elimination in overdose scenarios. Standard protocols recommend gastric if ingestion is recent (e.g., activated charcoal within 1-2 hours), followed by observation for cardiovascular or endocrine disturbances. In preclinical studies, high doses in animals produced reversible effects like reduced body weight and ECG changes, but these do not directly translate to human overdose risks. Immediate medical attention is advised, including contact with poison control centers for individualized management.

Clinical Evidence and Debates

Efficacy in Approved Indications

Dutasteride, at a dose of 0.5 mg daily, is approved by the U.S. (FDA) for the treatment of symptomatic (BPH) in men to improve symptoms, reduce the risk of acute urinary retention (AUR), and decrease the likelihood of BPH-related surgery. This approval, granted in 2001, is based on evidence from large-scale clinical trials demonstrating its inhibition of both type 1 and type 2 enzymes, leading to substantial reductions in (DHT) levels, which drive prostate growth. Efficacy was established in three pivotal phase III trials (ARIA3001, ARIA3002, and ARIB3003), which enrolled over 4,300 men with moderate to severe BPH symptoms and randomized them to dutasteride 0.5 mg or for 24 months in double-blind fashion. These studies showed dutasteride reduced serum DHT by a of 90.2% at 24 months (median 93.7%), compared to a 6.0% increase with . Total prostate volume decreased by approximately 25.7% from baseline with dutasteride, versus a 0.5% increase with , while transition zone volume (the primary site of BPH ) shrank by 27.3%. Symptom relief was measured via the American Urological Association Symptom Index (AUA-SI), where dutasteride provided an additional mean improvement of 3.0-4.3 points over at 24 months, alongside a 1.6-2.2 mL/s greater increase in maximum urinary flow rate (). The of AUR was reduced by 57% (57% of events), and the risk of invasive BPH-related surgery by 48%, with absolute risk reductions of 4.2% and 3.9%, respectively. A subsequent of randomized controlled trials corroborated these outcomes, confirming dutasteride's superiority in lowering levels, alleviating , and shrinking volume compared to or . Long-term extensions of these trials, up to 4 years, demonstrated sustained , with ongoing prostate volume reductions (up to 27.3% at 48 months) and persistent symptom score improvements without evidence of tolerance. In men with mild-to-moderate symptoms, secondary analyses from the REduction by DUtasteride of prostate Cancer Events (REDUCE) trial indicated a lower risk of BPH clinical progression ( 0.47, 95% CI 0.37-0.59). These findings position dutasteride as a reliable monotherapy for BPH management, particularly in patients with enlarged s, though individual responses vary based on baseline prostate size and symptom severity.

Evidence Gaps and Criticisms

Despite its demonstrated efficacy in reducing prostate volume and improving in (BPH), dutasteride's long-term safety profile remains incompletely characterized, particularly for durations exceeding four years, as most pivotal trials like and REDUCE were limited to that timeframe. Systematic reviews highlight a scarcity of prospective data on chronic use, with patients often requiring indefinite , yet insufficient monitoring for rare or delayed adverse events such as persistent endocrine disruptions. This gap is exacerbated by reliance on industry-sponsored studies, which may underemphasize discontinuation effects due to structured withdrawal protocols that do not capture real-world persistence. A notable criticism pertains to the interpretation of risk from the REDUCE trial, where dutasteride reduced overall biopsy-detectable by 23% but was associated with a higher incidence of high-grade (Gleason 8-10) tumors (0.5% vs. 0.2% in , 1.83). The U.S. issued a warning in citing this as evidence of elevated risk for aggressive disease, prompting label updates. However, persists over whether this reflects true —potentially via altered tumor biology from DHT suppression—or detection bias from dutasteride-induced prostate shrinkage facilitating earlier identification of preexisting high-grade lesions during protocol-mandated biopsies. Long-term follow-up data have not shown increased mortality, but the absence of randomized mortality endpoints leaves unresolved whether the risk-benefit favors chemoprevention, leading regulators to contraindicate dutasteride for this purpose. For off-label applications like androgenetic alopecia (AGA), evidence gaps include a paucity of large, placebo-controlled trials specific to this indication, with most data derived from small cohorts or post-hoc analyses of BPH studies, limiting generalizability to younger populations. Bibliometric analyses of AGA therapies underscore underrepresentation of dutasteride in rigorous endpoints beyond hair count surrogates, alongside concerns over amplified risks from its dual inhibition compared to . Patient-reported persistent —encompassing erectile issues, reduced , and ejaculatory disorders lasting beyond discontinuation—represents another evidentiary shortfall, documented in case series but contested by trial data showing resolution rates over 90% within one year, potentially attributable to underreporting or effects in controlled settings. These discrepancies highlight needs for independent, long-term to quantify incidence and causality, especially given dutasteride's more profound DHT suppression (up to 98%).

Comparisons to Finasteride

Dutasteride inhibits both type I and type II isoforms of 5α-reductase, achieving approximately 90-95% serum dihydrotestosterone (DHT) suppression, whereas finasteride primarily targets the type II isoform, resulting in about 70% DHT reduction. This dual inhibition by dutasteride leads to more profound intraprostatic DHT lowering compared to finasteride's selective action. In treating (BPH), both drugs reduce prostate volume, lower (PSA) levels, and improve , with randomized trials showing comparable overall efficacy after 12 months of use. Some studies indicate dutasteride provides greater reductions in total prostate volume (TPV) and PSA, alongside improved International Prostate Symptom Score (IPSS), potentially due to its broader enzyme inhibition. However, meta-analyses and head-to-head comparisons confirm no clinically significant differences in symptom relief or peak urinary flow rates between the two. For off-label use in male androgenetic alopecia (AGA), dutasteride demonstrates superior hair regrowth and reversal of miniaturization compared to finasteride, with randomized controlled trials showing higher rates of moderate-to-marked improvement (e.g., 35% vs. 21% in evaluator-blinded assessments). Systematic reviews support dutasteride's greater efficacy in Basic and Specific Androgenetic Alopecia Phototrichogram Scale (BASP) classifications, attributed to its more complete DHT suppression in scalp tissue. As with finasteride, individual variability in response exists, with approximately 10-20% of patients exhibiting limited efficacy due to factors such as genetics and disease progression. Adverse event profiles are similar, with no significant differences in rates of , , or other common side effects observed in clinical trials for both BPH and AGA indications. Dutasteride's longer half-life (approximately 5 weeks vs. finasteride's 6-8 hours) may prolong recovery from side effects upon discontinuation, though meta-analyses report equivalent overall safety. Neither shows a differential risk for development in BPH patients.
AspectDutasterideFinasteride
DHT Suppression~90-95% (serum and )~70% (primarily )
BPH EfficacyComparable symptom relief; potentially greater TPV/PSA reductionComparable symptom relief
AGA Efficacy (off-label)Superior hair regrowthEffective but inferior to dutasteride
Safety ProfileSimilar AEs; longer Similar AEs

Controversies

Sexual and Reproductive Dysfunction

Dutasteride, a dual , is associated with sexual adverse effects in clinical trials for (BPH), including (incidence 7.3%), decreased (4.2%), and ejaculatory disorders (2.2%), rates higher than but often decreasing over time with continued use. While these ejaculatory disorders may relate to dutasteride, symptoms like ejaculation discomfort and post-ejaculation issues are not always caused by the drug and could stem from alternative causes such as mild infections, stress, or pelvic floor problems; professional medical evaluation is needed to confirm the etiology. In phase III trials such as ARIA3001 and ARIA3002, these effects occurred in approximately 5-10% of patients, with discontinuation rates due to sexual side effects around 1-2%. For in androgenetic alopecia, sexual adverse events range from 2% to 16%, potentially higher in younger men due to prolonged exposure. Persistent sexual dysfunction after discontinuation, akin to post-finasteride syndrome observed with , has been reported with dutasteride, including ongoing , reduced , and orgasmic issues in a subset of users. data indicate that 5α-reductase inhibitors like dutasteride elevate risks of sustained impairment ( ~1.69) and ( ~1.55) beyond treatment cessation, though causality remains debated due to confounding factors like effects or preexisting conditions. Regarding reproductive function, dutasteride reduces semen parameters, with studies showing 20-30% decreases in ejaculate volume, count, and during treatment, attributed to DHT suppression in the and . These changes are generally mild and reversible within 6-24 weeks post-discontinuation in short-term use, as evidenced by recovery in BPH trials. However, chronic administration in young men for alopecia has demonstrated more pronounced, potentially longer-lasting impairments in and volume, raising concerns for in reproductive-age users. Animal reproduction studies reveal dutasteride's inhibition of fetal external genitalia development at doses approximating exposure, leading to contraindications in and warnings against handling by women of childbearing potential. data on are limited to analyses, with no large-scale conception outcome studies, but mechanistic DHT reduction suggests caution for men planning fatherhood, particularly with off-label low-dose regimens.

Prostate Cancer Associations

In the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial, a multicenter, randomized, double-blind, placebo-controlled study of 8,231 men aged 50 to 75 years with serum prostate-specific antigen (PSA) levels between 2.5 and 10.0 ng per milliliter and a negative prostate biopsy, dutasteride at 0.5 mg daily over four years reduced the overall risk of prostate cancer detection on protocol-mandated biopsies by 22.8% (absolute risk reduction from 25.1% in placebo to 19.9% in dutasteride; hazard ratio 0.77, 95% CI 0.70-0.85). This effect was primarily driven by a decrease in low-grade tumors (Gleason score 5-6), with fewer such cancers detected in the dutasteride arm. The trial also reported a numerically higher incidence of high-grade prostate cancers (Gleason score 8-10) in the dutasteride group (1.0%) compared to (0.5%; 1.83, 95% CI 0.94-3.56), though the difference lacked . For intermediate-grade cancers (Gleason score 7), rates were similar between groups. Explanations for the high-grade finding include potential promotion of aggressive disease via pathway alterations or, more plausibly, detection from dutasteride-induced prostate volume shrinkage (approximately 25% reduction), which may concentrate high-grade lesions and lower PSA thresholds for . Meta-analyses of randomized trials, including REDUCE, confirm dutasteride's association with a 34% in overall detectable cancers (meta-hazard 0.66, 95% CI 0.52-0.85), predominantly low-grade, with no statistically significant elevation in high-grade (Gleason 8-10) (meta-hazard 1.53, 95% CI 0.86-2.74). Two-year post-trial follow-up of REDUCE participants showed low new cancer diagnosis rates (1.3% overall), comparable between original treatment arms, indicating no evidence of accelerated progression. Despite these data, which derive from high-quality randomized evidence, concerns over high-grade associations have led agencies like the FDA to contraindicate 5-alpha-reductase inhibitors, including dutasteride, for chemoprevention outside clinical trials, emphasizing shared decision-making on . Long-term observational data suggest no increase in mortality with dutasteride use.

Mental Health Risks

Dutasteride, a dual , has been associated in observational studies with an increased risk of depression among users treated for (BPH), though causality remains unestablished and confounded by factors such as age and underlying conditions. A 2022 analyzing Danish registry data found that dutasteride exposure was linked to a of 1.68 (95% CI, 1.14-2.48) for new-onset depression, independent of comparisons, attributing potential mechanisms to reduced levels like that modulate GABA receptors and mood regulation. Similarly, a 2025 systematic review and of inhibitors (5-ARIs), including dutasteride, reported a 31% elevated depression risk (HR 1.31, 95% CI 0.98–1.76), with high heterogeneity across studies highlighting variability in dosing and patient populations. These findings align with smaller case series noting depressive symptoms in up to 50% of men reporting persistent effects post-discontinuation, though such reports often overlap with debated post-5ARI phenomena lacking confirmation. Regarding suicidality, large-scale analyses have generally not detected an elevated risk specifically attributable to dutasteride. A 2023 population-based study in comparing and dutasteride users for BPH found no increased suicidal behavior odds (adjusted OR 0.56 for dutasteride vs. ), even after adjusting for and comorbidities. Earlier U.S. data from 2017 similarly showed no suicide association for 5-ARIs overall (incidence rate ratio 0.88, 95% CI 0.53-1.45), despite heightened signals, suggesting depression mediation without progression to completed in most cases. However, regulatory bodies have issued warnings: in May 2025, the recommended monitoring for suicidal thoughts with both and dutasteride, particularly in younger patients or off-label use, based on reports, though these emphasize discontinuation upon symptom onset rather than proven causation. Mechanistic hypotheses link these risks to dutasteride's potent suppression of (DHT) and neuroactive steroids in the , potentially disrupting emotional processing, as evidenced by preclinical models showing anxiogenic effects from 5AR inhibition. Clinical trials for BPH, such as the ARIA3001/3002 studies, rarely reported psychiatric events (<1%), but post-marketing surveillance and voluntary registries reveal underreporting biases, with some patient advocacy data indicating persistent anxiety or cognitive fog in subsets. Critics of causal claims argue observational biases and nocebo effects inflate perceived risks, as placebo-controlled trials like CombAT show no significant mood differences, underscoring the need for prospective studies isolating dutasteride's effects from finasteride's more scrutinized profile. Overall, while depression signals warrant informed consent, evidence does not support routine mental health screening beyond standard adverse event monitoring.

Implications for Off-Label Uses

Dutasteride has been investigated off-label primarily for androgenetic alopecia (AGA), with clinical trials demonstrating superior hair regrowth compared to finasteride, including increased hair counts and reversal of miniaturization in men. A meta-analysis of randomized controlled trials confirmed dutasteride's greater efficacy in improving Basic and Specific Androgenetic Alopecia Phototrichogram scales, alongside similar rates of adverse events such as sexual dysfunction. Low-dose (0.2 mg) and intermittent regimens have shown positive outcomes in hair density without elevated safety concerns, suggesting potential dose optimization to balance benefits and risks. Topical formulations, evaluated in phase II trials, exhibited efficacy comparable to or exceeding oral finasteride with minimal systemic absorption and no significant skin irritation, potentially mitigating long-term risks associated with oral administration. However, implications extend to heightened risks given dutasteride's dual inhibition of 5α-reductase isoforms, which may amplify persistent sexual and reproductive side effects observed in approved uses, particularly for cosmetic indications like AGA where benefits are subjective and reversible upon discontinuation. In women, off-label applications for hirsutism, acne, or female pattern hair loss carry contraindications due to teratogenic potential and limited evidence, with studies noting efficacy in reducing androgen-dependent symptoms but emphasizing pregnancy avoidance and monitoring for hormonal disruptions. For suppression of dihydrotestosterone in transgender hormone regimens, dutasteride's use lacks robust randomized data, relying on anecdotal or small-scale reports, and may exacerbate known risks like ejaculatory disorders or mood alterations without proven superiority over established antiandrogens. Overall, while off-label efficacy supports targeted applications in refractory AGA, the absence of regulatory approval underscores the need for informed consent regarding unverified long-term safety, especially amid debates on post-finasteride syndrome analogs.

Chemistry and Formulations

Chemical Structure and Properties

Dutasteride is a synthetic 4-azasteroid compound with the molecular formula C27H30F6N2O2 and a molecular weight of 528.53 g/mol. Its IUPAC name is (1S,3aS,3bS,5aR,9aR,9bS,11aS)-N-[2,5-bis(trifluoromethyl)phenyl]-3-oxo-2,3,3a,3b,4,5,5a,6,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopentaphenanthrene-1-carboxamide, featuring a modified androstane steroid nucleus with a nitrogen atom replacing carbon at position 4 and a carboxamide linkage to a 2,5-bis(trifluoromethyl)aniline moiety at position 17. The structure includes six fluorine atoms in trifluoromethyl groups, contributing to its lipophilicity, and specific stereochemistry at multiple chiral centers that confers selectivity for 5α-reductase inhibition. Physically, dutasteride appears as a white to off-white crystalline powder with a ranging from 242°C to 250°C. It exhibits low in (insoluble), but is soluble in organic solvents such as (44 mg/mL), (64 mg/mL), and 400 (3 mg/mL). These properties influence its formulation into soft capsules for , as the compound's poor aqueous necessitates solubilization in lipophilic vehicles. Chemically, it is stable under standard storage conditions at -20°C and demonstrates no significant flammability.

Pharmaceutical Forms

Dutasteride is formulated exclusively as soft gelatin capsules for , with each capsule containing 0.5 mg of the . This is designed to enhance of the lipophilic compound, which is dissolved in a vehicle consisting of mono- and diglycerides of caprylic/ along with as an . The capsules are opaque, dull yellow, oblong, and imprinted with "GX CE2" on one side, measuring approximately 17.9 mm in length. The approved strength is limited to 0.5 mg, administered once daily for . A fixed-dose combination product, Jalyn, pairs 0.5 mg dutasteride with 0.4 mg tamsulosin in a single soft capsule of similar composition but modified to accommodate the additional . Generic equivalents of both Avodart and Jalyn maintain the same soft capsule formulation and 0.5 mg strength for dutasteride. No other pharmaceutical forms, such as tablets, injectables, or topicals, have received regulatory approval from the FDA.

History

Development and Early Trials

Dutasteride, initially designated as GG745, was developed by GlaxoSmithKline (GSK) during the as a dual inhibitor of the type 1 and type 2 isoforms of , enzymes responsible for converting testosterone to (DHT). This approach aimed to surpass the efficacy of , a type 2-specific inhibitor, by achieving greater DHT suppression to address conditions like (BPH). Preclinical studies established its potent biochemical activity, with in vitro assays showing inhibition constants in the nanomolar range for both isoforms. Early-phase clinical trials commenced in the late , with results from demonstrating rapid and profound DHT reduction: a 0.5 mg daily dose suppressed serum DHT by approximately 90% within two weeks, compared to 70% suppression observed with . These phase I and II studies, involving small cohorts of healthy volunteers and BPH patients, confirmed dose-dependent , with maximal DHT inhibition at 0.5 mg and minimal accumulation upon repeated dosing. Safety profiles in these trials indicated good tolerability, though monitoring focused on potential hormonal disruptions given the drug's mechanism. These findings paved the way for larger efficacy evaluations, culminating in the submission of a (NDA) to the U.S. in 2001, supported by data from initial trials showing sustained prostate volume reduction and symptom relief without severe adverse events predominating over . Approval followed on November 20, 2001, for BPH treatment under the brand name Duagen (later Avodart).

Regulatory Approvals and Post-Marketing Surveillance

Dutasteride, marketed as Avodart by GlaxoSmithKline, received approval from the U.S. Food and Drug Administration (FDA) on November 20, 2001, for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate, either as monotherapy or in combination with an alpha-blocker like tamsulosin, to improve symptoms, reduce the risk of acute urinary retention, and decrease the need for BPH-related surgery. The FDA rejected a supplemental new drug application in 2011 for prostate cancer risk reduction due to concerns over increased high-grade prostate cancer detection in trials, prompting GlaxoSmithKline to abandon global pursuit of that indication. In the , Avodart obtained marketing authorization on January 17, 2003, for similar BPH indications, with decentralized approval processes facilitating use across member states. Approvals followed in other regions, including in 2009 and in July 2009 for BPH treatment. Post-marketing surveillance has identified additional adverse reactions beyond pre-approval trials, including reactions such as , pruritus, urticaria, localized , serious skin reactions, and , as well as rare reports of and testicular pain or swelling, though causality remains unestablished due to voluntary reporting biases. The FDA updated Avodart labeling in June 2011 to include warnings on high-grade risk based on post-approval data analysis. Non-interventional studies, such as a Korean post-marketing surveillance initiated in 2011, have monitored real-world safety and efficacy in BPH patients, reporting tolerability consistent with trials but noting persistent sexual side effects. Recent (EMA) Pharmacovigilance Risk Assessment Committee (PRAC) reviews, initiated in October 2024, examined signals of associated with dutasteride and , leading to endorsed measures in June 2025, including patient alert cards, mood monitoring recommendations, and updated labeling to advise discontinuation if psychiatric symptoms emerge, though data linkage to dutasteride specifically remains under evaluation amid confounding off-label uses. These updates reflect ongoing without altering core BPH approval status.

Society and Culture

Generic and Brand Names

The generic name of the medication is dutasteride. It is marketed under the primary brand name Avodart by GlaxoSmithKline (GSK). Other brand names include Duagen. Generic equivalents of dutasteride 0.5 mg oral capsules became available in the United States following the expiration of Avodart's patent exclusivity, with launching an authorized generic version on October 12, 2015.

Availability and Regulatory Status

Dutasteride received approval from the United States Food and Drug Administration (FDA) on November 20, 2001, for the treatment of symptomatic (BPH) in men with an enlarged prostate, marketed as Avodart soft gelatin capsules. The approval covers its use as monotherapy to improve symptoms, reduce the risk of acute , and decrease the need for BPH-related , or in combination with tamsulosin. It is not approved for prevention or female use due to risks including birth defects in male fetuses. In the US, dutasteride is available by prescription only, with generics introduced after patent challenges and expiration around 2018. In the , dutasteride is authorized for BPH treatment through national approvals and centralized procedures, with generic versions like Dutasteride 0.5 mg soft capsules available since at least 2014. The (EMA) oversees ongoing safety reviews, including confirmation in May 2025 of as a for dutasteride and related 5-alpha reductase inhibitors, prompting updated labeling and risk minimization measures across member states. It remains a prescription in EU countries such as , where formulations like Dutasteride Cinfa require medical authorization. Worldwide, dutasteride is prescription-required in major markets including , , , and the , where it is dispensed for BPH under brands like Avodart or generics. Although not FDA-approved for androgenetic alopecia, it holds regulatory approval for this indication in , , and , facilitating broader elsewhere for despite lacking such endorsement in the or . Availability has expanded post-patent, with production and distribution by manufacturers like GlaxoSmithKline and generics firms, though import/export may face controls in regions like requiring verification against national drug authority lists.

Recent Research and Future Directions

Studies from 2023-2025

A multicenter, randomized, double-blind, placebo-controlled phase III trial published in 2025 evaluated the efficacy and safety of low-dose oral dutasteride (0.2 mg daily) for male androgenetic alopecia (AGA) over 24 weeks, involving 120 participants; it reported significant improvements in hair count, thickness, and global assessment scores compared to placebo, with a favorable safety profile including reduced serum dihydrotestosterone (DHT) levels without notable impacts on testosterone or adverse sexual events beyond one case of erectile dysfunction leading to withdrawal. A phase II randomized, double-blind trial in 2025 assessed topical dutasteride solutions (0.01%, 0.02%, and 0.05% w/v) against placebo and oral finasteride for AGA, finding dose-dependent hair growth enhancements, particularly at 0.05%, with minimal systemic absorption and low incidence of side effects like scalp irritation. Long-term observational data from a 2024 Korean study on dutasteride 0.5 mg daily for AGA in men followed for at least five years indicated sustained efficacy in maintaining density and patient satisfaction, alongside a tolerable safety profile with no new signals of serious adverse events beyond known class effects such as decreased in a minority. Intermittent dosing regimens were explored in a 2025 pilot , where twice- or thrice-weekly dutasteride 0.5 mg proved noninferior to daily dosing for AGA treatment in terms of regrowth, suggesting potential for reduced cumulative exposure while preserving benefits. Conversely, a 2024 case series on dutasteride for AGA reported no significant gains in density or diameter after multiple sessions, highlighting variability in topical delivery methods. In prostate-related research, a 2024 phase II randomized trial examined adding dutasteride to combined for patients with recurrent or metastatic salivary duct , yielding improved without excess toxicity, though the small sample size limits generalizability. A secondary of the Reduction by Dutasteride of Events (REDUCE) trial data, published in 2025, linked to larger volumes over four years, with dutasteride's DHT inhibition potentially modulating this association independently of metabolic factors. Beyond and , a randomized placebo-controlled trial tested dutasteride 1 mg daily for alcohol use disorder in men, demonstrating reductions in heavy drinking days and weekly drinks, attributed to its modulation of neurosteroids influencing reward pathways, with good tolerability. A 2025 study warned of risks, noting that prolonged dutasteride use in young men persistently impaired volume and , potentially leading to reversible only after extended discontinuation. A network meta-analysis in 2025 ranked oral dutasteride 0.5 mg as the most effective monotherapy for AGA hair density at 24 weeks among comparators like and , based on standardized mean differences from aggregated trials.

Emerging Therapeutic Applications

Dutasteride has shown preliminary efficacy in treating vulgaris, particularly in male patients with comorbid androgenetic alopecia (AGA). A 2023 review of 5-alpha reductase inhibitors in highlighted dutasteride's potential as an adjunctive , noting its ability to suppress levels more potently than , which contributes to sebum production implicated in acne . A evaluating oral dutasteride at 0.5 mg/day in males with demonstrated improvements in lesion counts and AGA severity, attributed to reduced androgen-driven activity, though larger randomized controlled trials are needed to confirm long-term benefits and safety. In women with , dutasteride has been investigated off-label for reducing excess hair growth by inhibiting type I and II 5-alpha reductase enzymes, leading to greater DHT suppression than . A 2024 safety analysis of antiandrogens for female AGA and related hyperandrogenic conditions, including and , reported tolerable profiles at low doses (e.g., 0.1-0.5 mg/day), with reductions in Ferriman-Gallwey scores observed in small cohorts, but emphasized monitoring for potential fetal risks due to teratogenicity. These applications leverage dutasteride's dual-enzyme inhibition, yet evidence remains limited to retrospective and small-scale studies, with calls for prospective data to assess efficacy against standards like . Emerging evidence supports dutasteride's role in (HS), an inflammatory condition linked to follicular occlusion and androgen influence. Off-label use at 0.5 mg/day has been associated with decreased lesion severity and drainage in case series, potentially via lowered DHT-mediated inflammation in apocrine glands, as detailed in dermatologic therapeutic summaries. Similarly, for frontal fibrosing alopecia (FFA), low-dose regimens have yielded hairline stabilization in observational reports, outperforming in some refractory cases due to superior scalp DHT reduction. These dermatologic expansions highlight dutasteride's versatility but underscore the need for randomized trials to mitigate risks like and , which occur at rates comparable to or exceeding in systemic use. Topical formulations represent a frontier for minimizing systemic exposure in these applications. Phase II trials from 2023-2025 have tested dutasteride solutions (0.01-0.05% w/v) for AGA, showing comparable hair count improvements to oral forms with fewer adverse effects, suggesting adaptability for , , or HS where localized androgen blockade is desirable. Ongoing research into nanocarrier delivery aims to enhance follicular penetration while preserving efficacy. Despite promise, regulatory approval for these indications lags, confined to off-label prescribing informed by DHT's causal role in hyperandrogenic dermatoses.

References

  1. https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/021319s015lbl.pdf
  2. https://www.accessdata.fda.gov/drugsatfda_docs/label/2001/21319lbl.pdf
  3. https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/021319s023s025lbl.pdf
  4. https://www.nejm.org/doi/full/10.1056/NEJMoa0908127
  5. https://pubmed.ncbi.nlm.nih.gov/18318566/
  6. https://pubmed.ncbi.nlm.nih.gov/22428659/
  7. https://ishrs.org/patients/treatments-for-hair-loss/medications/dutasteride/
  8. https://pmc.ncbi.nlm.nih.gov/articles/PMC12405733/
  9. https://pubmed.ncbi.nlm.nih.gov/29095730/
  10. https://pmc.ncbi.nlm.nih.gov/articles/PMC1550785/
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC5023004/
  12. https://pubmed.ncbi.nlm.nih.gov/23173718/
  13. https://gmr.scholasticahq.com/article/88531-finasteride-and-dutasteride-for-the-treatment-of-male-androgenetic-alopecia-a-review-of-efficacy-and-reproductive-adverse-effect
  14. https://www.ncbi.nlm.nih.gov/books/NBK603726/
  15. https://www.sciencedirect.com/science/article/abs/pii/S0090429504000688
  16. https://www.bmj.com/content/346/bmj.f2109
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC8984969/
  18. https://pubmed.ncbi.nlm.nih.gov/19825505/
  19. https://pubmed.ncbi.nlm.nih.gov/24127818/
  20. https://www.verywellhealth.com/dutasteride-vs-finasteride-similarities-and-differences-7693199
  21. https://pubmed.ncbi.nlm.nih.gov/21631695/
  22. https://bmcurol.biomedcentral.com/articles/10.1186/s12894-016-0170-6
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC9561294/
  24. https://pubmed.ncbi.nlm.nih.gov/17110217/
  25. https://pubmed.ncbi.nlm.nih.gov/8077349/
  26. https://www.mayoclinic.org/drugs-supplements/dutasteride-oral-route/description/drg-20063575
  27. https://www.tandfonline.com/doi/abs/10.2147/CIA.S192435
  28. https://www.jaad.org/article/S0190-9622%2806%2901287-4/fulltext
  29. https://www.jaad.org/article/S0190-9622%2813%2901171-7/fulltext
  30. https://pubmed.ncbi.nlm.nih.gov/30863034/
  31. https://www.jaadinternational.org/article/S2666-3287%2825%2900101-4/fulltext
  32. https://www.cureus.com/articles/375228-a-randomized-double-blind-placebo-and-active-controlled-phase-ii-study-to-evaluate-the-safety-and-efficacy-of-novel-dutasteride-topical-solution-001-002-and-005-wv-in-male-subjects-with-androgenetic-alopecia
  33. https://pubmed.ncbi.nlm.nih.gov/35816059/
  34. https://www.actasdermo.org/en-rf-mesotherapy-with-dutasteride-a-future-articulo-S1578219020301396
  35. https://pubmed.ncbi.nlm.nih.gov/18588452/
  36. https://www.urotoday.com/recent-abstracts/urologic-oncology/prostate-cancer/155073-5-reductase-inhibitors-and-prostate-cancer-mortality-beyond-the-abstract.html
  37. https://www.spandidos-publications.com/10.3892/ol.2014.2388
  38. https://jamanetwork.com/journals/jamaoncology/fullarticle/2792528
  39. https://www.nejm.org/doi/full/10.1056/NEJMp1106783
  40. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2822868
  41. https://www.cancer.gov/types/prostate/hp/prostate-prevention-pdq
  42. https://theoncologynurse.com/articles/ton-3189
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC2856356/
  44. https://pubmed.ncbi.nlm.nih.gov/10526249/
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC10366043/
  46. https://www.sciencedirect.com/science/article/abs/pii/S0190962218326732
  47. https://pubmed.ncbi.nlm.nih.gov/30312645/
  48. https://transcare.ucsf.edu/guidelines/feminizing-hormone-therapy
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC6007530/
  50. https://www.uptodate.com/contents/transgender-women-evaluation-and-management
  51. https://pubmed.ncbi.nlm.nih.gov/34756934/
  52. https://pmc.ncbi.nlm.nih.gov/articles/PMC8484383/
  53. https://www.ncbi.nlm.nih.gov/books/NBK555930/
  54. https://tau.amegroups.org/article/view/111026/html
  55. https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/021319s032lbl.pdf
  56. https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-5-alpha-reductase-inhibitors-5-aris-may-increase-risk-more-serious
  57. https://reference.medscape.com/drug/avodart-dutasteride-342823
  58. https://www.auanet.org/guidelines-and-quality/guidelines/disorders-of-ejaculation
  59. https://pubmed.ncbi.nlm.nih.gov/20357281/
  60. https://pmc.ncbi.nlm.nih.gov/articles/PMC6479083/
  61. https://news.northwestern.edu/stories/2017/march/hair-loss-and-prostate-drugs-linked-to-persistent-erectile-dysfunction-in-men
  62. https://pmc.ncbi.nlm.nih.gov/articles/PMC6055634/
  63. https://www.ema.europa.eu/en/news/measures-minimise-risk-suicidal-thoughts-finasteride-dutasteride-medicines
  64. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2799858
  65. https://www.nature.com/articles/s41598-023-32356-3
  66. https://pubmed.ncbi.nlm.nih.gov/28632494/
  67. https://pmc.ncbi.nlm.nih.gov/articles/PMC7308241/
  68. https://pmc.ncbi.nlm.nih.gov/articles/PMC7994662/
  69. https://go.drugbank.com/drugs/DB01126
  70. https://www.tga.gov.au/sites/default/files/auspar-avodart.pdf
  71. https://www.webmd.com/drugs/2/drug-64364/dutasteride-oral/details
  72. https://www.accessdata.fda.gov/drugsatfda_docs/nda/2001/21319_Duagen_medr_P1.pdf
  73. https://pubmed.ncbi.nlm.nih.gov/12350480/
  74. https://www.goldjournal.net/article/S0090-4295%2802%2901905-2/abstract
  75. https://pubmed.ncbi.nlm.nih.gov/24246318/
  76. https://www.europeanurology.com/article/S0302-2838%2804%2900324-0/fulltext
  77. https://jcadonline.com/adverse-effects-and-safety-of-5-alpha-reductase-inhibitors-finasteride-dutasteride-a-systematic-review/
  78. https://tcr.amegroups.org/article/view/23887/19565
  79. https://pmc.ncbi.nlm.nih.gov/articles/PMC3612406/
  80. https://onlinelibrary.wiley.com/doi/10.1111/jocd.16427
  81. https://bookcafe.yuntsg.com/ueditor/jsp/upload/file/20240618/1718672963573025091.pdf
  82. https://www.medicaljournals.se/acta/content/html/10.2340/00015555-3035
  83. https://tau.amegroups.org/article/view/91877/html
  84. https://pmc.ncbi.nlm.nih.gov/articles/PMC1472914/
  85. https://bjui-journals.onlinelibrary.wiley.com/doi/abs/10.1111/j.1464-410X.2011.10195.x
  86. https://wjmh.org/DOIx.php?id=10.5534/kja.2012.30.1.45
  87. https://pmc.ncbi.nlm.nih.gov/articles/PMC2963784/
  88. https://ijdvl.com/superiority-of-dutasteride-over-finasteride-in-hair-regrowth-and-reversal-of-miniaturization-in-men-with-androgenetic-alopecia-a-randomized-controlled-open-label-evaluator-blinded-study/
  89. https://pmc.ncbi.nlm.nih.gov/articles/PMC6388756/
  90. https://www.pagepress.org/journals/dr/article/view/9909/9546
  91. https://wjmh.org/DOIx.php?id=10.5534/wjmh.230327
  92. https://www.sciencedirect.com/science/article/abs/pii/S1743609515333166
  93. https://www.sciencedirect.com/science/article/abs/pii/S0302283803001982
  94. https://karger.com/drm/article/240/5-6/833/913258/Dutasteride-for-the-Treatment-of-Androgenetic
  95. https://www.psychiatrist.com/jcp/why-odds-ratios-can-be-tricky-statistics/
  96. https://pubmed.ncbi.nlm.nih.gov/17299062/
  97. https://academic.oup.com/jcem/article-abstract/92/5/1659/2598215
  98. https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/021319s027lbl.pdf
  99. https://ecerm.org/m/journal/view.php?number=1373
  100. https://pubmed.ncbi.nlm.nih.gov/23589750/
  101. https://pubmed.ncbi.nlm.nih.gov/23021996/
  102. https://www.gsk.com/en-gb/media/press-releases/large-long-term-study-shows-dutasteride-reduced-prostate-cancer-risk-in-men-at-increased-risk-of-the-disease/
  103. https://www.medrxiv.org/content/10.1101/2025.08.21.25333991.full
  104. https://pmc.ncbi.nlm.nih.gov/articles/PMC10066399/
  105. https://pmc.ncbi.nlm.nih.gov/articles/PMC5818776/
  106. https://www.psychiatrist.com/jcp/analytical-review-depression-suicidality-finasteride/
  107. https://pmc.ncbi.nlm.nih.gov/articles/PMC12318778/
  108. https://pmc.ncbi.nlm.nih.gov/articles/PMC5237684/
  109. https://www.gendergp.com/medical-guide/dutasteride-in-gender-affirming-care/
  110. https://pubchem.ncbi.nlm.nih.gov/compound/Dutasteride
  111. https://www.chemicalbook.com/ChemicalProductProperty_EN_CB3254628.htm
  112. https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/022460s000lbl.pdf
  113. https://www.drugs.com/dosage/dutasteride.html
  114. https://pmc.ncbi.nlm.nih.gov/articles/PMC1472916/
  115. https://www.sciencedirect.com/science/article/abs/pii/S0090429502019052
  116. https://www.accessdata.fda.gov/drugsatfda_docs/nda/2001/21319_Duagen.cfm
  117. https://www.accessdata.fda.gov/drugsatfda_docs/appletter/2011/021319s023%2Cs025ltr.pdf
  118. https://www.gsk.com/en-gb/media/press-releases/gsk-receives-fda-complete-response-letter-for-avodart-for-prostate-cancer-risk-reduction-supplemental-indication/
  119. https://www.medicines.org.uk/emc/product/6758/smpc
  120. https://www.pmda.go.jp/files/000245812.pdf
  121. https://clinicaltrials.gov/study/NCT01299571
  122. https://www.ema.europa.eu/en/medicines/human/referrals/finasteride-dutasteride-containing-medicinal-products
  123. https://www.hpra.ie/safety-information/safety-notices/article/finasteride-and-dutasteride---new-measures-to-minimise-the-risk-of-suicidal-ideation
  124. https://www.famhp.be/en/news/prac_may_2025_new_risk_mitigation_measures_for_finasteride_and_dutasteride_and_start_of_a
  125. https://www.rxlist.com/dutasteride/generic-drug.htm
  126. https://www.drugs.com/dutasteride.html
  127. https://www.rxlist.com/avodart-drug.htm
  128. https://www.tevausa.com/news-and-media/press-releases/teva-announces-exclusive-launch-of-generic-avodart-capsules-in-the-united-states/
  129. https://www.drugs.com/availability/generic-avodart.html
  130. https://www.drugpatentwatch.com/p/generic-api/dutasteride
  131. https://www.geneesmiddeleninformatiebank.nl/pars/h117492.pdf
  132. https://oladoctor.com/en/medicines/spain/dutasterida-cinfa-05-mg-capsulas-blandas-efg
  133. https://www.medicalmex.com/avodart-dutasteride/
  134. https://www.reddit.com/r/bali/comments/1llaq4k/dutasteride_indonesia/
  135. https://pubmed.ncbi.nlm.nih.gov/40736519/
  136. https://pubmed.ncbi.nlm.nih.gov/38321615/
  137. https://www.sciencedirect.com/science/article/pii/S2666328725001014
  138. https://www.jaadcasereports.org/article/S2352-5126%2824%2900398-9/fulltext
  139. https://pubmed.ncbi.nlm.nih.gov/39304797/
  140. https://pubmed.ncbi.nlm.nih.gov/40955380/
  141. https://pubmed.ncbi.nlm.nih.gov/38684046/
  142. https://pubmed.ncbi.nlm.nih.gov/40114308/
  143. https://pubmed.ncbi.nlm.nih.gov/41051009/
  144. https://pmc.ncbi.nlm.nih.gov/articles/PMC11172682/
  145. https://nextstepsinderm.com/derm-topics/dutasteride-therapeutic-cheat-sheet/
  146. https://www.tandfonline.com/doi/abs/10.1080/20415990.2024.2437973
Add your contribution
Related Hubs
User Avatar
No comments yet.