Dutasteride is an oral drug that blocks both forms of 5α-reductase, the enzyme that converts testosterone into the more potent androgen dihydrotestosterone (DHT). It is FDA-approved at 0.5 mg/day as Avodart, and in a combined capsule with tamsulosin as Jalyn, to treat an enlarged prostate (benign prostatic hyperplasia, BPH). It is not FDA-approved for hair loss, but it has been tested in randomized trials for male pattern hair loss and is prescribed for it in South Korea and Japan.
It is the close relative of finasteride, and the two drugs share most of their warnings. The main differences are that dutasteride also blocks the type 1 enzyme, lowers serum DHT by about 90–95% rather than about 70%, and has a half-life of about 5 weeks instead of about 6 hours. That long half-life means the drug stays in the body for months after the last dose. In the context of anabolic steroids, the key trial found that blocking DHT with dutasteride did not reduce testosterone’s effect on muscle, but at those testosterone levels it also did not reduce prostate size, PSA or skin oil.
This page summarizes what the FDA label, the major randomized trials and large observational studies report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Dual (type 1 and type 2) 5α-reductase inhibitor (4-azasteroid) |
| Brands / approval | Avodart 0.5 mg (NDA 021319, approved November 2001); Jalyn 0.5 mg dutasteride + 0.4 mg tamsulosin (NDA 022460, approved June 2010); generics available |
| Route | Oral soft gelatin capsule, swallowed whole |
| Labeled dose | 0.5 mg once daily, alone or with tamsulosin 0.4 mg (BPH only) |
| Half-life (label) | About 5 weeks at steady state; still detectable in serum for 4–6 months after stopping |
| Effect on serum DHT | Median about 90% lower after 2 weeks and 93–95% lower over 4 years |
| US status | Prescription only; not a scheduled anabolic steroid |
| WADA status | Not named on the 2026 Prohibited List |
What it is
Dutasteride is a synthetic 4-azasteroid with the formula C₂₇H₃₀F₆N₂O₂ and a molecular weight of 528.5 (Avodart label; PubChem). It is not a hormone and does not bind the human androgen receptor. It is insoluble in water, so each capsule holds 0.5 mg dissolved in an oily mixture of mono- and diglycerides.
Humans make DHT with two 5α-reductase isozymes. According to the label, type 2 is mainly active in the reproductive tissues, while type 1 also converts testosterone in the skin and liver. Dutasteride is a competitive inhibitor of both and forms a stable complex with the enzyme that comes apart extremely slowly. Finasteride, by contrast, is far more selective for type 2 (see the finasteride page for the isozyme details).
| Feature | Dutasteride | Finasteride |
|---|---|---|
| Isozymes blocked | Type 1 and type 2 | Mainly type 2 |
| Serum DHT, head-to-head in BPH (24 weeks) | −94.7% on 0.5 mg | −70.8% on 5 mg |
| Serum DHT, head-to-head in healthy men (1 year) | −94% on 0.5 mg | −73% on 5 mg |
| Plasma half-life | About 5 weeks | About 6–8 h |
| US-approved doses | 0.5 mg (BPH) | 5 mg (BPH); 1 mg (hair loss) |
| US hair-loss approval | No | Yes (Propecia 1 mg) |
Sources: Clark et al., JCEM 2004; Amory et al., JCEM 2007; Avodart label; finasteride labels.
In the Clark trial, 399 men with BPH were randomized to one of five dutasteride doses (0.01–5 mg), finasteride 5 mg or placebo for 24 weeks. Besides the deeper average drop, DHT suppression was much less variable on dutasteride (standard deviation 3.3%) than on finasteride (18.3%), and reached 98.4% on 5 mg dutasteride.
Pharmacokinetics
From the Avodart label:
| Parameter | Value |
|---|---|
| Time to peak | 2–3 h after a single 0.5 mg dose |
| Oral bioavailability | About 60% (range 40–94%, in 5 subjects); food lowers peak level by 10–15%, not clinically relevant |
| Volume of distribution | 300–500 L |
| Protein binding | 99.0% to albumin; 96.6% to alpha-1 acid glycoprotein |
| Metabolism | Extensive, by CYP3A4 and CYP3A5; one metabolite (6β-hydroxydutasteride) is about as active as the parent drug |
| Excretion | Mainly in feces; under 1% unchanged in urine |
| Terminal half-life | About 5 weeks at steady state |
| Steady-state level | About 40 ng/mL on 0.5 mg/day; 65% of steady state after 1 month and about 90% after 3 months |
| After stopping | Serum levels stay above 0.1 ng/mL for 4–6 months |
The half-life lengthens with age. After a single 5 mg dose, it was about 170 h in men aged 20–49, about 260 h at 50–69 and about 300 h over 70. The longer 5-week figure applies at steady state, after months of daily dosing.
Dutasteride also reaches semen. In 26 healthy men on 0.5 mg/day for a year, semen levels averaged 3.4 ng/mL (range 0.4–14 ng/mL), about 11.5% of the serum level.
Hormonal effects
| Measure | Result on 0.5 mg/day |
|---|---|
| Serum DHT | Median −85% at 1 week, −90% at 2 weeks, −93% to −95% over 1–4 years |
| Serum testosterone | Median +19% at 1–2 years, +26% at 3 years, +22% at 4 years, within the normal range |
| LH | Median +12% at 6 months and +19% at 12 and 24 months (men with BPH) |
| SHBG, estradiol, FSH, free T4, DHEA | No clinically significant change vs placebo over 52 weeks (healthy men) |
| Prostate tissue (5 mg/day for up to 12 weeks) | DHT 784 vs 5,793 pg/g on placebo; testosterone 2,073 vs 93 pg/g |
| Lipids and bone density | No change over 52 weeks (healthy men) |
In the 52-week healthy-volunteer study, total testosterone rose by 97.1 ng/dL more than placebo at week 8, and thyroid-stimulating hormone (TSH) by 0.4 mcIU/mL at week 52. Both returned to baseline within 24 weeks of stopping (Avodart label).
Approved medical use
| Product | Indication | Labeled dose |
|---|---|---|
| Avodart 0.5 mg | Symptomatic BPH in men with an enlarged prostate: to improve symptoms and lower the risk of acute urinary retention and BPH-related surgery; also with tamsulosin | 0.5 mg once daily, with or without food |
| Jalyn (0.5 mg dutasteride + 0.4 mg tamsulosin) | Symptomatic BPH in men with an enlarged prostate | 1 capsule once daily, about 30 minutes after the same meal each day |
Both labels state that dutasteride is not approved to prevent prostate cancer (Jalyn label). Avodart is not indicated for women or children. Capsules must be swallowed whole, because the contents can irritate the mouth and throat. The patient information notes that a treatment period of at least 6 months is usually needed to judge whether it works.
What the research shows
Benign prostatic hyperplasia
Three identical 2-year trials (ARIA3001–3003) randomized 4,325 men aged 50 or older with moderate-to-severe symptoms and a prostate of at least 30 cm³ to dutasteride 0.5 mg/day or placebo (Roehrborn et al., Urology 2002). Serum DHT fell by a mean of 90.2% at 24 months. The pooled 2-year results in the label:
| Outcome at 24 months | Placebo | Dutasteride 0.5 mg |
|---|---|---|
| Acute urinary retention | 4.2% | 1.8% (57% risk reduction, 95% CI 38–71%) |
| BPH-related surgery | 4.1% | 2.2% (48% risk reduction, 95% CI 26–63%) |
| Prostate volume change | −2.2% | −26.7% |
| Symptom score change (0–35 scale, baseline ≈17) | −1.7 | −3.8 |
| Peak urine flow change | +0.7 mL/s | +1.8 mL/s |
The benefits were maintained through a further 2 years of open-label treatment.
Combination with tamsulosin
The 4-year CombAT trial randomized 4,844 men with BPH to dutasteride 0.5 mg, tamsulosin 0.4 mg (an alpha-blocker that relaxes prostate muscle) or both (Roehrborn et al., Eur Urol 2010). The label reports:
| Outcome | Combination | Dutasteride | Tamsulosin |
|---|---|---|---|
| Symptom score change at 24 months | −6.2 | −4.9 | −4.3 |
| Symptom score change at 48 months | −6.3 | −5.3 | −3.8 |
| Prostate volume change at 48 months | −27.3% | −28.0% | +4.6% |
| Ejaculation disorders (all trial) | 11% | 2% | 4% |
The combination improved symptoms more than either drug alone. For the 4-year risk of acute urinary retention or surgery, it beat tamsulosin but gave no benefit over dutasteride alone. There was no placebo arm.
Head-to-head with finasteride for BPH
The EPICS trial randomized 1,630 men with BPH to dutasteride 0.5 mg (n = 813) or finasteride 5 mg (n = 817) for 12 months (Nickel et al., BJU Int 2011). Despite dutasteride’s deeper DHT suppression, the two drugs shrank the prostate equally, with no significant difference in symptom scores, urine flow or adverse events. For the prostate, the extra type 1 inhibition did not translate into a measurable clinical advantage in this trial.
Prostate cancer prevention
The REDUCE trial randomized 8,231 men aged 50–75 with a PSA of 2.5–10.0 ng/mL and a recent negative biopsy to dutasteride 0.5 mg/day or placebo for 4 years, with scheduled biopsies at 2 and 4 years (Andriole et al., NEJM 2010):
| Outcome | Placebo | Dutasteride |
|---|---|---|
| Prostate cancer found on biopsy | 858 of 3,424 (25.1%) | 659 of 3,305 (19.9%); 22.8% relative reduction (95% CI 15.2–29.8) |
| Gleason 7–10 tumors, years 1–4 | 233 of 3,407 | 220 of 3,299 (no significant difference) |
| Gleason 8–10 tumors, years 3–4 | 1 | 12 (p = 0.003) |
| Gleason 8–10 tumors, whole trial (label) | 0.5% | 1.0% |
| Acute urinary retention | 6.7% | 1.6% |
The Gleason score grades how aggressive a prostate cancer looks under the microscope; 8–10 is high grade. The fall was in lower-grade tumors, and the small excess of high-grade tumors led to the warning on the label. As with finasteride, the FDA did not approve dutasteride for prevention.
Male pattern hair loss
Dutasteride is not FDA-approved for hair loss, but it is prescribed for male pattern hair loss in South Korea and Japan (Lee et al., Ann Dermatol 2025), and several randomized trials have tested it:
| Trial | Design | Main result |
|---|---|---|
| Olsen et al., JAAD 2006 | 416 men aged 21–45; dutasteride 0.05, 0.1, 0.5 or 2.5 mg, finasteride 5 mg or placebo; 24 weeks | Hair count rose with dose; 2.5 mg beat finasteride at 12 and 24 weeks |
| Eun et al., JAAD 2010 | 153 Korean men aged 18–49; 0.5 mg vs placebo; 6 months | +12.2 vs +4.7 hairs/cm² (p = 0.03) |
| Gubelin Harcha et al., JAAD 2014 | 917 men aged 20–50; dutasteride 0.02, 0.1 or 0.5 mg, finasteride 1 mg or placebo; 24 weeks | 0.5 mg increased hair count and hair width more than finasteride 1 mg (p = 0.003) and placebo; adverse events similar across groups |
| Tsunemi et al., J Dermatol 2016 | 120 Japanese men; open-label 0.5 mg; 52 weeks | Hair count and width improved; drug-related adverse events in 17%, none leading to withdrawal |
| Lee et al., Ann Dermatol 2025 | 139 Korean men; 0.2 mg, 0.5 mg or placebo; 24 weeks | Vertex hair count +21.5 on 0.2 mg vs +6.0 on placebo; 0.2 mg as effective as 0.5 mg |
Two meta-analyses pooled these data:
- Across 3 head-to-head trials with 576 men, dutasteride increased total hair count in the target area more than finasteride after 24 weeks (mean difference 28.6 hairs, 95% CI 18.8–38.4), with no significant difference in sexual side effects (Zhou et al., Clin Interv Aging 2019). One of these trials compared dutasteride 2.5 mg with finasteride 5 mg, not the hair-loss doses.
- A network meta-analysis of 23 studies ranked dutasteride 0.5 mg first for total hair count at 24 weeks, ahead of finasteride 1 mg by 7.1 hairs/cm² (95% CI 5.1–9.3). At 48 weeks, finasteride doses ranked highest for hair count (Gupta et al., JAMA Dermatol 2022).
The main limits are short follow-up (most trials lasted 24 weeks) and few placebo-controlled data beyond 6 months, compared with the 5-year data for finasteride.
Use alongside testosterone and other anabolic steroids
The most relevant trial for this library is the 5α-Reductase Trial (Bhasin et al., JAMA 2012). It enrolled 139 healthy men aged 18–50 and shut down their own testosterone with monthly leuprolide (a GnRH agonist). They then received testosterone enanthate at 50, 125, 300 or 600 mg/week for 20 weeks, plus either placebo or dutasteride 2.5 mg/day, five times the labeled dose. 102 men finished.
| Weekly testosterone dose | Mean testosterone, placebo / dutasteride | Fat-free mass gain, placebo | Fat-free mass gain, dutasteride |
|---|---|---|---|
| 50 mg | 385 / 519 ng/dL | +0.8 kg | +0.6 kg |
| 125 mg | 822 / 895 ng/dL | +3.5 kg | +2.6 kg |
| 300 mg | 1,702 / 1,706 ng/dL | +5.7 kg | +5.8 kg |
| 600 mg | 3,578 / 3,898 ng/dL | +8.1 kg | +7.1 kg |
DHT rose with dose in the placebo groups but stayed suppressed in all dutasteride groups. The dose-adjusted difference in fat-free mass was not significant (p = 0.18). Fat mass, leg and chest press strength, sexual function, hematocrit and cholesterol changes also did not differ between groups. The authors concluded that conversion to DHT is not essential for testosterone’s effects on muscle.
The same trial produced a less expected result. Prostate volume, PSA, forehead sebum (skin oil) and acne scores also did not differ between the dutasteride and placebo groups. The authors’ explanation is that DHT amplifies testosterone’s effect in tissues such as the prostate mainly when testosterone is low. At normal or high testosterone levels, testosterone alone appears enough to drive those tissues. They noted that blocking 5α-reduction “may not necessarily be effective in sparing the prostate, depending upon androgen dose.”
Important limits:
- No hair outcomes. The trial did not measure scalp hair, and no trial has tested whether dutasteride prevents hair loss caused by anabolic steroids.
- Short and small. Twenty weeks, about 17 men randomized per group (102 finished), all healthy men without prostate disease.
- Already 5α-reduced steroids. As with finasteride, dutasteride has no mechanism to change the effects of DHT itself or DHT-derived steroids. The theoretical concern that blocking 5α-reductase could strengthen nandrolone in some tissues (rat and in-vitro data) applies to both drugs and is covered on the finasteride page.
Side effects and risks
Sexual side effects
These are the most common adverse reactions on the label. They were concentrated in the first 6 months and became similar to placebo later. Pooled data from the three 2-year BPH trials (2,167 men on dutasteride, 2,158 on placebo):
| Event | Dutasteride, months 0–6 | Placebo, months 0–6 | Dutasteride, months 19–24 | Placebo, months 19–24 |
|---|---|---|---|---|
| Impotence | 4.7% | 1.7% | 0.8% | 0.9% |
| Decreased libido | 3.0% | 1.4% | 0.3% | 0.1% |
| Ejaculation disorders | 1.4% | 0.5% | 0.1% | 0.0% |
| Breast disorders (enlargement, tenderness) | 0.5% | 0.2% | 0.6% | 0.1% |
Withdrawal from the trials for adverse reactions occurred in 4% on dutasteride vs 3% on placebo, most often for impotence (1%). Adding tamsulosin raised the rate of ejaculation disorders (11% vs 2% on dutasteride alone in CombAT).
In younger men treated for hair loss:
- A randomized trial in 117 men aged 23–50 found sexual adverse events in 16% on dutasteride 0.5 mg vs 8% on placebo over 24 weeks. All were mild to moderate and resolved, and none led to stopping treatment (Tsai et al., J Dermatol 2018).
- A meta-analysis of 15 placebo-controlled hair-loss trials found a relative risk of sexual dysfunction of 1.37 (95% CI 0.81–2.32) for dutasteride, which was not statistically significant, and 1.66 (1.20–2.30) for finasteride. The authors noted that dutasteride data were limited (Lee et al., Acta Derm Venereol 2019).
Persistent symptoms after stopping
The label states that impotence, decreased libido and ejaculation disorders associated with dutasteride “may persist after treatment discontinuation,” and that the role of dutasteride in this persistence is unknown. How often this happens has not been measured.
Depression
“Depressed mood” is listed as a postmarketing reaction on the label. Two large cohort studies in older men reported separate or comparable results for dutasteride:
| Study | Population | Depression | Suicide |
|---|---|---|---|
| Welk et al., JAMA Intern Med 2017 | 93,197 Ontario men aged 66 or older starting finasteride or dutasteride | HR 1.94 (95% CI 1.73–2.16) in the first 18 months; HR 1.22 (1.08–1.37) afterward | HR 0.88 (0.53–1.45), not significant |
| Garcia-Argibay et al., JAMA Netw Open 2022 | 2,236,876 Swedish men; 8,774 started dutasteride | Dutasteride HR 1.68 (1.43–1.96), constant over time | Dutasteride HR 0.98 (0.62–1.54), not significant |
In the Ontario study, self-harm was also raised in the first 18 months (HR 1.88, 95% CI 1.34–2.64), and the type of drug did not change the associations. The Swedish study found no difference between finasteride and dutasteride for depression. Both are observational studies in older men, mostly treated for the prostate, and cannot prove cause.
High-grade prostate cancer and PSA
The label warns that 5α-reductase inhibitors may increase the risk of high-grade prostate cancer (REDUCE: Gleason 8–10 in 1.0% vs 0.5%). Dutasteride lowers PSA by about 50% within 3–6 months, including when cancer is present, so an unadjusted PSA can hide a rising value. See the Monitoring section.
Breast changes
Breast enlargement and tenderness are listed adverse reactions. Across the three 4-year BPH trials there was 1 case of male breast cancer on dutasteride and 1 on placebo, and none in CombAT or REDUCE. Male breast cancer has been reported after marketing. The label states that the relationship between long-term dutasteride use and male breast cancer is unknown.
Semen and fertility
The label reports a 52-week study in healthy men aged 18–52 (27 on dutasteride, 23 on placebo). Compared with placebo, mean total sperm count fell by 23%, semen volume by 26% and sperm motility by 18%. Sperm concentration and shape were unaffected and averages stayed in the normal range. However, total sperm count was still 23% below baseline 24 weeks after stopping, and 2 men had drops of more than 90% at 52 weeks, with only partial recovery. The effect on an individual’s fertility is unknown.
A separate trial in 99 healthy men compared dutasteride 0.5 mg, finasteride 5 mg and placebo for a year (Amory et al., JCEM 2007):
| Measure | Dutasteride | Finasteride |
|---|---|---|
| Total sperm count at 26 weeks | −28.6% | −34.3% |
| Semen volume at 52 weeks | −29.7% (significant) | −14.5% |
| Total sperm count 24 weeks after stopping | −23.3% | −6.2% |
The authors described the changes as mild and apparently reversible. The slower return on dutasteride fits its longer half-life.
Cardiac failure signal
In CombAT, the composite term “cardiac failure” occurred in 0.7% on the combination, 0.1% on dutasteride alone and 0.6% on tamsulosin alone. In REDUCE it occurred in 0.6% on dutasteride vs 0.4% on placebo. Most affected men had other risk factors, and the label states that no causal link has been established and that overall cardiovascular events were not imbalanced.
Pregnancy, handling and blood donation
- Pregnancy. Dutasteride is contraindicated in pregnancy. Blocking DHT can cause abnormal development of the external genitals of a male fetus; in rats and rabbits this occurred at doses below the human dose.
- Skin absorption. Based on animal studies, the label states that dutasteride can be absorbed through the skin. Women who are or may become pregnant should not handle the capsules, and skin that touches a leaking capsule should be washed with soap and water.
- Semen. Assuming complete absorption of 5 mL of semen, the label estimates a partner’s blood level about 100 times lower than levels that caused genital abnormalities in animal studies.
- Blood donation. Men should not donate blood until at least 6 months after the last dose, to avoid exposing a pregnant transfusion recipient.
Interactions and other cautions
- Strong CYP3A4 inhibitors. Dutasteride is cleared by CYP3A4/5. The label advises caution with potent, long-term inhibitors such as ritonavir; the effect has not been formally studied. Verapamil and diltiazem lowered dutasteride clearance by 37% and 44%, which the label does not consider clinically significant.
- No effect found on tamsulosin, terazosin, digoxin or warfarin kinetics, and cholestyramine did not reduce absorption.
- Liver. Hepatic impairment has not been studied; because the drug is extensively metabolized, exposure could be higher.
- Kidneys. No dose adjustment is needed.
- Hypersensitivity. Contraindicated after serious skin reactions or angioedema with dutasteride or another 5α-reductase inhibitor.
- Overdose. Volunteers received doses up to 40 mg (80 times the therapeutic dose) for 7 days without significant safety concerns, and 60 subjects took 5 mg/day for 6 months without additional adverse effects.
- Animal tumors. In a 2-year rat study, Leydig cell (testicular) adenomas increased at 135 times the maximum recommended human dose, which the label links to the rise in LH that follows 5α-reductase inhibition.
Monitoring
The label gives specific rules for reading PSA on dutasteride. The new baseline is set after 3 months, earlier than the 6 months used for finasteride:
| Situation | Label guidance |
|---|---|
| Starting treatment | Set a new PSA baseline at least 3 months after starting, then monitor periodically |
| Single PSA value after 3 or more months on treatment | Double it before comparing with normal ranges for untreated men |
| Any confirmed rise from the lowest on-treatment value | Evaluate for prostate cancer, even if still in the normal range |
| Percent free PSA | No adjustment needed |
| Missed doses | Can affect PSA results |
Legal status and use outside medicine
In the US, dutasteride is a prescription-only drug, with brand and generic products listed on Drugs@FDA. It is not named in Schedule III (21 CFR 1308.13), where anabolic steroids are listed. Its only US-approved use is BPH; use for hair loss in the US is off-label.
Dutasteride and other 5α-reductase inhibitors are not named on the WADA 2026 Prohibited List. Anti-doping laboratories still regard 5α-reductase inhibitors as potential confounders of the urinary steroid profile, because they change how testosterone and related steroids are broken down (Iannella et al., Drug Test Anal 2021). That study tested finasteride, not dutasteride.
Key takeaways
- A deeper, longer-lasting DHT blocker than finasteride. Dutasteride blocks both 5α-reductase isozymes and lowers serum DHT by about 90–95%, compared with about 70% for finasteride. Its half-life is about 5 weeks, and it stays detectable for 4–6 months after stopping.
- Approved in the US only for BPH. At 0.5 mg/day it cut the 2-year risk of urinary retention by 57% and of surgery by 48%, but it performed no better than finasteride 5 mg in a head-to-head BPH trial.
- Effective for male pattern hair loss in short trials. At 0.5 mg it grew more hair than finasteride 1 mg over 24 weeks, but long-term placebo-controlled data are limited, and it is not FDA-approved for this use.
- Muscle gains intact, but no proven tissue protection at high testosterone levels. Blocking DHT did not reduce lean-mass gains from testosterone up to 600 mg/week. At those doses it also did not reduce prostate volume, PSA or sebum, and hair was not studied.
- Sexual effects, mood and fertility are the main concerns. Sexual side effects were two to three times as common as on placebo in the first 6 months, then fell to placebo levels. Depression risk was raised in large cohorts, and sperm count stayed about 23% lower 6 months after stopping in a label study.
- Handling and PSA rules matter. It is absorbed through the skin, so pregnant women should not handle capsules; blood donation is deferred for 6 months; and PSA values must be doubled after 3 months on treatment.
Sources
- Waylis Therapeutics. Avodart (dutasteride) soft gelatin capsules, prescribing information, DailyMed version March 2025. DailyMed; Drugs@FDA, NDA 021319.
- Waylis Therapeutics. Jalyn (dutasteride and tamsulosin hydrochloride) capsules, prescribing information, DailyMed version March 2026. DailyMed; Drugs@FDA, NDA 022460.
- National Center for Biotechnology Information. Dutasteride, PubChem CID 6918296. PubChem.
- Clark RV, Hermann DJ, Cunningham GR, et al. Marked suppression of dihydrotestosterone in men with benign prostatic hyperplasia by dutasteride, a dual 5alpha-reductase inhibitor. J Clin Endocrinol Metab. 2004;89(5):2179–2184. PubMed.
- Amory JK, Wang C, Swerdloff RS, et al. The effect of 5alpha-reductase inhibition with dutasteride and finasteride on semen parameters and serum hormones in healthy men. J Clin Endocrinol Metab. 2007;92(5):1659–1665. PubMed.
- Roehrborn CG, Boyle P, Nickel JC, et al. Efficacy and safety of a dual inhibitor of 5-alpha-reductase types 1 and 2 (dutasteride) in men with benign prostatic hyperplasia. Urology. 2002;60(3):434–441. PubMed.
- Roehrborn CG, Siami P, Barkin J, et al. The effects of combination therapy with dutasteride and tamsulosin on clinical outcomes in men with symptomatic benign prostatic hyperplasia: 4-year results from the CombAT study. Eur Urol. 2010;57(1):123–131. PubMed.
- Nickel JC, Gilling P, Tammela TL, et al. Comparison of dutasteride and finasteride for treating benign prostatic hyperplasia: the Enlarged Prostate International Comparator Study (EPICS). BJU Int. 2011;108(3):388–394. PubMed.
- Andriole GL, Bostwick DG, Brawley OW, et al. Effect of dutasteride on the risk of prostate cancer. N Engl J Med. 2010;362(13):1192–1202. PubMed.
- Olsen EA, Hordinsky M, Whiting D, et al. The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. J Am Acad Dermatol. 2006;55(6):1014–1023. PubMed.
- Eun HC, Kwon OS, Yeon JH, et al. Efficacy, safety, and tolerability of dutasteride 0.5 mg once daily in male patients with male pattern hair loss: a randomized, double-blind, placebo-controlled, phase III study. J Am Acad Dermatol. 2010;63(2):252–258. PubMed.
- Gubelin Harcha W, Barboza Martínez J, Tsai TF, et al. A randomized, active- and placebo-controlled study of the efficacy and safety of different doses of dutasteride versus placebo and finasteride in the treatment of male subjects with androgenetic alopecia. J Am Acad Dermatol. 2014;70(3):489–498.e3. PubMed.
- Tsunemi Y, Irisawa R, Yoshiie H, et al. Long-term safety and efficacy of dutasteride in the treatment of male patients with androgenetic alopecia. J Dermatol. 2016;43(9):1051–1058. PubMed.
- Lee S, Kim JE, Lew BL, et al. Efficacy and safety of low-dose (0.2 mg) dutasteride for male androgenic alopecia: a multicenter, randomized, double-blind, placebo-controlled, parallel-group phase III clinical trial. Ann Dermatol. 2025;37(4):183–190. PubMed.
- Zhou Z, Song S, Gao Z, et al. The efficacy and safety of dutasteride compared with finasteride in treating men with androgenetic alopecia: a systematic review and meta-analysis. Clin Interv Aging. 2019;14:399–406. PubMed.
- Gupta AK, Venkataraman M, Talukder M, Bamimore MA. Relative efficacy of minoxidil and the 5-α reductase inhibitors in androgenetic alopecia treatment of male patients: a network meta-analysis. JAMA Dermatol. 2022;158(3):266–274. PubMed.
- Bhasin S, Travison TG, Storer TW, et al. Effect of testosterone supplementation with and without a dual 5α-reductase inhibitor on fat-free mass in men with suppressed testosterone production: a randomized controlled trial. JAMA. 2012;307(9):931–939. PubMed; PMC.
- Tsai TF, Choi GS, Kim BJ, et al. Prospective randomized study of sexual function in men taking dutasteride for the treatment of androgenetic alopecia. J Dermatol. 2018;45(7):799–804. PubMed.
- Lee S, Lee YB, Choe SJ, Lee WS. Adverse sexual effects of treatment with finasteride or dutasteride for male androgenetic alopecia: a systematic review and meta-analysis. Acta Derm Venereol. 2019;99(1):12–17. PubMed.
- Welk B, McArthur E, Ordon M, et al. Association of suicidality and depression with 5α-reductase inhibitors. JAMA Intern Med. 2017;177(5):683–691. PubMed.
- Garcia-Argibay M, Hiyoshi A, Fall K, Montgomery S. Association of 5α-reductase inhibitors with dementia, depression, and suicide. JAMA Netw Open. 2022;5(12):e2248135. PubMed.
- Iannella L, Colamonici C, Curcio D, et al. 5α-reductase inhibitors: evaluation of their potential confounding effect on GC-C-IRMS doping analysis. Drug Test Anal. 2021;13(11-12):1852–1861. PubMed.
- US Code of Federal Regulations. 21 CFR 1308.13, Schedule III. eCFR.
- World Anti-Doping Agency. The 2026 Prohibited List. WADA.