Dutasteride 500micrograms/5ml oral solution
Requires a prescription from a doctor or prescriber
Dutasteride is an oral synthetic 4-azasteroid commonly marketed under the trade name Avodart.
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
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Drug safety updates
MHRA alerts for Dutasteride
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Dutasteride
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Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Dutasteride
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
WHO defined daily dose (DDD)
500 microgram
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Tablets & capsules
(2)Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 29 · Randomised trials: 17 · 2010–2026
Showing the 50 most relevant studies, sorted by most relevant.
Zhongbao Zhou, Shiqiang Song, Zhenli Gao, et al.
Clinical Interventions in Aging, 2019
Solam Lee, Young Bin Lee, S. Choe, et al.
Acta dermato-venereologica, 2019
Almuntaserbellah Almudaimeegh, Hanadi M ALMutairi, Fatimah AlTassan, et al.
Dermatology Reports, 2024
Almeziny A, Alghamdi A, Alajlan A, et al.
2025
- Alopecia
- 5-alpha Reductase Inhibitors
- Dutasteride
BackgroundAndrogenic alopecia (AGA) is a common condition characterized by progressive hair loss influenced by dihydrotestosterone (DHT). While oral dutasteride has shown efficacy in treating AGA, concerns about systemic side effects have prompted interest in localized treatments such as intralesional administration.AimsThis systematic review evaluates the effectiveness and safety of intralesional dutasteride for treating AGA in adults.MethodsFollowing PRISMA guidelines, we conducted a comprehensive search of multiple databases for studies involving adults (≥ 18 years) with AGA treated with intralesional dutasteride. Eligible studies included randomized controlled trials, non-randomized studies, cohort studies, and observational studies. Exclusion criteria were animal studies, duplicate publications, and studies lacking relevant outcome data. The primary outcomes were improvements in hair density, hair thickness, and photographic evidence of hair growth. Secondary outcomes assessed safety, including local and systemic adverse events. Data extraction and quality assessment were independently performed by two reviewers.ResultsIncluded studies consistently reported improvements in hair density and thickness following intralesional dutasteride treatment, with photographic evidence supporting visual improvement. Treatment was generally well tolerated, with minimal adverse events such as mild scalp irritation and no significant systemic effects reported. However, the studies varied in methodology, sample size, and follow-up duration.ConclusionsIntralesional dutasteride appears to be a promising treatment option for AGA, offering localized efficacy with a favorable safety profile. Nonetheless, the current evidence is limited by heterogeneity and a lack of large-scale, high-quality trials. Further standardized research is needed to confirm these findings.
Abstract licence: CC BY
Niaga KJK, Rinaldi FX, Nathania N, et al.
2025
PurposeAlpha-blockers and 5-alpha reductase inhibitors (5ARIs) are well-established treatments for symptoms of benign prostatic hyperplasia (BPH). Despite their therapeutic benefits, concerns have been raised regarding a potential association between these medications and an increased risk of dementia. However, current evidence remains inconsistent, highlighting the need for further evaluation. This study aims to assess the potential dementia risk among patients receiving alpha-blockers and 5ARIs.MethodsFollowing PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-analyses) guidelines (PROSPERO CRD42025643431), 7 databases were systematically searched through December 2024 for studies examining the association between alpha-blockers or 5ARIs and dementia risk in patients with BPH. Risk of bias was assessed using the ROBINS-I (Risk of Bias in Non-randomized Studies of Interventions) tool. A Bayesian network meta-analysis was performed to estimate risk ratios with 95% credible intervals and to generate surface under the cumulative ranking curve (SUCRA) values.ResultsFive multicenter studies involving 3,650,434 patients (mean age, 71.1 years) and demonstrating an overall low risk of bias were included. The network analysis indicated that neither alpha-blockers nor 5ARIs were significantly associated with an increased risk of dementia compared with no treatment. However, SUCRA values suggested a relatively higher probability of dementia risk for 5ARIs (finasteride and dutasteride), followed by tamsulosin, doxazosin, terazosin, and alfuzosin.ConclusionThis study found no significant association between the use of alpha-blockers or 5ARIs and increased dementia risk. These findings may assist clinicians in making more informed prescribing decisions, particularly for older male patients with BPH. Further large-scale research with extended follow-up periods is needed to strengthen the evidence across all BPH medications.
Abstract licence: CC BY-NC
Hyun-Min Seo
2023
Złotowska A, Jastrząb-Miśkiewicz B, Krajewski PK
2026
Introduction5α-reductase inhibitors (5-ARIs) are most commonly used to treat benign prostatic hyperplasia (BPH) and androgenetic alopecia (AGA). Preclinical and clinical studies suggest that in patients with AGA treated with 5-ARIs, a subset reports sexual adverse events, including decreased libido, erectile dysfunction, and ejaculatory disorders. This review explores the development of sexual dysfunction in patients with androgenetic alopecia due to the use of 5-ARIs, emphasizing their importance in the clinical diagnosis of health disorders coexisting with hair loss.MethodsA systematic review was conducted by searching electronic databases, including MEDLINE, Scopus, Web of Science and Google Scholar, according to the PRISMA guidelines. The search was limited to articles published in English and up to December 2025. Key search terms included "5α-reductase inhibitors" or "5-ARIs" or "finasteride" or "dutasteride" AND "side effects" or "sexual side effects" or "sexual" or "sexual dysfunction" AND "androgenetic alopecia" or "male pattern hair loss" or "female pattern hair loss." Data synthesis included findings from 41 studies, comprising 33 primary-evidence studies in AGA/MPHL/FPHL populations and 8 supporting-evidence studies providing pharmacokinetic, mixed-indication, or comparative context.Results5-ARIs are effective therapies for androgenetic alopecia and are generally well tolerated. Across placebo-controlled RCTs evaluating oral finasteride 1 mg in men with AGA, sexual adverse events were reported in 1.9-6.7% of treated patients compared with 0.9-3.9% in placebo groups, with most events mild and reversible upon discontinuation. Topical finasteride 0.25% was associated with lower rates of sexual adverse events (2.8%) compared with oral finasteride (4.8%). For dutasteride 0.5 mg, sexual adverse events ranged from 4.1 to 12.0% across RCTs, compared with 4.0-5.0% in placebo groups. No sexual adverse effects were consistently reported in women treated with 5-ARIs for AGA. In most reports, the effects were transient and reversible after discontinuation.ConclusionOverall, clinicians should counsel patients that most sexual side effects reported in controlled AGA studies are infrequent, mild, and reversible, but individual susceptibility varies. Shared decision-making, careful monitoring of sexual function, and further high-quality long-term studies-using standardized definitions of sexual dysfunction and persistence-are needed to quantify risks better and identify vulnerable subgroups.
Abstract licence: CC BY
Zhongbao Zhou, Yuanshan Cui, Jitao Wu, et al.
BMC Urology, 2019
Hirshburg Jm, Kelsey Pa, Therrien Ca, et al.
The Journal of clinical and aesthetic dermatology, 2016
Hehir CM, Calpin GG, Cullivan O, et al.
2026
- Prostatic Hyperplasia
- Postoperative Complications
- Transurethral Resection of Prostate
ObjectiveTo critically evaluate the existing evidence base surrounding the efficacy of preoperative 5-alpha reductase inhibitor (5ARI) administration in the reduction of perioperative complication rates in transurethral resection of prostate (TURP).MethodsIn April 2025, a systematic search of on-line databases was conducted to identify randomised controlled trials (RCTs) that compared surgical outcomes and complication rates in patients undergoing TURP for benign prostatic hyperplasia (BPH) who were treated preoperatively with 5ARI (finasteride or dutasteride) as compared to placebo/none. The efficacy of preoperative finasteride was evaluated through outcomes related to blood loss, rate of blood transfusion, and operative time. The physiological mechanism of 5ARI treatment was evaluated through microvessel density (MVD) and vascular endothelial growth factor (VEGF) expression of the resected specimen.ResultsA total of 30 RCTs met the inclusion criteria for this meta-analysis in which a total of 2974 patients underwent TURP for BPH (1464 5ARI: 1410 Control). Intraoperative blood loss was significantly lower among 5ARI-treated patients (Z = 6.37, mean difference [MD] = -82.58 mL, 95% confidence interval [CI] -107.98 to -57.18; P 3, P ConclusionPreoperative administration of 5ARIs significantly reduces intraoperative blood loss and risk of requiring blood transfusion in patients undergoing TURP for BPH. Even short durations (2 weeks) of 5ARI therapy can significantly reduce prostate vascularity.
Abstract licence: CC BY-NC
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
1 found
Half-life
Not available
Mechanism
The 5α-reductase is a nuclear-bound steroid intracellular enzyme primarily locat…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
0.5 mg
Half-life
5 weeks
Protein binding
99%
[L10568]
Volume of distribution
300 to 500 L
Metabolism
Elimination
1-15%
Clearance
0.01 to 40 mg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L10568]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 785 interactions
The estimated dermal LD50 of dutasteride in rabbits is > 2,000 mg/kg.
[L6256]
Overdose
In studies of volunteers receiving single doses of dutasteride up to 40 mg (which is 80 times the therapeutic dose) for 7 days, there were no reports of clinically significant adverse events.
[L10568]
Low incidences of impotence, reduced libido, gynecomastia, and ejaculation disorder occurred significantly more often in dutasteride than placebo recipients.
[A178345]
There are no known antidotes for dutasteride. In case of overdose, appropriate symptomatic and supportive treatment should be given.
[L10568]
Nonclinical Toxicology
In a 2-year carcinogenicity mouse study, there was an increased incidence of benign hepatocellular adenomas in female mice receiving 250 mg/kg/day.
[L10568]
An increased incidence of Leydig cell hyperplasia was observed in male rats receiving doses of 7.5 mg/kg/day and greater. At tumorogenic doses, the luteinizing hormone (LH) levels in rats were increased by 167%.
There was no demonstrated a genotoxic potential of dutasteride or its metabolites in a bacterial mutagenesis assay, a chromosomal aberration assay in CHO cells, and a micronucleus assay in rats.
[L10568]
At much higher doses than the maximum recommended human dose (MRHD) in sexually mature male rats, dutasteride caused a dose- and time-dependent decrease in fertility, reduced cauda epididymal (absolute) sperm counts but not sperm concentration (at 50 and 500 mg/kg/day), reduced weights of the epididymis, prostate, and seminal vesicles, and microscopic changes in the male reproductive organs.
[L10568]
At exposures 425- and 315-fold the expected clinical exposure of dutasteride in rats and dogs, respectively, there were some signs of non-specific, reversible, centrally-mediated toxicity without associated histopathological changes.
[L10568]
Pregnancy and Lactation
As DHT is a necessary hormone for the development of male genitalia, exposure to dutasteride in pregnant women bearing male fetuses may cause fetal harm.
[L10568]
In animal reproduction and developmental toxicity studies, dutasteride inhibited normal development of external genitalia in male fetuses.
[L10568]
Although it is not known whether dutasteride is excreted in human milk, the use of dutasteride in women of childbearing potential, including nursing women.
[L10568]
In elderly patients, the half-life of dutasteride may increase. As the renal elimination of dutasteride is very minimal, the use of dutasteride in patients renal insufficiency is reported to be safe.
[L6256]
There are no specific dosage adjustment recommendations for use in elderly patients or patients with renal impairment.
[L10568]
By forming a stable complex with both type I and type II 5α-reductase, dutasteride inhibits its enzymatic action of converting testosterone to 5α-dihydrotestosterone (DHT), which is the androgen primarily responsible for the initial development and subsequent enlargement of the prostate gland. It is proposed that DHT is the principal androgen responsible for prostatic growth in later life-normal masculinization of the external genitalia and maturation of the prostate gland during development-thus reducing the serum DHT levels results in reduced prostatic volume and increased epithelial apoptosis.[A178375] Dutasteride is a competitive and specific inhibitor of both Type I and Type II 5α-reductase isoenzymes and when evaluated under in vitro and in vivo conditions, the dissociation of the drug from the drug-enzyme complex is reported to be extremely slow.[L10568] Dutasteride does not bind to the human androgen receptor.[L10568]
After 1 and 2 weeks of daily dosing with dutasteride 0.5 mg, median serum DHT concentrations were reduced by 85% and 90%, respectively.[L10568] The serum concentrations of DHT were maintained to be decreased by more than 90% in 85% of patients following 1 years' administration of oral dutasteride 0.5 mg/day.[A178345] As evident from the clinical studies, dutasteride may also cause decreases in serum PSA in the presence of prostate cancer.[L10568]
How the body processes this drug — absorption, distribution, metabolism, and elimination
While food intake reduced the maximum serum concentrations by 10 to 15%, food intake is reported to have a negligible effect on the bioavailability of the drug.
[L10568]
[L10568]
[L10568]
[L10568]
[L10568]
Therefore, on average, the dose unaccounted for approximated 55%, with a range between 5% and 97%.
[L10568]
[A178363]
Proteins and enzymes this drug interacts with in the body
PMID:20637498 PMID:38821050
Acts as a polyprenal reductase that mediates the reduction of polyprenal into dolichal in a NADP-dependent mechanism .
PMID:38821050
Dolichols are required for the synthesis of dolichol-linked monosaccharides and the oligosaccharide precursor used for N-glycosylation .
PMID:20637498 PMID:38821050
Also able to convert testosterone (T) into 5-alpha-dihydrotestosterone (DHT) PMID:17986282 PMID:26855069
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
Appears to function in modulating the activity of the immune system during the acute-phase reaction
ATC G04CB02
ATC G04CA52
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Dutasteride
Additional database identifiers
Drugs Product Database (DPD)
12580
ChemSpider
5293502
BindingDB
50340481
ZINC
ZINC000003932831
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11284
GenAtlas
SRD5A1
GeneCards
SRD5A1
GenBank Gene Database
M32313
GenBank Protein Database
177767
UniProt Accession
S5A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11285
GenAtlas
SRD5A2
GeneCards
SRD5A2
GenBank Gene Database
M74047
GenBank Protein Database
338469
Guide to Pharmacology
2633
UniProt Accession
S5A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:25812
GeneCards
SRD5A3
UniProt Accession
SR5A3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
UniProt Accession
SC6A3_MOUSE
UniProt Accession
VMAT2_MOUSE
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72