Cyproterone 50mg tablets
Requires a prescription from a doctor or prescriber
An anti-androgen that, in the form of its acetate (cyproterone acetate), also has progestational properties.
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MHRA alerts for Cyproterone
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 Cyproterone
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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 Cyproterone
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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.
16 branded products available
MHRA licensed products
View all licensed products for Cyproterone on the MHRA register
Androcur 50mg tablets
Cyprostat 50mg tablets
Cyproterone 50mg tablets
Cyproterone 50mg tablets
Cyproterone 50mg tablets
Cyproterone 50mg tablets
Cyproterone 50mg tablets
Cyproterone 50mg tablets
Cyproterone 50mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
100 mg
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
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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(4)
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Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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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
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NHS UK identifiers
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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: 12 · Randomised trials: 16 · 1975–2026
Showing the 50 most relevant studies, sorted by most relevant.
M. Pavone‐Macaluso, H. J. Voogt, G. Viggiano, et al.
The Journal of urology, 1986
Vercellini P, Vercellini P, Buffo C, et al.
2025
- Endometriosis
- Contraceptives, Oral, Combined
BackgroundNo conceptually new drugs for the safe and successful cure of endometriosis are likely to become available soon. Hormonal modulation of ovarian function and suppression of menstruation remain the pillars of disease control. However, existing drugs may be used following novel modalities to limit the consequences of endometriosis progression.ObjectivesThe aims of this review were to propose a pharmacological approach aimed at limiting the potential detrimental effects of the recent dramatic increase in postmenarcheal repetitive ovulatory menses and to define the type of hormones and the routes of administration that can be used to maximize safety and tolerability in the medical treatment of endometriosis.MethodsFor this narrative review, we selected the best quality evidence, prioritizing RCTs, systematic reviews, meta-analyses, network meta-analyses, and international guidelines, preferably published in the last decade.OutcomeMedical treatment of endometriosis should be included into all aspects of prevention. Very-low-dose combined oral contraceptives can be used for years to counteract the increased risk of ovarian cancer observed in patients with endometriosis. This primary prevention measure saves lives and can effectively integrate targeted risk-reducing surgery. Secondary pharmacological prevention, based on a working diagnosis of early onset adenomyosis-endometriosis selectively in adolescents with severe dysmenorrhea and heavy menstrual bleeding, can potentially impede the development of advanced disease forms, and reduce the need for management of complications due to a delay in diagnosis and treatment. Tertiary prevention, i.e., medical therapy of established disease, is based initially on the safest available estrogen-progestogen combinations and progestogen monotherapies. Whenever possible, ethinyl estradiol and cyproterone acetate should be avoided because of thromboembolic and meningioma risks, respectively. Estradiol can be administered transdermally. Switching to gonadotropin-releasing hormone agonists and antagonists should not be delayed when the first-line agents fail.Conclusions and outlookTwo-thirds of symptomatic endometriosis patients can be managed satisfactorily for many years using, with the right modality, the existing safe, effective, and well-tolerated medications. Despite the constant plea for new drugs, this already appears to be an excellent clinical outcome, unsurpassed when managing other human chronic inflammatory diseases. Cohort studies are needed to verify whether turning off the recurrent inflammation caused by repeated ovulation and menstruation could also affect the risk of systemic conditions associated with endometriosis.
Abstract licence: CC BY
Hudelist B, Roux A, Huet-Mignaton E, et al.
2026
BackgroundMeningiomas are the most common primary brain tumours in adults. Concerns have emerged about a possible link between progestogen use and intracranial meningioma; we assessed this association.MethodsIn this systematic review and meta-analysis, we searched PubMed/MEDLINE, Embase, Cochrane Library, EPI-PHARE database (from inception up to November 01, 2025), pharmacovigilance reports, and backward snowballing. Eligible publications were English or French epidemiological studies, reporting associations between progestogens and intracranial meningiomas. We excluded non-original reports, abstracts-only, and studies without eligible progestogen exposure or meningioma outcomes. We extracted summary data from published reports. Risk of bias was assessed with the Newcastle-Ottawa Scale, and certainty of evidence with GRADE. The primary outcome was intracranial meningioma. Secondary outcomes were malignancy, location, and regression. Random-effects models were used, and heterogeneity was assessed with I2; a narrative synthesis was also performed.FindingsOf 542 records screened, 78 studies were included in the review, and 14 high-quality observational studies in meta-analysis; all 14 were NOS high quality, although residual confounding and potential outcome misclassification cannot be excluded. Cyproterone acetate (CPA) was associated with increased meningioma risk (5 studies; 1047 exposed; pooled-OR 12.36 (95% CI: 7.47-20.45); I2: 73.8%; GRADE: moderate). Depot medroxyprogesterone acetate was also associated (6 studies; 842 exposed; pooled-OR 2.68 (95% CI: 1.72-4.19); I2: 92.7%; GRADE: low). Chlormadinone acetate (CMA), nomegestrol acetate (NOMAC), promegestone, medrogestone, and desogestrel showed signals of increased risk (CMA 3 studies, 164-683 exposed; NOMAC 3, 171-969; promegestone 1, 83; medrogestone 1, 42; desogestrel 2, 115-287). We did not pool these estimates due to sparse, heterogeneous evidence. No signal was found for norgestrel, levonorgestrel, progesterone, dydrogesterone, or spironolactone; evidence for dienogest and hydroxyprogesterone was insufficient. Regression after withdrawal was reported for CPA and NOMAC. Tumours were predominantly anterior/middle skull base, and malignant meningiomas were more frequent with CPA, CMA, and NOMAC.InterpretationThe certainty of evidence was limited by the observational design, residual confounding, heterogeneity, and imprecision for some exposures. Use of specific progestogens, particularly high dose macroprogestogens may be associated with an increased risk of intracranial meningioma. Transparent patient information and careful clinical and, where appropriate, imaging follow-up are essential.FundingNone.
Abstract licence: CC BY
Lane S, Lynn E, Bobbins A, et al.
2024
S. Venturoli, O. Marescalchi, F. Colombo, et al.
The Journal of clinical endocrinology and metabolism, 1999
J. Irani, L. Salomon, Rostand Oba, et al.
The Lancet. Oncology, 2010
K. Lee, John J. Y. Zhang, R. Kirollos, et al.
Scientific Reports, 2022
Angus LM, Leemaqz SY, Kasielska-Trojan AK, et al.
2025
- Breast
- Spironolactone
- Cyproterone Acetate
ContextTransgender people with sex recorded male at birth desiring feminization commonly use cyproterone acetate or spironolactone as antiandrogens with estradiol, but the optimal antiandrogen is unclear.ObjectiveWe aimed to assess the effect of antiandrogens on breast development. We hypothesized this would be greater in those treated with cyproterone acetate than spironolactone due to more potent androgen receptor antagonism and suppression of serum total testosterone concentrations.MethodsA randomized clinical trial was conducted between 2020-2022 at an outpatient endocrinology clinic. Transgender people aged 18+ years old commencing feminizing gender affirming hormone therapy were included. The intervention was standardized estradiol therapy plus either spironolactone 100 mg daily or cyproterone acetate 12.5 mg daily for 6 months. The primary outcome was breast development as measured by the breast-chest distance. Secondary outcomes included estimated breast volume, suppression of serum total testosterone concentration ResultsSixty-three people (median age 25 years) were enrolled, randomized, and included in intention to treat analysis (cyproterone acetate n = 32, spironolactone n = 31). At 6 months, there was no between-group difference in breast-chest distance (mean difference 0.27 cm, 95% CI -0.82 to 1.35, P = .6) or estimated breast volume (mean difference 17.26 mL, 95% CI -16.94 to 51.47, P = .3). Cyproterone acetate was more likely to suppress serum testosterone concentration to ConclusionAntiandrogen choice should be based on clinician and patient preference with consideration of side effects. Further research is needed to optimize breast development in transgender people.
Abstract licence: CC BY-NC-ND
Mesbah Shams, Azar Sattarinezhad, Hossainali Rostamipour, et al.
Reviews in Clinical Medicine, 2025
Eka Rusdianto Gunardi, Irma Bernadette, Riyan Hari Kurniawan, et al.
Indonesian Journal of Obstetrics and Gynecology, 2026
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
None known
Half-life
96 hours
Mechanism
The direct antiandrogenic effect of cyproterone is blockage of the binding of di…
Food interactions
2 warnings
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
96 hours
Metabolism
Elimination
60%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 903 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:19022849
Transcription factor activity is modulated by bound coactivator and corepressor proteins like ZBTB7A that recruits NCOR1 and NCOR2 to the androgen response elements/ARE on target genes, negatively regulating androgen receptor signaling and androgen-induced cell proliferation .
PMID:20812024
Transcription activation is also down-regulated by NR0B2. Activated, but not phosphorylated, by HIPK3 and ZIPK/DAPK3
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC G03HB01
ATC G03HA01
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Cyproterone acetate
Matched from: Cyproterone
Additional database identifiers
Drugs Product Database (DPD)
7572
ChemSpider
9496
BindingDB
50094569
PDB
CA4
ZINC
ZINC000003814423
HUGO Gene Nomenclature Committee (HGNC)
HGNC:644
GenAtlas
AR
GeneCards
AR
GenBank Gene Database
M20132
GenBank Protein Database
178628
Guide to Pharmacology
628
UniProt Accession
ANDR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6364
GeneCards
KLK3
Guide to Pharmacology
2373
UniProt Accession
KLK3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2594
GenAtlas
CYP19A1
GeneCards
CYP19A1
GenBank Gene Database
M22246
GenBank Protein Database
179002
Guide to Pharmacology
1362
UniProt Accession
CP19A_HUMAN
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