Trilostane 60mg capsules
Trilostane is an inhibitor of 3 beta-hydroxysteroid dehydrogenase used in the treatment of Cushing's syndrome.
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
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.
View Drug Analysis Profile
Suspected adverse reactions reported for Trilostane
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
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.
View EudraVigilance report
Suspected adverse reactions reported for Trilostane
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
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)
360 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
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
Official UK regulator monitoring and safety alerts
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: 6 · Randomised trials: 2 · 1978–2026
Showing the 50 most relevant studies, sorted by most relevant.
Shanlly S, Slessor J, Yan W, et al.
2025
Cushing's syndrome is one of the most common endocrine disorders in dogs and is typically managed with long-term medical treatment. Several pharmacological agents are available: trilostane, mitotane, ketoconazole, cabergoline, selegiline, and aminoglutethimide, but their comparative effects on survival remain unclear. This systematic review and meta-analysis compared the impact of these agents on survival outcomes in dogs with naturally occurring diseases. A comprehensive search of MEDLINE, Embase, Web of Science, Academic Search Complete, and the Cochrane Library was conducted between 1 September 2024 to 3 January 2025. Eligible studies included dogs diagnosed with Cushing's syndrome that reported survival outcomes for at least one of the specified treatments. Five studies (n = 295 dogs) met the inclusion criteria, with trilostane and mitotane providing sufficient data for meta-analysis. Pooled mean difference in survival time across four studies was 85.1 days (95% CI: -255.9 to 85.7, p = 0.21) with substantial heterogeneity (I2 = 89%), indicating no statistically significant difference between the drugs. In contrast, pooled survival rates at fixed intervals favored trilostane, with an 11% higher survival at 36 months (p = 0.005) and no heterogeneity observed (I2 = 0%). These findings suggest trilostane may offer long-term survival benefits over mitotane.
Abstract licence: CC BY
Gordon O. Potts, J. E. Creange, H. R. Harding, et al.
Steroids, 1978
Guilherme Luiz Carvalho de Carvalho, L. Meirelles, C. D. da Silva, et al.
Research in veterinary science, 2022
- Pituitary ACTH Hypersecretion
- Cushing Syndrome
- Dog Diseases
Reto Neiger, I. Ramsey, J. O'Connor, et al.
Veterinary Record, 2002
P. A. le Roux, S. Tregoning, P. Zinn, et al.
Human reproduction, 2002
Ali R. Olaimat, Parastoo Jafarzadehbalagafsheh, Mohammad Gol, et al.
Animals : an Open Access Journal from MDPI, 2025
Simple Summary Drugs rarely are aimed at a single target. More frequently, drugs can affect the functioning of multiple systems as a consequence of the different levels of activity of the aimed target or because of the effects caused by drug interactions with the other possible targets. Trilostane is a veterinary drug used for very specific diseases, but the array of possible beneficial effects generated by trilostane could be useful for diseases different from those indicated for the use of this drug. Additionally, although abandoned as a drug to treat diseases in human patients, the use of trilostane in animals to address conditions still needing effective therapies could give trilostane appeal for a new appraisal in disorders common to humans and animals, such as epilepsy, anxiety, and depression. This review of the present evidence suggests that trilostane is a powerful tool to stimulate the production of hormones (steroids), making the brain more resilient to injuries and traumatic events, preventing more negative consequences caused by the triggered neuroinflammatory responses (a consequence common to seizures and, but not only, depression), which definitely could lead to more severe conditions.
Abstract licence: CC BY
J. Lemetayer, S. Blois
The Canadian veterinary journal = La revue veterinaire canadienne, 2018
N. Ruckstuhl, C. Nett, C. Reusch
American journal of veterinary research, 2002
P. Komanicky, R. Spark, J. Melby
The Journal of clinical endocrinology and metabolism, 1978
Su‐Min Park, Kyeong‐Bo Kim, Woo‐Jin Song, et al.
2021
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
8 hours
Mechanism
Trilostane produces suppression of the adrenal cortex by inhibiting enzymatic co…
Food interactions
None known
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Half-life
8 hours
Metabolism
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1045 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
Specifically converts dihydrotestosterone to its inactive form 5alpha-androstanediol, that does not bind androgen receptor/AR. Also converts androstanedione, a precursor of testosterone and estrone, to epiandrosterone .
PMID:1401999 PMID:2139411
Expected to use NAD(+) as preferred electron donor for the 3beta-hydroxy-steroid dehydrogenase activity and NADPH for the 3-ketosteroid reductase activity (Probable)
Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF-kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA-binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter.
Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP.
Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3 .
PMID:17922032
Maintains neuronal survival in response to ischemic reperfusion injury when in the presence of circulating estradiol (17-beta-estradiol/E2) (By similarity)
ATC H02CA01
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)
Trilostane
Additional database identifiers
Drugs Product Database (DPD)
7334
ChemSpider
570949
BindingDB
50247882
ZINC
ZINC000100038546
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5217
GenAtlas
HSD3B1
GeneCards
HSD3B1
GenBank Gene Database
M27137
GenBank Protein Database
306889
UniProt Accession
3BHS1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5218
GenAtlas
HSD3B2
GeneCards
HSD3B2
GenBank Gene Database
M67466
GenBank Protein Database
184401
UniProt Accession
3BHS2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3467
GenAtlas
ESR1
GeneCards
ESR1
GenBank Gene Database
X03635
GenBank Protein Database
31234
Guide to Pharmacology
620
UniProt Accession
ESR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3468
GenAtlas
ESR2
GeneCards
ESR2
GenBank Gene Database
AB006590
GenBank Protein Database
2911152
Guide to Pharmacology
621
UniProt Accession
ESR2_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