Trientine 150mg tablets
Requires a prescription from a doctor or prescriber
Triethylenetatramine (TETA), also known as trientine, is a potent and selective copper (II)-selective chelator.
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Safety monitoring data
Yellow Card reports
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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.
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Suspected adverse reactions reported for Trientine
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1 branded products available
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Cuprior 150mg tablets
WHO defined daily dose (DDD)
450 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
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
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: 10 · Randomised trials: 2 · 1982–2026
Showing the 50 most relevant studies, sorted by most relevant.
Hafiz Muhammad Ehsan Arshad, Muhammad Zain Raza, Musab Maqsood, et al.
Rare, 2025
J. Farrant, Susanna Dodd, C. Vaughan, et al.
Heart, 2023
- Cardiomyopathy, Hypertrophic
- Trientine
- Heart
M. Schilsky, A. Członkowska, M. Zuin, et al.
The lancet. Gastroenterology & hepatology, 2022
J. Walshe
Lancet, 1982
G. Brewer, F. Askari, M. Lorincz, et al.
Archives of neurology, 2006
G. Brewer, F. Askari, R. Dick, et al.
Translational research : the journal of laboratory and clinical medicine, 2009
I. Herbert Scheinberg, Marvin E. Jaffe, Irmin Sternlieb
New England Journal of Medicine, 1987
C. O. F. Kamlin, Timothy M Jenkins, Jamie L Heise, et al.
Drugs, 2024
- Hepatolenticular Degeneration
- Trientine
- Penicillamine
Trientine tetrahydrochloride (TETA-4HCl, Cuvrior®) is a copper chelating agent with the active moiety triethylenetetramine (trientine), developed by Orphalan, Inc. to address the unmet needs in the treatment of Wilson disease. The journey from bench to bedside builds upon the documented safety profile of trientine hydrochloride capsules developed initially to meet the needs of individuals intolerant to d-penicillamine (DPA). Trientine hydrochloride capsules are inherently unstable requiring strict cold chain storage conditions from production, transportation, and use at home by the patient. Trientine tetrahydrochloride has a distinctive, patent-protected unique polymorphic form, which permits the production at scale of film-coated scored tablets deemed room temperature stable for 36 months. Trientine tetrahydrochloride is supported by a well-characterized pharmacodynamic, pharmacokinetic, and metabolic profile demonstrating reliable and predictable dose linearity and dose proportionality kinetics. Trientine tetrahydrochloride is the only trientine formulation that has been compared with DPA in a prospective randomized clinical trial, demonstrating non-inferiority to DPA in adults with stable Wilson disease. On 28 April, 2022, the US Food and Drug Administration approved TETA-4HCl for use in adult patients with Wilson disease who are de-coppered and tolerant to DPA. Health authorities in multiple countries worldwide have approved TETA-4HCl for the treatment of adults and children aged 5 years or more who are intolerant to DPA including the European Union, UK, Saudi Arabia, Switzerland, Colombia, Australia, New Zealand, and China. This article aims to provide a comprehensive narrative review of the key milestones in the development of TETA-4HCl.
Abstract licence: CC BY-NC 4.0
J. Yoshii, H. Yoshiji, S. Kuriyama, et al.
International Journal of Cancer, 2001
Rupert Purchase
Drugs, 2025
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
13.8 to 16.5 hours
Mechanism
Wilson's disease is an autosomal recessive genetic disorder that leads to copper accumulation in the tissues.
Food interactions
3 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
6%
[A18803]
…
Half-life
13.8 to 16.5 hours
[L41730]
Volume of distribution
645 L
Metabolism
[A18803]
…
Elimination
1%
[L41730]
…
Clearance
69.5 L/h
[A18803]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
TETA has been investigated in clinical trials for the treatment of heart failure in patients with diabetes.[A18804][A19332][A19333][A19334][A19335]
[L41730]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 810 interactions
[L41735]
Occasional cases of trientine overdose have been reported. A large overdose of 60 g of trientine hydrochloride resulted in nausea, vomiting, dizziness, mild acute kidney injury, mild hypophosphatemia, low serum zinc, and low serum copper: the patient recovered following intravenous hydration and supportive measures.
There is no antidote for an acute overdose from trientine. Chronic use of trientine at dosages above the maximum recommended dosage has resulted in sideroblastic anemia.
[L41730]
In preliminary studies, TETA was shown to ameliorate left ventricular hypertrophy in both human and animal subjects with diabetes. In animal models, TETA was also shown to reverse manifestations of diabetic nephropathy, including nephromegaly, renal fibrosis, glomerulosclerosis, and albuminuria, without lowering hyperglycemia.[A18804] This finding may be explained by TETA chelating copper cations, which are pro-oxidant and activate pathways that produce excessive reactive oxygen species (ROS) that cause tissue injury.[A19335] TETA was shown to possess anti-angiogenesis properties, as copper is an essential element for angiogenesis in cancer cells. TETA was shown to inhibit telomerase, suggesting that it may exhibit an inhibitory effect or cytotoxicity on tumor growth. Based on these early findings, TETA has been studied for its anticancer effects.[A19333]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A18803]
TETA has the potential to chelate non-copper cations in mineral supplements and other oral drugs, resulting in altered drug absorption; thus, TETA should be administered at least one hour apart from these medications.
[L41730]
The median Tmax ranges from 1.25 to 2 hours. Mean Cmax (± SD) of triethylenetetramine (TETA) was 2030 ± 981 ng/mL following oral administration of 900 mg TETA and 3430 ± 1480 ng/mL following administration of 1500 mg TETA. The systemic exposure (AUC) of TETA increased in a dose-proportional manner over the range of 900 mg to 1500 mg TETA.
The mean AUCinf (± SD) was 9750 ± 4910 ngxh/mL at 900 mg and 17200 ± 9470 ngxh/mL at 1500 mg.
[L41730]
[L41730]
[A19333]
In healthy adult volunteers receiving oral capsules of TETA, the apparent volume of distribution of steady state was 645 L.
[A18803]
[A18803]
TETA undergoes acetylation mediated by diamine acetyltransferase, also known as spermidine/spermine N1-acetyltranferase,[A18804][A19333] to form two major active metabolites, N1-acetyltriethylenetetramine (MAT) and N1,N10-diacetyltriethylenetetramine (DAT).
[L41730]
The chelating activity of MAT is significantly lower than that of TETA.
[A19333]
[L41730]
Approximately less than 1% of the administered dose is renally excreted as unchanged drug within the first six hours of dosing. About 8% of the dose is excreted as two major metabolites of TETA, MAT and DAT. Urinary excretion of metabolites occurs later than the excretion of the unchanged parent drug: it continues for 26 hours or longer.
[A18803]
[A18803]
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC A16AX12
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)
Triethylenetetramine
Matched from: Trientine
Additional database identifiers
Drugs Product Database (DPD)
23507
ChemSpider
21106175
BindingDB
50323751
PDB
104
ZINC
ZINC000019364225
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1372
GeneCards
CA14
GenBank Gene Database
AB025904
GenBank Protein Database
6009640
Guide to Pharmacology
2598
UniProt Accession
CAH14_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10540
GenAtlas
SAT1
GeneCards
SAT1
GenBank Gene Database
M77693
GenBank Protein Database
338392
UniProt Accession
SAT1_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