Trimetazidine 35mg modified-release tablets
Requires a prescription from a doctor or prescriber
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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 Trimetazidine
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2 branded products available
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)
40 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.
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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: 25 · Randomised trials: 24 · 1994–2026
Showing the 50 most relevant studies, sorted by most relevant.
Vacharanukrauh P, Miller KJ, Alif SM, et al.
2025
- Breast Neoplasms
- Anthracyclines
- Cardiotonic Agents
PurposeThis study aimed to systematically assess the efficacy of cardioprotective agents in preventing anthracycline-induced cardiotoxicity in patients with breast cancer using a comprehensive network meta-analysis (NMA).MethodsThis study included patients with breast cancer undergoing anthracycline-based chemotherapy. Randomized controlled trials (RCTs) published before March 2020 were identified through systematic searches in MEDLINE, Cochrane CENTRAL, Web of Science, and CINAHL. The primary outcome was left ventricular ejection fraction (LVEF), assessed using cardiac magnetic resonance imaging, multigated radionuclide angiography, or echocardiography. The NMA integrated direct and indirect comparisons to estimate the relative effectiveness of pharmacological interventions.ResultsThe systematic review included 31 RCTs with 3,228 participants, whereas the NMA synthesized 25 effect sizes from 15 RCTs. Mineralocorticoid receptor antagonists (MRAs) [standardized mean difference (SMD): -1.78, 95% confidence interval (CI): -2.81 to -0.75] and trimetazidine (SMD: -1.12, 95%CI: -2.32 to -0.09) exhibited the most substantial cardioprotective effects. Dexrazoxane (SMD: -0.53, 95%CI: -1.90 to -0.02) and β-blockers (SMD: -0.34, 95%CI: -0.70 to 0.02) showed potential benefits, albeit with greater uncertainty. Direct comparisons showed that dexrazoxane was more effective than β-blockers (SMD: -1.25, 95%CI: -2.22 to -0.48), with mineralocorticoid receptor antagonists (MRAs) outperforming both. Despite heterogeneity and potential publication bias, mineralocorticoid receptor antagonists (MRAs) and trimetazidine consistently ranked as the most effective interventions. LVEF findings confirmed the cardioprotective benefits of β-blockers, ARBs, ACE inhibitors, and dexrazoxane.ConclusionsRCT evidence suggested that cardioprotective drugs effectively mitigate anthracycline-induced LVEF decline. However, the lack of direct head-to-head trials limits definitive conclusions on comparative efficacy, warranting trials in patients with lower baseline LVEF to optimize cardioprotective strategies.
Abstract licence: CC BY
Budiarto RM, Tri Saputra PB, Kurniawan RB, et al.
2024
- Trimetazidine
- Vasodilator Agents
- Ankle Brachial Index
Zeng M, Chen Z, Zhang Y, et al.
2024
- Myocarditis
- Ubiquinone
- Trimetazidine
IntroductionCoenzyme Q10 (CoQ10) is considered to be beneficial for patients with acute viral myocarditis (AVM). In addition, trimetazidine may be also beneficial to patients with AVM by promoting cardiac energy metabolism. This systematic review and meta-analysis examined the efficacy and safety of combining trimetazidine and CoQ10 with respect to CoQ10 alone in patients suffering from AVM.MethodologyPubMed, Embase, the Cochrane Library, Wanfang, and China National Knowledge Infrastructure (CNKI) databases were searched for relevant randomized controlled trials (RCTs). An analysis of random effects was employed to combine the results.ResultsSixteen RCTs that included 1,364 patients with AVM contributed to the meta-analysis. Overall, 687 patients received the combined treatment, while 677 received the CoQ10 alone for a duration of 2-12 weeks (mean: 5.2 weeks). In contrast to monotherapy with CoQ10, combined treatment with trimetazidine and CoQ10 significantly improved overall therapy effectiveness (risk ratio [RR]: 1.19, 95% confidence interval [CI]: 1.13 to 1.24, p 0.05). The combined treatment was associated with improved myocardial enzyme levels and recovery of cardiac systolic function as compared to CoQ10 alone (p all ConclusionsTrimetazidine combined with CoQ10 is an effective and safe treatment for AVM.
Abstract licence: CC BY
Lukwaro A, Lu Y, Chen J, et al.
2024
- Trimetazidine
- Contrast Media
- Coronary Angiography
BackgroundContrast-induced acute kidney injury (CI-AKI) is a known complication after coronary angiography (CAG) or percutaneous coronary intervention (PCI). Clinical evidence suggests that trimetazidine (TMZ), an anti-ischemic drug, may prevent CI-AKI. We aimed to evaluate the role of trimetazidine in preventing CI-AKI in patients with pre-existing renal dysfunction undergoing CAG or PCI.MethodsWe searched PubMed, Cochrane Library, EBSCOhost, Web of Science, and Google Scholar databases from January 2004 to January 2024. We reviewed RCTs involving participants aged ≥ 18 years with pre-existing renal insufficiency who underwent CAG or PCI. Outcomes should include the incidence of CI-AKI, adverse events, and changes in serum creatinine (Scr) levels at different time intervals. Two reviewers independently extracted the data, evaluated the quality and relevance of the studies, and graded the strength of evidence for each study through consensus.ResultsNine RCTs met the inclusion criteria and assessed the role of TMZ in patients with renal dysfunction who underwent CAG or PCI. All RCTs showed a significant decrease in the incidence of CI-AKI in the TMZ group compared to the control group (RR 0.36, 95% CI, [0.25, 0.52] P ConclusionThe addition of TMZ to standard hydration protocols may offer a promising strategy for lowering the incidence of CI-AKI, adverse events, and postoperative SCr levels in patients with renal insufficiency within 72 h after CAG or PCI. However, large-scale RCTs are necessary to definitively establish the efficacy and safety of TMZ in patients with renal insufficiency after CAG or PCI.
Abstract licence: CC BY-NC-ND
Zhang X, Duan Z, Yu Y, et al.
2025
- Myocardial Reperfusion Injury
- Trimetazidine
- Vasodilator Agents
D. Handoko, S. Nassiri, A. A. Bovenkamp, et al.
Open Heart, 2024
- Trimetazidine
- Vasodilator Agents
- Heart Failure
Anna Marielle B. Dy, Lorenzo Luis G. Limjoco, Roland Dominic G. Jamora
Frontiers in Neurology, 2020
Importance: Trimetazidine (TMZ) is a medication given to patients with stable coronary artery disease. While it is reportedly well-tolerated, there are increasing numbers of reports of adverse events such as parkinsonism. Objectives: The purpose of this study was to systematically review the currently available literature on TMZ-induced parkinsonism. Evidence Review: A search of Scopus, MEDLINE, EMBASE, the Cochrane Library, the Health Technology Assessment Database, PubMed, Science Direct, and Google Scholar was conducted on or before November 7, 2019. The literature search included cohort studies, prospective and/or retrospective studies, meta-analysis, and other systematic reviews published as an original article, including abstracts and full texts. We included patients taking TMZ who developed one or more of the parkinsonian symptoms of bradykinesia, tremors, rigidity, and postural instability, where these symptoms improved after withdrawal of the said medication. Findings: There are currently five studies on TMZ use and associated parkinsonism. The literature included two case reports, one case series, and one retrospective and one prospective study. We found no results from randomized clinical trials. Overall, 88 patients developed TMZ-induced parkinsonism. Regression of parkinsonism was reported in all of the participants after withdrawal of TMZ. A total of 49 patients (55.7%) had complete regression of symptoms, while 39 patients (44.3%) had significant reduction of symptoms. The duration between TMZ (dose, 60–80 mg/day) intake and onset of symptoms ranged from 4 months to 20 years. The most commonly reported extrapyramidal symptoms were akinesia, rigidity, postural disturbances, and gait disorders, which were usually mild and symmetric. Conclusions and Relevance: The current literature suggests that TMZ can induce parkinsonism that is reversible with drug withdrawal. It is warranted to examine patients, especially the elderly, on TMZ for parkinsonian symptoms and those with pre-existing neurodegenerative diseases. Further studies are needed to assess the risk-benefit ratio of this drug, especially in the elderly age group.
Abstract licence: CC BY 4.0
Pramana KAAP, Cahyani NGAMSD, Pintaningrum Y, et al.
2024
M. Marzilli, Dragos Vineareanu, G. Lopaschuk, et al.
International journal of cardiology, 2019
Ashkan Heshmatzadeh Behzadi, Behzad Amoozgar, Shalini Jain, et al.
Medicine, 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
7.81 hours
Mechanism
During myocardial ischemia, anaerobic metabolism takes over, increasing levels of lactic acid.
Food interactions
2 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
35 mg
Half-life
7.81 hours
Protein binding
15%
[A7692][L33015]
Trimetazidine can bind to human serum albumin.
[A233175]
Volume of distribution
4.8 L/kg
[L33015]
Metabolism
[A233230]
…
Elimination
79-84%
[A7692][L33015]
…
Clearance
8 mL/min
[L33015]
…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Acidic conditions, caused by anaerobic metabolism and fatty acid oxidation, in response to myocardial ischemia, activate sodium-hydrogen and sodium-calcium antiport systems.[A233215] The increased intracellular calcium decreases contractility.[A233215] It is hypothesized that trimetazidine inhibits 3-ketoacyl coenzyme A thiolase, which decreases fatty acid oxidation but not glucose metabolism, preventing the acidic conditions that exacerbate ischemic injury.[A7688][L33020] However, evidence for this mechanism is controversial.[A233215]
Trimetazidine is not FDA approved. However, it has been approved in France since 1978.[L33020]
[L33015]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 1 of 1 interactions
[L33015]
Treat overdoses with symptomatic and supportive therapy.
[L33015]
The oral LD50 in rats is 1700 mg/kg, and in mice is 1550 mg/kg.
[L33025]
The subcutaneous LD50 in rats is 1500 mg/kg, and in mice is 410 mg/kg.
[L33025]
This injury to the myocardium raises concentrations of catecholamines, which activate hormone sensitive lipase, and increasing fatty acid concentrations in plasma.[A233215] When the myocardium is repurfused, fatty acid oxidation becomes the dominant form of ATP production, maintaining an acidic pH, and further exacerbating the injury.[A233215]
The mechanism of action of trimetazidine is not fully understood.[A233215] Trimetazidine may inhibit mitochondrial 3-ketoacyl coenzyme A thiolase, decreasing long chain fatty acid β-oxidation but not glycolysis in the myocardium.[A7688][L33020] The decreased long chain fatty acid β-oxidation is compensated for by increased use of glucose, preventing a lowered myocardial pH, and further decreases in contractility.[A7688][L33020] However, another study suggests that 3-ketoacyl coenzyme A thiolase may not be trimetazidine's target, and that this mechanism may be incorrect.[A233215]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A7692]
In young, healthy patients, the same dose reaches a mean Cmax of 91.2 µg/L, with a Tmax of 2.0-6.0 hours, and an AUC0-12h 720 h\*µg/L.
[A7692]
[A7692][L33015]
In patients over 65, the half life increases to 11.7 hours.
[A7692][L33015]
[A7692][L33015]
Trimetazidine can bind to human serum albumin.
[A233175]
[L33015]
[A233230]
Trimetazidine can also be N-formylated, N-acetylated, or N-methylated at the piperazine ring to form N-formyltrimetazidine, N-acetyltrimetazidine, and N-methyltrimetazidine respectively.
[A233230]
Alternatively, trimetazidine can be demethylated at the 2, 3, or 4 position of the 2,3,4-trimethoxybenzyl moiety to form 2-desmethyltrimetazidine, 3-desmethyltrimetazidine, or 4-desmethyltrimetazidine.
[A233230]
The desmethyltrimetazidine metabolites can undergo sulfate conjugation or glucuronidation prior to elimination.
[A233230]
[A7692][L33015]
In a study of 4 healthy subjects, individual metabolites made up 0.01-1.4% of the dose recovered in urine.
[A233230]
In the urine, 2-desmethyltrimetazidine made up 0-1.4% of the recovered dose, 3- and 4-desmethyltrimetazidine made up 0.039-0.071% each, N-methyltrimetazidine made up 0.015-0.11%, trimetazidine ketopiperazine made up 0.011-0.4%, N-formyltrimetazidine made up 0.035-0.42%, N-acetyltrimetazidine made up 0.016-0.19%, desmethyl trimetazidine O-sulphate made up 0.01-0.65%, and an unknown metabolite made up0.026-0.67%.
[A233230]
[L33015]
In eldery patients with a creatinine clearance of 72 ± 8 mL/min, trimetazidine clearance was 15.69 L/h.
[A7692]
In young, healthy patients with a creatinine clearance of 134 ± 18 mL/min, trimetazidine clearance was 25.2 L/h.
[A7692]
Proteins and enzymes this drug interacts with in the body
Also displays hydrolase activity on various fatty acyl-CoAs .
PMID:25478839
Thereby, could be responsible for the production of acetate in a side reaction to beta-oxidation (Probable). Abolishes BNIP3-mediated apoptosis and mitochondrial damage PMID:18371312
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
ATC C01EB15
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)
Trimetazidine
Additional database identifiers
ChemSpider
19853
BindingDB
80613
ZINC
ZINC000019358638
HUGO Gene Nomenclature Committee (HGNC)
HGNC:83
GeneCards
ACAA2
UniProt Accession
THIM_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_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