Brivaracetam 75mg tablets
Requires a prescription from a doctor or prescriber
Brivaracetam is a racetam derivative of levetiracetam used in the treatment of partial-onset seizures.
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Yellow Card
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Drug safety updates
MHRA alerts for Brivaracetam
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 Brivaracetam
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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 Brivaracetam
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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.
4 branded products available
MHRA licensed products
View all licensed products for Brivaracetam on the MHRA register
Briviact 75mg tablets
Briviact 75mg tablets
Briviact 75mg tablets
Briviact 75mg 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(2)
Cenobamate for treating focal onset seizures in epilepsy (TA753)
Epilepsies in children, young people and adults (NG217)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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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: 31 · Randomised trials: 11 · 2007–2026
Showing the 50 most relevant studies, sorted by most relevant.
Ting Song, Lingjun Feng, Yulei Xia, et al.
Frontiers in Neurology, 2023
Howard A, Mo M, Bencsik C, et al.
2026
- Status Epilepticus
- Pyrrolidinones
- Anticonvulsants
M. Rasool, Attia Qayyum, Ammara Zamir, et al.
Molecular Medicine Communications, 2024
Tai Y, Huang C, Wei Z, et al.
2026
Le Z, Ou Z, Yan R, et al.
2026
- Epilepsies, Partial
- Anticonvulsants
ObjectiveAntiseizure medications (ASMs) are the cornerstone of epilepsy treatment. However, evidence on direct comparison of ASMs is lacking. This network meta-analysis evaluated the comparative efficacy and safety of approved and investigational add-on third-generation ASMs for focal epilepsy in adolescents and adults.MethodsData were retrieved through an extensive literature search of PubMed, Embase, Cochrane Library, and ClinicalTrial.gov databases from inception through August 2025. Findings were reported following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guideline (CRD420251180027). Primary efficacy outcomes were ≥50 % and 100 % responder rates at 12-weeks maintenance duration. Secondary outcomes were corresponding responder rates at 8-weeks maintenance duration. Tolerability was assessed as retention rate. Treatment-emergent adverse events (TEAEs) and TEAEs leading to treatment discontinuation were the safety outcomes.ResultsThe literature search retrieved 345 studies, of which 35 studies were included. All ASMs showed significantly higher responder rates compared with placebo. Significantly higher 100 % responder rate was observed with cenobamate (CNB; 400mg/d: Risk ratio [RR] 15; 95 % CI, 7.0-39; 200mg/d: RR 8.7; 95 % CI, 3.9-22) at a maintenance duration of 12 weeks and 8 weeks (400mg/d: RR 15; 95 % CI, 7.0-41; 200mg/d: RR 8.6; 95 % CI, 4.0-24). All ASMs showed a patient retention rate comparable with placebo. For overall TEAEs, brivaracetam (BRV; 50mg/d) and BRV ranked the lowest for individual and pooled doses, respectively; placebo ranked the highest in both cases. For TEAEs leading to treatment discontinuation, CNB ranked lower than the placebo.SignificanceAll approved and investigational ASMs were effective add-on treatments for focal epilepsy, with CNB demonstrating the greatest likelihood of achieving seizure freedom.
Abstract licence: CC BY
Bekenova N, Aitkaliyev A, Kassiyeva B, et al.
2025
ObjectiveCognitive impairment is a common comorbidity in epilepsy, negatively affecting patients' quality of life. Although various treatments-antiepileptic drugs (AEDs), vagus nerve stimulation (VNS), and surgery-may influence cognition, comparative data on their effects on executive functions and memory remain limited. This systematic review aimed to evaluate studies assessing the impact of these treatments on executive functions and memory using the EpiTrack cognitive screening tool.MethodsA systematic search identified 1,008 publications, of which 35 full-text articles were reviewed. After applying inclusion criteria, seven studies were included, examining cognitive changes in patients undergoing various treatments.ResultsPerampanel and Cenobamate exhibited a neutral cognitive profile, with scores stable at "moderate impairment" (29.67-30.04). Lamotrigine and Levetiracetam demonstrated persistent severe impairment. Brivaracetam improved from severe to moderate impairment (not clinically significant). Only Topiramate showed a clinically significant decline (30.0 to 26.6). VNS therapy led to slight improvement over five years (severe to moderate impairment), while combined VNS + 1-2AEDs produced clinically meaningful gains. In contrast, VNS with 3-4 AEDs maintained severe impairment.ConclusionThis review underscores the importance of accurate cognitive assessment in epilepsy management, with a monitoring frequency of no more than every six months for patients receiving AED therapy.
Abstract licence: CC BY
Yu Zhang, Huihui Liu, Xin Wang, et al.
Frontiers in Pharmacology, 2026
S. Halloush, N. Alkhatib, Osamah M. Alfayez, et al.
Medicine, 2025
- Epilepsies, Partial
- Seizures
- Pyrrolidinones
This study conducts a cost-effectiveness analysis of brivaracetam (BRV) compared to other 3rd-generation antiseizure medications (AEDs) for the treatment of pharmacoresistant focal-onset seizures in Jordan. A Markov model was constructed over a 2-years’ time horizon for a hypothetical cohort of focal-onset seizures patients. A cycle of 3-months was adopted in our economic evaluation (total cycles of 8 cycles). Four health states were defined: seizure free, partial responders (≥50% reduction in seizure frequency), non-responders, and discontinuation. In addition to BRV, 3 treatment comparators were included in this economic evaluation: eslicarbazepine (ESL), lacosamide (LCM), and perampanel (PER). Clinical data were retired from a previously published network meta-analysis of 65 randomized controlled trials. Cost inputs were obtained from the Jordan Food and Drug Administration and local healthcare providers. Incremental Cost-Effectiveness Ratio (ICER) was calculated using the percentage of complete response (CR) in the denominator. Probabilistic sensitivity analysis was conducted to assess the robustness of the study findings. BRV was associated with the highest gains in CR over all AEDs included in this economic evaluation. The 2-year cost of ESL is JOD 4139; LCM is JOD 3078; PER is JOD 5541; BRV is JOD 3925. The incremental gain in CR with BRV was higher by 29.0%, 30.9%, and 26.4% compared to ESL, LCM, and PER, respectively. Despite these higher gains in CR with BRV versus all other AEDs in this economic evaluation, it was associated with lower cost when compared to ESL and PER at saving ICER of -JOD 737 per 1% CR achieved and -JOD 6113 per 1% CR achieved, respectively. However, BRV was associated with the ICER of JOD 2744 per 1% of CR achieved compared with LCM. These estimates were confirmed by the probabilistic sensitivity analysis. Compared to ESL and PER, BRV was associated with cost-savings. Compared to LCM, the BRV was cost-effective at the World Health Organization recommended willingness-to-pay threshold of 3× of Jordanian gross domestic product per capita.
Abstract licence: CC BY
Fröling E, Morales Sahm M, Schmude M, et al.
2026
- Epilepsy
- Pyrrolidinones
- Anticonvulsants
Lin-Ming Zhang, Gaiqing Yang, Baikun Zhou, et al.
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
1 found
Half-life
7-8h
Mechanism
The precise mechanism of brivaracetam's anti-epileptogenic activity is unknown.
Food interactions
2 warnings
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
100%
[A19180]
Half-life
7-8h
[A19180]
Protein binding
20%
Volume of distribution
0.5L/kg
Metabolism
[A19188]
…
Elimination
95%
Clearance
0.7-1.07 mL/min
[A19187]
Clearance is primarily metabolic with less than 10% of the parent drug excreted unchanged.
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1661 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A19180]
[A19180]
[A19188]
Another metabolite is created via oxidation of the propyl side chain by CYP2C8 as well as CYP3A4, CYP2C19, and CYP2B6. Some conjugation with glucuronic acid and taurine account for a small amount of metabolism.
[A19187]
Clearance is primarily metabolic with less than 10% of the parent drug excreted unchanged.
Proteins and enzymes this drug interacts with in the body
The influx of Na+ ions provokes membrane depolarization, initiating the propagation of electrical signals throughout cells and tissues. The accessory beta subunits participate in localization and functional modulation of the Nav channels .
PMID:24297919
Modulates the activity of SCN1A/Nav1.1 .
PMID:33712547
Modulates the activity of SCN2A/Nav1.2 PMID:24297919
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N03AX23
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)
Brivaracetam
Additional database identifiers
Drugs Product Database (DPD)
22702
ChemSpider
8012964
BindingDB
50422531
PDB
VLX
ZINC
ZINC000003979899
HUGO Gene Nomenclature Committee (HGNC)
HGNC:20566
GenAtlas
SV2A
GeneCards
SV2A
GenBank Gene Database
AB018279
GenBank Protein Database
40788343
UniProt Accession
SV2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10585
GenAtlas
SCN1A
GeneCards
SCN1A
GenBank Gene Database
AF225985
GenBank Protein Database
12642270
Guide to Pharmacology
578
UniProt Accession
SCN1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10582
GenAtlas
SCN10A
GeneCards
SCN10A
GenBank Gene Database
AF117907
GenBank Protein Database
4838145
Guide to Pharmacology
585
UniProt Accession
SCNAA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10583
GenAtlas
SCN11A
GeneCards
SCN11A
GenBank Gene Database
AF188679
GenBank Protein Database
6572950
UniProt Accession
SCNBA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10588
GenAtlas
SCN2A
GeneCards
SCN2A
GenBank Gene Database
M94055
GenBank Protein Database
457879
Guide to Pharmacology
579
UniProt Accession
SCN2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10590
GenAtlas
SCN3A
GeneCards
SCN3A
GenBank Gene Database
AJ251507
GenBank Protein Database
7414320
Guide to Pharmacology
580
UniProt Accession
SCN3A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10591
GenAtlas
SCN4A
GeneCards
SCN4A
GenBank Gene Database
M81758
GenBank Protein Database
338213
Guide to Pharmacology
581
UniProt Accession
SCN4A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10593
GenAtlas
SCN5A
GeneCards
SCN5A
GenBank Gene Database
M77235
GenBank Protein Database
184039
Guide to Pharmacology
582
UniProt Accession
SCN5A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10594
GeneCards
SCN7A
UniProt Accession
SCN7A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10596
GenAtlas
SCN8A
GeneCards
SCN8A
GenBank Gene Database
AF050736
GenBank Protein Database
4321647
Guide to Pharmacology
583
UniProt Accession
SCN8A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10597
GenAtlas
SCN9A
GeneCards
SCN9A
GenBank Gene Database
X82835
GenBank Protein Database
758110
Guide to Pharmacology
584
UniProt Accession
SCN9A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10586
GeneCards
SCN1B
GenBank Gene Database
L10338
GenBank Protein Database
307415
UniProt Accession
SCN1B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10589
GeneCards
SCN2B
GenBank Gene Database
AF007783
GenBank Protein Database
3309111
UniProt Accession
SCN2B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:20665
GeneCards
SCN3B
GenBank Gene Database
AJ243396
GenBank Protein Database
7160975
UniProt Accession
SCN3B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10592
GeneCards
SCN4B
GenBank Gene Database
AY149967
GenBank Protein Database
27465047
UniProt Accession
SCN4B_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:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2615
GeneCards
CYP2B6
GenBank Gene Database
M29874
GenBank Protein Database
181296
Guide to Pharmacology
1324
UniProt Accession
CP2B6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_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