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Clinical data
Pronunciation/ˌbrɪvəˈræsətəm/ BRIV-ə-RASS-ə-təm
Trade namesBriviact
License data
  • US: C (Risk not ruled out)
Routes of
Oral (tablets, oral solution), IV
ATC code
Legal status
Legal status
  • US: Schedule V
  • In general: ℞ (Prescription only)
Pharmacokinetic data
BioavailabilityNearly 100%
Protein binding≤20%
MetabolismHydrolysis by amidase, CYP2C19-mediated hydroxylation
Metabolites3 inactive metabolites
Elimination half-life≈9 hours
ExcretionKidneys (>95%)[1]
CAS Number
PubChem CID
ECHA InfoCard100.118.642 Edit this at Wikidata
Chemical and physical data
Molar mass212.15 g/mol g·mol−1
3D model (JSmol)
Specific rotation[α]D −60°
Melting point72 to 77 °C (162 to 171 °F)

Brivaracetam (trade name Briviact), a chemical analog of levetiracetam, is a racetam derivative with anticonvulsant (antiepileptic) properties.[2][3] It is marketed by the pharmaceutical company UCB. In India it is co-promoted and distributed by Dr. Reddy's Laboratories.

Medical uses

Brivaracetam is used to treat partial-onset seizures with or without secondary generalisation, in combination with other antiepileptic drugs. No data are available for its effectiveness and safety in patients younger than 16 years.[4][5]

It is sometimes prescribed as an alternative to the drug's analogue levetiracetam to avoid neuropsychiatric adverse effects such as mood swings, anxiety, emotional lability, and depression.

Adverse effects

The most common adverse effects include sleepiness, dizziness, nausea and vomiting. More rarely, coordination problems and changes in behaviour can occur.[4][5]


Coadministration of brivaracetam with carbamazepine may increase exposure to carbamazepine-epoxide, the active metabolite of carbamazepine, and could theoretically lead to reduced tolerability. Coadministration of brivaracetam with phenytoin may increase phenytoin levels. Coadministration of other antiseizure drugs are unlikely to affect brivaracetam exposure. Brivaracetam provides no added therapeutic benefit when administered in conjunction with levetiracetam that acts on the same protein.[6]


Mechanism of action

Brivaracetam is believed to act by binding to the ubiquitous synaptic vesicle glycoprotein 2A (SV2A), like levetiracetam. but with 20-fold greater affinity.[7][8] There is some evidence that racetams including levetiracetam and brivaracetam access the luminal side of recycling synaptic vesicles during vesicular endocytosis. They may reduce excitatory neurotransmitter release and enhance synaptic depression during trains of high-frequency activity, such as is believed to occur during epileptic activity. [9]


Brivaracetam exhibits linear pharmacokinetics over a wide dose range, is rapidly and completely absorbed after oral administration, has an elimination half-life of 7 to 8 hours, and has plasma protein binding of less than 20%. It is extensively metabolized (>90%), primarily via hydrolysis of the acetamide group, and secondarily through hydroxylation mediated by the liver enzyme CYP2C19. The three major metabolites (hydroxy, acid, and hydroxyacid) are pharmacologically inactive. Brivaracetam is eliminated as urinary metabolites, with over 95% of a radioactive test dose recovered in the urine within 72 hours, including only 8.6% as unchanged brivaracetam.[10]


As noted above, brivaracetam is primarily metabolized by hydrolysis, via amidase enzymes, to an inactive metabolite. To a lesser extent, it is also metabolized by a minor metabolic pathway via CYP2C19-dependent hydroxylation. Individuals who have no CYP2C19 enzyme activity, “CYP2C19 poor metabolizers”, will have a greater exposure to standard doses of brivaracetam. Because they are less able to metabolize the drug to its inactive form for excretion, they may have an increased risk of adverse effects. The most common adverse effects of brivaracetam therapy include sedation, fatigue, dizziness, and nausea.[11] The FDA-approved drug label for brivaracetam states that patients who are CYPC19 poor metabolizers, or are taking medicines that inhibit CYP2C19, may require a dose reduction.[12]

Chemical and physical properties

Levetiracetam, for comparison

Brivaracetam is the 4R-propyl analogue of the anticonvulsant levetiracetam.


Positive preliminary results from stage III trials were recorded in 2008,[13] along with evidence that it is around 10 times more potent for the prevention of certain types of seizure in mouse models than its analogue levetiracetam.[14]

On 14 January 2016, the European Commission,[5] and on May 12, 2016, the Food and Drug Administration[15] approved brivaracetam under the trade name Briviact. The Drug Enforcement Administration (DEA) has issued an interim final rule[clarification needed] placing brivaracetam into schedule V of the Controlled Substances Act (CSA) effective Mar 09, 2017.[16] As of May 2016, brivaracetam is not approved in other countries, including Australia, Canada and Switzerland. It was approved in Australia in 2018.


  1. ^ "Briviact (brivaracetam) Tablets, for Oral Use; Oral Solution; Injection, for Intravenous Use. CV. Full Prescribing Information" (PDF). UCB, Inc., Smyrna, GA 30080. Retrieved 27 August 2016.
  2. ^ von Rosenstiel P (Jan 2007). "Brivaracetam (UCB 34714)". Neurotherapeutics. 4 (1): 84–7. doi:10.1016/j.nurt.2006.11.004. PMID 17199019.
  3. ^ Malawska B, Kulig K (Jul 2005). "Brivaracetam UCB". Current Opinion in Investigational Drugs. 6 (7): 740–746. PMID 16044671.
  4. ^ a b briviact for Briviact.
  5. ^ a b c "Briviact". European Medicines Agency. Retrieved 30 May 2016.
  6. ^ Rolan P, Sargentini-Maier ML, Pigeolet E, Stockis A (2008). "The pharmacokinetics, CNS pharmacodynamics and adverse event profile of brivaracetam after multiple increasing oral doses in healthy men". Br J Clin Pharmacol. 66 (1): 71–5. doi:10.1111/j.1365-2125.2008.03158.x. PMC 2485265. PMID 18341673.
  7. ^ Rogawski MA, Bazil CW (Jul 2008). "New molecular targets for antiepileptic drugs: alpha(2)delta, SV2A, and K(v)7/KCNQ/M potassium channels". Current Neurology and Neuroscience Reports. 8 (4): 345–352. doi:10.1007/s11910-008-0053-7. PMC 2587091. PMID 18590620.
  8. ^ Haberfeld, H, ed. (2015). Austria-Codex (in German). Vienna: Österreichischer Apothekerverlag.
  9. ^ Rogawski MA (2016). "A new SV2A ligand for epilepsy". Cell. 167: 587. doi:10.1016/j.cell.2016.09.057. PMID 27768878.
  10. ^ Sargentini-Maier ML, Espié P, Coquette A, Stockis A (2008). "Pharmacokinetics and metabolism of 14C-brivaracetam, a novel SV2A ligand, in healthy subjects". Drug Metab. Dispos. 36 (1): 36–45. doi:10.1124/dmd.107.017129. PMID 17908923.
  11. ^ Dean, Laura (2012), Pratt, Victoria; McLeod, Howard; Rubinstein, Wendy; Dean, Laura (eds.), "Brivaracetam Therapy and CYP2C19 Genotype", Medical Genetics Summaries, National Center for Biotechnology Information (US), PMID 29763212, retrieved 2019-01-25
  12. ^ "DailyMed - BRIVIACT- brivaracetam tablet, film coated BRIVIACT- brivaracetam solution BRIVIACT- brivaracetam injection, suspension". Retrieved 2019-01-25.
  13. ^ Rogawski MA (Aug 2008). "Brivaracetam: a rational drug discovery success story". British Journal of Pharmacology. 154 (8): 1555–7. doi:10.1038/bjp.2008.221. PMC 2518467. PMID 18552880.
  14. ^ Matagne A, Margineanu DG, Kenda B, Michel P, Klitgaard H (Aug 2008). "Anti-convulsive and anti-epileptic properties of brivaracetam (ucb 34714), a high-affinity ligand for the synaptic vesicle protein, SV2A". British Journal of Pharmacology. 154 (8): 1662–71. doi:10.1038/bjp.2008.198. PMC 2518465. PMID 18500360.
  15. ^ "FDA approves Briviact to treat partial onset seizures". US FDA. May 12, 2016.
  16. ^ Drug Enforcement Administration Department of Justice (Nov 25, 2015). "Schedules of Controlled Substances: Placement of Brivaracetam Into Schedule V. Interim final rule, with request for comments". Fed Regist. 81 (92): 29487–92. PMID 27192732.

External links