Brivaracetam
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| Pronunciation | BRIV-a-RA-se-tam |
| Trade names | Briviact |
| AHFS/Drugs.com | Briviact |
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| Routes of administration |
Oral (tablets, oral solution), IV |
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| Pharmacokinetic data | |
| Bioavailability | Nearly 100% |
| Protein binding | ≤20% |
| Metabolism | Hydrolysis by amidase, CYP2C19-mediated hydroxylation |
| Metabolites | 3 inactive metabolites |
| Biological half-life | ~9 hours |
| Excretion | Kidneys (>95%) |
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| ECHA InfoCard | 100.118.642 |
| Chemical and physical data | |
| Formula | C11H20N2O2 |
| Molar mass | 212.15 g/mol |
| 3D model (Jmol) | |
| Specific rotation | [α]D −60° |
| Melting point | 72 to 77 °C (162 to 171 °F) |
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Brivaracetam (trade name Briviact), a chemical analog of levetiracetam, is a racetam derivative with anticonvulsant (antiepileptic) properties. It is marketed by the pharmaceutical company UCB.
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.
The most common adverse effects include sleepiness, dizziness, nausea and vomiting. More rarely, coordination problems and changes in behaviour can occur.
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.
Brivaracetam is believed to act by binding to the ubiquitous synaptic vesicle glycoprotein 2A (SV2A), like levetiracetam. but with 20-fold greater affinity. 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.
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.
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