Clearance of Brivaracetam may be reduced in patients with hepatic insufficiency, however the photo paroxysmal response model in patients diagnosed with photosensitive epilepsy has proven to be effective.
Brivaracetam is chemically related to the AED Levetiracetam and possesses a natural binding affinity for the 2A synaptic vesicle protein. A higher potency in suppressing epileptiform responses in vitro, roughly ten-fold above that of Levetiracetam, has been shown in comprehensive studies of Brivaracetam. The ability of Brivaracetam to suppress various seizure types in studies, including genetic forms of epilepsy in patients offers patients a novel inhibitory therapy.
Brivaracetam has a half-life of eight hours and virtually complete bioavailability. As Brivaracetam is mainly metabolized via hydrolysis of the acetamide group, as well as CYP2C8-mediated hydroxylation, its metabolites are not pharmacologically active.
Brivaracetam has been tested in a comprehensive trials for toxicology, safety and genotoxicity. A low acute toxicity has been found in patients who received therapy with Brivaracetam. Commonly reported adverse effects have been documented as mild, and include fatigue, dizziness, headache and somnolence.