Brivaracetam 99%

ChEBI: A non-proteinogenic amino acid derivative that is butanamide in which the pro-S hydrogen at position 2 is replaced by a (4R)-2-oxo-4-propylpyrrolidin-1-yl. Used for treatment of partial onset seizures related to epilepsy.
Brivaracetam is a non-proteinogenic amino acid derivative that is butanamide in which the pro-S hydrogen at position 2 is replaced by a (4R)-2-oxo-4-propylpyrrolidin-1-yl. Used for treatment of partial onset seizures related to epilepsy. It has a role as an anticonvulsant. It is a gamma-lactam and a non-proteinogenic amino acid derivative. It derives from a L-alpha-aminobutyric acid.|Brivaracetam is a DEA Schedule V controlled substance. Substances in the DEA Schedule V have a low potential for abuse relative to substances listed in Schedule IV and consist primarily of preparations containing limited quantities of certain narcotics.|Brivaracetam is a racetam derivative of levetiracetam used in the treatment of partial-onset seizures. Brivaracetam binds SV2A with 20 times higher affinity than levetiracetam. It is available under the brand name Briviact made by UCB. Briviact received FDA approval on February 19, 2016.|The mechanism of action of brivaracetam is as an Epoxide Hydrolase Inhibitor.|Brivaracetam is a relatively unique anticonvulsant that is typically used in combination with other antiepileptic medications for partial onset seizures. Brivaracetam has been linked to rare instances of serum aminotransferase and alkaline phosphatase elevations during treatment and is suspected of causing rare cases of clinically apparent drug induced liver disease.|Brivaracetam is an orally bioavailable levetiracetam derivative, with anticonvulsant activity. Although the exact mechanism through which brivaracetam exerts its effects is not fully known, this agent targets and binds to synaptic vesicle protein 2A (SV2A) in the brain. This prevents synaptic vesicle exocytosis and the synaptic release of certain, as of yet not fully known, excitatory neurotransmitters. This may inhibit impulse conduction across synapses, decrease neuronal (hyper-)excitability, and may modulate epileptogenesis. SV2A, a membrane glycoprotein present in neuronal synaptic vesicles, plays a key role in action potential-induced neurotransmitter release in the brain.