Briviact’s Mechanism of Action: How It Stops Seizures

Briviact (brivaracetam) is a medication used to manage epilepsy, a neurological condition characterized by recurrent seizures. It helps control partial-onset seizures. Approved by the FDA on February 19, 2016, Briviact is manufactured by UCB.

What Are Seizures?

Seizures are sudden, temporary disturbances in the brain’s electrical activity, resulting from abnormal or excessive firing of neurons. This uncontrolled electrical discharge can manifest in various ways, influencing behavior, movement, sensations, or levels of consciousness.

Some seizures involve subtle changes, such as brief moments of staring or lapses in attention, while others can cause more dramatic generalized convulsions and loss of consciousness. Most seizures typically resolve within a few minutes, usually lasting less than two minutes. However, a seizure extending beyond five minutes is considered a medical emergency.

These electrical surges can be caused by various factors, including underlying medical conditions, injuries, or illnesses.

How Brain Cells Communicate

The human brain relies on intricate communication between billions of neurons. This communication primarily occurs through a combination of electrical and chemical signals. Neurons transmit electrical signals, known as action potentials, along their length.

When an action potential reaches the end of a neuron, it arrives at a specialized junction called a synapse. At the synapse, the electrical signal is converted into a chemical signal. This involves the release of chemical messengers, called neurotransmitters, into a tiny gap between neurons known as the synaptic cleft. These neurotransmitters then diffuse across the cleft and bind to specific receptors on the neighboring neuron, influencing its activity by either exciting or inhibiting it.

The Role of Synaptic Vesicle Protein 2A (SV2A)

Synaptic Vesicle Protein 2A (SV2A) is a transmembrane protein located on synaptic vesicles, which are small sacs within neurons that store neurotransmitters. SV2A is found throughout the central nervous system in nearly all synaptic terminals.

SV2A is understood to play a role in regulating the release of neurotransmitters. It is thought to participate in a pre-fusion maturation step during vesicular exocytosis. Studies have indicated that SV2A influences the coupling between calcium entry into the neuron and the subsequent release of neurotransmitters.

Mice lacking SV2A expression experience severe seizures and typically do not survive beyond three weeks, highlighting its importance for normal nervous system function and survival. Reduced SV2A expression has also been observed in brain tissue from animal models of epilepsy and in patients with drug-resistant temporal lobe epilepsy.

Briviact’s Action on SV2A

Briviact (brivaracetam) exerts its therapeutic effect by specifically targeting and binding to Synaptic Vesicle Protein 2A (SV2A) in the brain. This binding occurs with high affinity, forming a strong connection with the SV2A protein. By interacting with SV2A, Briviact modulates its function, influencing the process of neurotransmitter release.

It is hypothesized that Briviact’s binding may stabilize the conformation of SV2A, enabling it to perform a protective role during seizure activity. The modulation of SV2A by Briviact results in a reduction in the release of neurotransmitters, particularly excitatory ones like glutamate.

This reduced release helps to stabilize neuronal activity, preventing the excessive and uncontrolled electrical discharges that characterize seizures. Briviact’s action on SV2A is similar to that of levetiracetam, another antiepileptic drug, but Briviact demonstrates a notably higher affinity for SV2A, being 15 to 30 times more potent in its binding.

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