SV2A

Pioneering research undertaken by UCB scientists led to the discovery that levetiracetam (Keppra®) binds to an isoform of SV2A (synaptic vesicle protein 2A). Levetiracetam's mechanism of action is unique among anti-epileptic drugs, which often act by modulating ion channels, neurotransmitter receptors and pathway enzymes.  Levetiracetam alone acts on the SV2 proteins, a unique class of presynaptic proteins, and a new target for drug discovery in epilepsy and perhaps other neurological disorders.

Since epilepsy is a disorder characterised by periods of abnormal neural activity and levetiracetam moderates this disease, it is hypothesised that SV2A may be involved in the pathophysiology of epilepsy and other neurological disorders involving hyper-excitability and hypersynchronisation.  By binding to SV2A, levetiracetam may modulate one or more of its actions, ultimately affecting neural excitability but does not appear to affect neural activity in normal brains. Consequently, it seems that levetiracetam's modulation of SV2A function only has relevance in pathophysiological conditions.

UCB has active research programmes around both the function of SV2 proteins, and the development of additional therapeutics that act by binding to SV2.  These studies may also contribute to our understanding of the pathophysiological basis of epilepsy, with the aim of improving and refining our treatment of this heterogeneous and debilitating disease, as well as other neurological disorders involving abnormalities in neural excitability.