Rationale A significant body of evidence implicates sodium channels in mediating the pathophysiological components of both neuropathic and nociceptive pain. This is supported by clinical evidence suggesting that local anaesthetics, anticonvulsants and tricyclic compounds that block voltage-gated sodium channels may act as useful therapeutics for managing and treating pain. The use of these sodium channel blockers has, however, been limited by the lack of selectivity for different sodium channel subtypes with often additional central nervous system (CNS) and cardiovascular side effects. Therefore, a key to improvement on the limitations of most existing sodium channel blockers is to selectively target those that are involved in pain mechanisms whilst sparing those channels involved in cardiovascular function.