a recent UPS article on new drug b nding sites on Ca2+ channels, S Jedding and colleagues make the a:sertion that the experimental neuroprotective agent, lifarizine, is less selective for Na+ channels than p lenytoin, riluzole and lamotriginei. I- owever, the authors do not specify M hat this alleged lack of selectivity relates to. Many agents that inhibit Na+ cur- rents do so by selectively binding to the inactivated state of the channel, thereby impeding the voltage-depen- dent transition of the channel back to the resting state that would occur in the absence of drug. This effectively reduces the population of resting state channels which, in turn, results in fewer channels available to open in response to depolarization. Clearly, the higher the affinity of a drug for its t: rget site on the inactivated channel, tl le lower the concentration needed to remove a given proportion of chan- nels from the total ‘active’ pool. In voltage-clamp experiments, the con- centration of lifarizine interacting M ith 50% of inactivated state Na+ channels (I$) is 0.19 =