4-Aminopyridine

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Background

IC50: 170 and 230 μM at KV1.1 and KV1.2, respectively
K+ channels function to conduct K+ ions down their electrochemical gradient, doing so both rapidly and selectively. Biologically, these channels act to set or reset the resting potential in a number of cells. In excitable cells, such as neurons, the delayed counterflow of potassium ions shapes the action potential. 4-Aminopyridine (4-AP or fampridine) is a potassium channel-blocking agent.
In vitro: 4-AP acts by selectively blocking fast, voltage-gated K+ channels in excitable tissues. In axons, K+ channel blockade increases the safety factor1 across demyelinated internodes and 4-AP can, therefore, restore conduction in focally demyelinated axons. 4-AP also increases calcium (Ca2+) influx at presynaptic terminals thereby enabling an enhancement of neuroneuronal or neuromuscular transmission in normally myelinated neurons [1].
In vivo: Investigations of the effects of 4-AP on neurologic deficits in animal in vivo models of demyelinating disease or SCI have yielded inconsistent results. Some trials have shown indications of potential neurological benefit, such as enhanced motor evoked potentials or reflex activity, while others have yielded no evident gains in function [1].
Clinical trial: The randomized clinical trials which have been completed to date indicate that K+ channel blockade by 4-Aminopyridine may prove to be a useful strategy for ameliorating central conduction deficits. Diverse neurological gains have been reported for both motor and sensory domains [1].

Reference:[1] Hayes KC. The use of 4-aminopyridine (fampridine) in demyelinating disorders. CNS Drug Rev. 2004 Winter;10(4):295-316.