Fampridine-SR ("4-aminopyridine", "4-AP", “fampridine”) is an investigational oral, sustained-release tablet formulation of 4-aminopyridine. In laboratory studies fampridine has been found to improve impulse conduction in nerve fibers in which the insulating layer, called myelin, has been damaged.
Clinical History of Fampridine-SR in Multiple Sclerosis (MS)
Acorda recently completed a Phase 3 clinical study of Fampridine-SR to evaluate its safety and efficacy in improving walking ability in people with all types of MS.
View a video* illustrating Fampridine-SR’s mechanism of action:
Researchers have shown that, contrary to popular belief, most people with spinal cord injury (SCI) do not have severed cords; rather, most have blunt damage to the cord. The great majority of such individuals have some axons within the spinal cord that survive the injury. However, these surviving axons often are damaged and lose part of their myelin, the insulating sheath that permits electrical impulses to be conducted down the axon. Nerve impulses "short circuit" in demyelinated axons, much like electricity in a wire whose insulation is stripped. Thus, even though a demyelinated axon is alive, it cannot transmit motor or sensory impulses. In multiple sclerosis (MS), the myelin is believed to be damaged by the body's own immune system, rather than by physical trauma as in SCI.
Fampridine-SR's major action is to block specialized potassium channels on axons. When an axon is demyelinated after injury, large numbers of these potassium channels are exposed and "leak" potassium ions, causing the axon to "short circuit".
By closing the exposed potassium channels, Fampridine-SR permits the axon to transmit impulses again, even in a demyelinated state.
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