Sponsored by:
Acorda Therapeutics
Information provided by:
Acorda Therapeutics
ClinicalTrials.gov Identifier:
NCT00053417
Purpose
Multiple Sclerosis (MS) is a disorder of the body's immune system that affects the Central Nervous System (CNS). Normally, nerve fibers carry electrical impulses through the spinal cord, providing communication between the brain and the arms and legs. In people with MS, the fatty sheath that surrounds and insulates the nerve fibers (called "myelin") deteriorates, causing nerve impulses to be slowed or stopped. As a result patients with MS may experience periods of muscle weakness and other symptoms such as numbness, loss of vision, loss of coordination, paralysis, spasticity, mental and physical fatigue and a decrease in the ability to think and/or remember. These periods of illness may come (exacerbations) and go (remissions). Fampridine-SR is an experimental drug that increases the ability of the nerve to conduct electrical impulses. This study will evaluate the effects of Fampridine-SR on the walking ability of subjects with MS, as well as to examine the effects on muscle strength and spasticity. The study will also examine the possible risks of taking Fampridine-SR.
Multiple Sclerosis Drug: Fampridine-SR (4-aminopyridine, 4-AP) Phase II This study has been completed. 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 completed enrollment of its second Phase 3 clinical trial of Fampridine-SR to evaluate its safety and efficacy in improving walking ability in people with MS. Data is expected second quarter 2008. 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. 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. From: Acorda Therapeutics Inc.
