Antihistamine Could Act As a Remyelinating Agent in Multiple Sclerosis

In a surprisingly fast translation of lab research into discoveries into a treatment with the potential to profit patients, UC San Francisco researchers have effectively finished a Phase II clinical trial demonstrating that an FDA- approved antihistamine nervous sensory system function in patients with chronic multiple sclerosis (MS).

In light of past lab laboratory of the antihistamine compound at UCSF, the specialists said, the medication most likely exerted its impact by repairing damage MS had inflicted on myelin, a protecting membrane that speeds transmission of electrical signals in the nervous system.

Research demonstrates an over-the-counter antihistamine could act as a remyelinating agent in multiple sclerosis. Current treatments for multiple sclerosis (MS) mean to decrease the risk of further inflammation-mediated damage to the myelin sheath, which surrounds neuronal axons.

Preliminary research has demonstrated that clemastine fumarate, an over-the-counter medication at first marketed as an antihistamine, has potential as a remyelinating agent.

Analysts found a significant reduction in visual-evoked potential latency delay (a measure that is some of the time used to confirm a diagnosis of MS) after patients with relapsing MS were treated with clemastine fumarate.

In a crossover research published in The Lancet (online, 10 October 2017), 50 patients with relapsing MS were randomly assigned to clemastine fumarate or placebo for 90 days, before switching treatment for 60 days, notwithstanding their current immunomodulatory treatment.

The group found a significant reduction in visual-evoked potential latency delay (a measure that is once in a while used to confirm a diagnosis of MS) after treatment with clemastine fumarate. The impacts were consistent in the two groups and persisted even after patients switched to placebo.

The results were related to fatigue; however, no serious adverse events were reported. The outcomes are the main evidence of drug-induced myelin repair in a chronic neurodegenerative condition, the group concluded.

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