NeuroScientific Biopharmaceuticals’ Lead Candidate, EmtinB, Shows Promise in Preclinical Model of MS

NeuroScientific Biopharmaceuticals (NSB)’s lead candidate EmtinB induces significantly greater myelin regeneration in a cellular model of multiple sclerosis (MS) than the market-leading therapy Copaxone, the company announced.

“These results represent a potential breakthrough in the treatment of MS as there are currently no approved therapeutic drugs available to patients that have demonstrated the ability to regenerate myelin in the central nervous system” Matthew Liddelow, NSB’s CEO and managing director, said in a press release.

EmtinB is a lab-made molecule designed to mimic the neuroregenerative and neuroprotective effects of a protein called metallothionein-II (MT-II). EmtinB resembles the portion of MT-II that binds to LRP1 and LRP2, two cell surface receptors present in several types of brain cells.

By binding to these receptors, EmtinB is expected to activate signaling pathways that promote nerve cell survival and regeneration, and also suppress neuroinflammation.

Previous data in a cellular model of MS showed that EmtinB significantly increased the number of oligodendrocytes — the cells that produce myelin, which is the protective sheath surrounding nerve fibers that is lost in MS. The study was conducted by an independent, French-based contract research organization called Neuron Experts, at NSB’s request.

Now, NSB asked the same organization to assess EmtinB’s ability to promote myelin regeneration in a cellular model of MS and compare it with that of Copaxone, the leading marketed disease-modifying therapy for MS.

Copaxone (glatiramer acetate injection), marketed by Teva Pharmaceuticals, is believed to work by suppressing the activity of immune cells that wrongly attack myelin. While it was shown to lower relapse rates and halt disease progression in MS patients, Copaxone is not meant to promote remyelination and thus cannot reverse the damage that MS already caused.

The new independent, preclinical study evaluated the regeneration of myelin around nerve fibers after treatment with either one of five doses of EmtinB (15, 30, 60, 120 or 150 micrograms per milliliter, mcg/ml), or a dose of Copaxone (10 mcg/ml).

Data showed that almost every dose of EmtinB resulted in a significant increase in myelin sheet around nerve fibers, compared with untreated cells. The only exception was the lower EmtinB dose of 15 mcg/ml.

At the higher doses (120 and 150 mcg/ml), EmtinB’s boost in myelin regeneration was significantly superior — by more than 25–30% — to that achieved with Copaxone.

“Whilst we previously showed that EmtinB could positively influence the proliferation of myelin-forming oligodendrocytes in an MS model, these results go a step further to demonstrate that EmtinB significantly increases actual myelin formation”, Liddelow said.

The study’s full results are expected to be released later this month.

EmtinB also is being evaluated as a potential treatment for Alzheimer’s disease and degenerative conditions of the optic nerve. NSB expects to launch Phase 1 clinical trials for both indications this year.