Multiple sclerosis

Multiple sclerosis (MS) is a chronic disease in which the immune system attacks myelin (the fatty coating around neurons) in the brain, optic nerves and spinal cord, impairing signal transmission and potentially resulting in loss of neurons themselves. Approved disease-modifying drugs modulate the immune system, which may reduce relapses and slow disability progression. There are no approved drugs that can promote repair and improve function.

Multiple Sclerosis and NVG-291

In multiple sclerosis, scar-like plaques, called lesions, form in areas of the brain and spinal cord where myelin is damaged. Although remyelination can occur spontaneously, it ultimately fails in the areas where lesions develop. These lesions are associated with molecules called chondroitin sulfate proteoglycans (CSPGs), which might initially help to contain the damage, but in the long term the interaction of CSPGs with their cellular receptor, protein tyrosine phosphatase sigma (PTPσ), interferes with the repair of damaged myelin.

In animal models, NVG-291-R relieves the inhibitory effects of CSPGs and thus NervGen’s lead drug candidate, NVG-291, is expected to enable neural repair by promoting formation of myelin and improving connections among neurons.

In an MS model, animals treated with NVG-291-R had substantially greater remyelination compared to placebo treated animals after 21 days, and NVG-291-R restored motor function even when administered after symptoms were fully developed (Luo et al., 2018).

In animal models of MS, NVG-291-R has been shown to

stimulate the production of oligodendrocyte precursor cells

allow remyelination and regeneration of damaged neurons
increase specific proteases that digest and break down the glial scar tissue (CSPGs) that otherwise keep neurons from regenerating and oligodendrocytes from remyelinating

A list of select scientific publications that give an overview of the robust effects of NVG-291-R seen in animal models is provided in our list of Journals & Publications