Neuroprotection and Remyelination

Bionure seeks to change the life of patients suffering AON, NMO and MS

Neuroprotection refers to the mechanisms and strategies used to prevent and protect axons, neurons and myelin against neuronal injury or degeneration in order to restore their functioning with preservation of the quality of vision.

In optic neuritis, inflammation of the optic nerve induces significant demyelination and axonal damage. Once inflammation is removed by natural mechanisms or accelerated by the use of corticosteroids, optic nerve tissue remains damaged. Axons that have been damaged during the inflammatory attack cannot be restored or replaced and its loss becomes irreversible, leading to permanent visual dysfunction. Further, lack of myelin seems to contribute to permanent axonal degeneration in the long-term.

This leads to a significant impact in patients’ sight, with most than half of people that have suffered an optic neuritis episode referring impairment of visual function in the long-term, limiting their quality of life. Consequently, a key unmet need in AON patients is to prevent axonal damage during the attack in order to prevent subsequent disability.

Our main candidate BN201 has been shown to promote neuroprotection by protecting and preventing axonal loss and neuronal death in several animal models driven by different mechanisms of damage: demyelination in the lysolecithin-induced demyelination model, inflammation in the experimental autoimmune encephalomyelitis model and hypertension in the hypertensive glaucoma model.

Further to its compelling neuroprotective activity in axons and neurons, BN201 has proved to be remyelinating by differentiating oligodendrocyte precursor cells (OPCs) into mature oligodendrocytes and promoting the formation of myelin sheaths around neurons, in a collaboration established with the Myelin Repair Foundation.