Neuraxpharm pays US$650m for MS drug commercialisation

Together with a fee of US$12.5m for the launch of the B cell suppressant antibody to treat relapsing/remitting mulitple sclerosis (rMS), the US$140m upfront payment and success-dependent milestones of US$492.5m, the deal can is valued at up to US$645m. In addition, TG will receive tiered double-digit royalties on net product sales up to 30%. Neuraxpharm’s dedicated neurology focus and established European presence makes them an attractive partner the European launch of ublituximab-xiiy, targeted within the next six months

Ublituximab-xiiy (BRIUMVI) is the first and only anti-CD20 monoclonal antibody approved in the United States (US) and European Union (EU) for adult patients with relapsing forms of multiple sclerosis (RMS) that can be administered in a one-hour infusion, twice a year, following the starting dose. Neuraxpharm is backed by funds advised by the global private equity firm, Permira.

Neuraxpharm will have the exclusive right to commercialise BRIUMVI in territories outside the United States, Canada, and Mexico, which are retained by TG, and excluding certain Asian countries previously partnered. Additionally, TG Therapeutics retains an option to buy back all rights under the commercialisation agreement for a period of two years in the event of a acquisition of TG.

BRIUMVI is currently approved and commercially available in the US for patients with rMS, to include clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease, in adults. BRIUMVI has also been approved by the European Commission (EC) for the treatment of adult patients with RMS who have active disease defined by clinical or imaging features. With this approval, the centralised marketing authorisation is valid in all EU Member States, Iceland, Norway and Liechtenstein. Approval in the United Kingdom (UK) and Switzerland will also be pursued.

BRIUMVI is a novel monoclonal antibody that targets a unique epitope on CD20-expressing B-cells. BRIUMVI is uniquely designed to lack certain sugar molecules normally expressed on CD10-antibodies. Removal of these sugar molecules allows for efficient B-cell depletion at low doses.