BRUSSELS, July 29, 2020 /PRNewswire/ — UCB today announced an agreement to enter into a world-wide, exclusive license agreement with Roche and Genentech, a member of the Roche Group, for the global development and commercialization of UCB0107 in Alzheimer’s Disease (AD). The transaction remains subject to obtaining antitrust clearance and other customary closing conditions.
Charl van Zyl, Executive Vice President UCB and Head of Neurology said: “We are excited that Roche and Genentech, with their deep and wide-ranging expertise, capacity and know-how in Alzheimer’s Disease, will collaborate with UCB on UCB0107 with a shared ambition to offer people living with Alzheimer’s Disease a new treatment option. Our science driven, patient centric development approach, and leading experience in neurological diseases provides a uniquely holistic view towards the unmet needs and the potential for an effective anti-Tau antibody in the treatment of neurodegenerative diseases like Alzheimer’s Disease and progressive supranuclear palsy. In-line with our ongoing and longstanding commitment to the neurodegeneration community, this partnership represents an important step in the potential development of this exciting new medicine.”
James Sabry, Global Head of Roche Pharma Partnering said: “In Alzheimer’s Disease, we are continuing to explore new molecules that address the key pathways of this complex disease. We are pleased to embark on this journey together with UCB to help expand our efforts on tau. Our commitment remains strong on exploring multiple approaches with the hope that our research and development, including this collaboration with UCB, will lead to a disease-modifying medicine that could positively impact millions of people with Alzheimer’s Disease.”
UCB0107 is an investigational monoclonal antibody drug being developed by UCB as a potential treatment for patients with tauopathies such as progressive supranuclear palsy (PSP) and Alzheimer’s Disease.
UCB will provide an exclusive, world-wide license to Roche and Genentech to develop and commercialize UCB0107 in AD. In return, UCB will receive an initial upfront payment of US $120 million. UCB will fund and perform a proof-of-concept study in AD and, upon availability of the results of that study, Genentech has the right to progress with the development or return full rights back to UCB. After Genentech’s decision to proceed with further clinical development, UCB will be eligible to receive further potential cost reimbursement, development and sales milestone payments as well as royalties with a total potential consideration approaching US $2 billion upon receipt of certain regulatory approvals and satisfying certain clinical and sales milestones.
This license agreement does not impact UCB’s 2020 financial outlook.
UCB continues to develop UCB0107 in progressive supranuclear palsy (PSP), with a confirmatory phase 3 study due to commence in Q2 2021.
UCB0107 is a recombinant, humanized, full-length IgG4 monoclonal antibody, targeting a central Tau epitope, which is being developed to block/reduce the spread of Tau pathology.
Tau is a microtubule-associated protein expressed in the central nervous system, which supports the assembly and stabilization of neuronal microtubules. In tauopathies, Tau becomes pathogenic, forming tangles, which cause cell damage and ultimately neuronal death.[1.2.3] It is hypothesised that the spread of Tau protein from neuron to neuron underpins disease progression in tauopathies providing the rationale for antibody therapies.
UCB, Brussels, Belgium (www.ucb.com) is a global biopharmaceutical company focused on the discovery and development of innovative medicines and solutions to transform the lives of people living with severe diseases of the immune system or of the central nervous system. With more than 7 500 people in approximately 40 countries, UCB generated revenue of € 4.9 billion in 2019. UCB is listed on Euronext Brussels (symbol: UCB). Follow us on Twitter: @UCB_news
- Courade J-P et al. Acta Neuropathol. 2018;136(5):729–45.
- Albert M et al. Brain. 2019; 142:1736–50.
- Fontaine S et al. Cell Mol Life Sci. 2015;72(10):1863–79.
- Ling H. J Mov Disord. 2016;9(1):3–13.