Kiniksa Enters Global License Agreement with Genentech for Fibrosis Drug
August 4, 2022
Kiniksa Pharmaceuticals entered into a global license agreement with Roche and Genentech, a member of the Roche Group, for the rights to develop and commercialize vixarelimab, a fully human monoclonal antibody targeting oncostatin M receptor beta (OSMRβ).
Genentech will focus development of vixarelimab in fibrosis, where oncostatin M (OSM)-mediated pathogenesis is thought to be an important pathway for intervention in multiple fibrotic indications.
“Pursuing novel therapies in fibrosis is central to Genentech’s focus on developing medicines for patients with respiratory diseases,” said James Sabry, global head of Roche Pharma partnering. “Developing vixarelimab, a first-in-class fully human monoclonal antibody, in fibrosis is another example of how we are taking an innovative approach to meet patients’ unmet needs.”
Under the terms of the global license agreement, Kiniksa will receive $100 million in upfront and near-term payments, and is eligible to receive up to approximately $600 million in certain clinical, regulatory, and sales-based milestones, before fulfilling upstream financial obligations. Kiniksa is also eligible to receive royalties on annual net sales. Genentech will obtain rights for the development and commercialization of vixarelimab.
“Our work underscores the differentiated potential of the OSMRβ mechanism as well as its potential to help patients with serious unmet need,” said Sanj Patel, chairman and CEO of Kiniksa. “The agreement provides an optimal infrastructure for the further development of vixarelimab. We plan to allocate the non-dilutive capital received from this transaction towards synergistic opportunities across our portfolio, including the expansion of our ARCALYST cardiovascular franchise.”
Kiniksa has completed screening patients for the phase 2b clinical trial of vixarelimab in prurigo nodularis. The company plans to complete the trial but will no longer disclose data in the second half of 2022.
Author: Rare Daily Staff
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