Pandion Therapeutics and Astellas Pharma have signed a $795m agreement for the research, development and commercialisation of locally acting immunomodulators to treat Type 1 diabetes, as well as other autoimmune diseases of the pancreas.

Under the license and collaboration agreement, the modular biologics and functional immunology expertise of Pandion will combine with Astellas’ therapeutics development and global commercialisation capabilities to treat these diseases.

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Pandion will leverage its modular immune effector and tissue tether platform to design and discover bispecific drug candidates.

Astellas will carry out preclinical, clinical and commercialisation activities for selected candidates developed during the partnership.

Astellas representative director corporate executive vice president, chief strategy officer and chief financial officer Naoki Okamura said: “Astellas positions antigen-specific immune modulation (ASIM) as one of our strategic areas of primary focus and we are engaged in the development of novel therapies for autoimmune diseases using new modality / technology.

“Pandion’s tissue-specific immune modulation technology is anticipated to be the potential next-generation modality for ASIM, which can potentially expand its application to various other autoimmune diseases.”

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As part of the collaboration, Pandion is eligible to receive upfront and payments of up to $45m related to research and preclinical activities.

Additionally, upon the development and commercialisation of multiple candidates for multiple pancreatic autoimmune diseases by Astellas, Pandion may receive future development and commercial milestone payments of more than $750m from Astellas.

Furthermore, Pandion will receive royalties on global net sales of any commercial products developed through the partnership.

Pandion CEO Rahul Kakkar said: “Type 1 diabetes involves the autoimmune destruction of the patient’s own pancreas. Our tissue targeted immune effectors are designed to directly address this aberrant immune response and modify the disease at the site of immune attack.”