Astellas and Pandion partner on locally acting immunomodulators

Pharmaceutical

Astellas and Pandion have announced that they have signed a License and Collaboration Agreement to research, develop and commercialise immunomodulators for pancreatic autoimmune diseases. The partnership allows the parties to use Pandion’s modular biologics and immunology expertise with Astellas' therapeutics development and global commercialization capabilities for the treatment of autoimmune diseases. The former will be in charge of the design and discovery of the bispecific drug and the latter will be responsible for managing clinical, commercialised and preclinical activities.

Naoki Okamura, Astellas’ Representative Director Corporate EVP, CSO and CFO, 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. We will continue to dedicate our efforts in delivering novel treatments for diseases with high unmet medical needs, pursuing cutting-edge science and technological advances.”

“Astellas and Pandion have signed a License and Collaboration Agreement to research, develop and commercialise immunomodulators for pancreatic autoimmune diseases. “

Rahul Kakkar, Pandion’s CEO, said: "We are excited to collaborate with Astellas, a partner whose strategic vision for the potential of local immunomodulation in type 1 diabetes, and deep commitment and capabilities in immunology, will greatly accelerate our R&D efforts and build upon our existing collaboration with the JDRF T1D Fund. 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.”

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