BOSTON, Mass., and SEATTLE, Wash., and EMERYVILLE, Calif., June 15th, 2022 – Affini-T Therapeutics, Inc., a biotechnology company unlocking the power of T cells against oncogenic driver mutations, and Metagenomi, Inc., a genetic medicines company with a versatile portfolio of next-generation, wholly-owned gene editing tools, today announced a partnership to enable Affini-T’s next generation ex vivo T cell receptor (TCR) cell therapies for solid tumor patients using Metagenomi’s novel proprietary gene editing systems.
“We are delighted to announce our partnership with Metagenomi and to apply their next-generation gene editing systems to our cell therapies targeting oncogenic and viral driver genes, including KRAS and p53, to provide the greatest impact for patients across a variety of hard-to-treat solid tumor types,” said Jak Knowles, M.D., Co-founder, President and Chief Executive Officer, Affini-T Therapeutics. “By working with Metagenomi, we will gain access to powerful, novel gene editing tools to make precise and multiplex edits to immune cells, thereby optimizing the effector function of our cell-based therapeutics.”
“With this collaboration, Metagenomi is executing on its ex vivo therapeutics partnering strategy in the immuno-oncology space. We are especially excited to partner with the outstanding team at Affini-T and its scientific founder Dr. Phil Greenberg, who has fundamentally advanced this field. We believe that cell therapy, combined with our powerful gene editing tools, is the future of immuno-oncology, treating patients with the highest unmet medical need,” said Brian C. Thomas, Ph.D., Founder and Chief Executive Officer of Metagenomi. “Our strategy in cell therapy strives to create a broad pipeline of licensed, partnered and in-house development programs with leading scientific teams.”
The partnership will leverage Metagenomi’s proprietary gene editing systems to complement Affini-T’s state-of-the-art TCR discovery and synthetic biology platforms to generate groundbreaking cell therapy products. Affini-T will have the option to exclusively license Metagenomi’s technology to make gene edits in autologous TCR T cell therapies for specific tumor targets, with the option to expand non-exclusively to editing certain allogeneic approaches. In the future the parties will discuss further targets for co-development and co-commercialization.
Under the terms of the agreement, Metagenomi will be entitled to receive tiered payments for each optioned cancer target plus additional milestone and royalty payments.
Metagenomi is a gene editing company committed to developing potentially curative therapeutics by leveraging a proprietary toolbox of next-generation gene editing systems to accurately edit DNA where current technologies cannot. Our metagenomics-powered discovery platform and analytical expertise reveal novel cellular machinery sourced from otherwise unknown organisms. We adapt and forge these naturally evolved systems into powerful gene
editing systems that are ultra-small, extremely efficient, highly specific and have a decreased risk of immune response. These systems fuel our pipeline of novel medicines and can be leveraged by partners. Our goal is to revolutionize gene editing for the benefit of patients around the world. For more information, please visit https://metagenomi.co/.
About Affini-T Therapeutics
Affini-T is unlocking the power of T cells and targeting core oncogenic drivers to develop potentially curative therapies for solid tumor cancers. Our differentiated cell therapy platform harnesses state-of-the-art engineering and synthetic biology capabilities to target even the most devastating cancer-driving mutations, beginning with KRAS. We leverage these tools to optimize T cell functions and rewrite the rules of the solid tumor microenvironment, enabling the potential for sustained clinical outcomes in patients. Building on the world-class innovation inherent in our leadership team, founders and technologies, we are powered to develop transformational medicines that last. Follow us on LinkedIn and Twitter.
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