Medigene Presents Preclinical Data on Optimal Affinity TCRs Targeting the Neoantigen Mutant KRAS

Planegg/Martinsried, May 15, 2024. Medigene AG (Medigene or the “Company”, FSE: MDG1, Prime Standard), an immuno-oncology platform company focusing on the discovery and development of T cell immunotherapies for solid tumors, today presents the company’s proprietary T cell receptor (TCR) discovery process to obtain optimal affinity 3S (sensitive, specific and safe) TCRs at the 21^th Association for Cancer Immunotherapy (CIMT) Annual Meeting in Mainz from May 15 - 17, 2024. Data presented also shows the clear benefit of adding the PD1-41BB costimulatory switch protein (CSP) to further armor and enhance these 3S TCR-T cells, which enables them to overcome the immunosuppressive tumor microenvironment.

The poster with the title “Selection of superior KRAS G12V mutation-specific T cell receptors with unique characteristics for 3rd generation armored and enhanced T cell therapy” will be available on Wednesday, May 15, 2024, following the presentation on Medigene’s website: https://medigene.com/science/abstracts/

“The discovery process of unique TCR sequences is the first key step to generate TCR-T cells with optimal safety, efficacy and durability,” said Dr. Selwyn Ho, Chief Executive Officer at Medigene. “Employing a high-throughput process as part of our End-To-End (E2E) Platform enabled us to discover unique TCR sequences with distinct features with respect to specificity, sensitivity and safety (3S). These potential best-in-class 3S TCRs hold promise for utilization across diverse modalities, here focusing on T cell receptor engineered T cell (TCR-T) therapies, but also for use in T cell engagers and TCR natural killer cell therapies. “

He continued: “Our TCRs can undergo further enhancement through integration of various technologies within our E2E Platform such as with our exclusive PD1-41BB CSP, which significantly enhances TCR-T cell functionality, persistence and proliferation and offers the promise of highly effective and durable TCR-T therapies in patients.”

The presented data highlighted the specificity and sensitivity of TCR-T cells co-expressing the PD1-41BB CSP alongside one of three distinct 3S TCRs targeting the mKRAS G12V neoantigen. These TCR-T cells displayed markedly increased secretion of interferon gamma (IFNγ) observed upon TCR-T cell stimulation with mKRAS G12V-positive tumor cells, contrasting with the absence of IFN γ secretion upon stimulation with any tumor or healthy cell expressing naturally occurring wild-type KRAS protein.