Medigene AG, an immuno-oncology platform company focusing on the discovery and development of differentiated T cell immunotherapies for solid tumors and BioNTech SE have announced that their collaboration to advance T cell receptor immunotherapies against cancer will extend beyond the initial three-year term outlined at the signing of the agreement in February 2022.
Planegg/Martinsried, May 21, 2024. Medigene AG (Medigene or the “Company”, FSE: MDG1, Prime Standard), an immuno-oncology platform company focusing on the discovery and development of differentiated T cell immunotherapies for solid tumors and BioNTech SE (Nasdaq: BNTX, “BioNTech”) have announced that their collaboration to advance T cell receptor (TCR) immunotherapies against cancer will extend beyond the initial three-year term outlined at the signing of the agreement in February 2022. This extension will enable ongoing and future work required to potentially generate novel TCRs directed against multiple newly nominated antigen targets that could further expand the BioNTech warehouse of TCR candidates.
“We are pleased about the extension of our partnership with BioNTech aiming at the development of highly differentiated TCR-based therapies for patients suffering from solid tumors. The collaboration solidifies our position as a leader in the field of TCR generation while we continue to deliver very promising TCR candidates,” said Dr. Selwyn Ho, Chief Executive Officer at Medigene. “The ongoing work between our scientific teams reflects the strength of our partnership in the fight against cancer, and we look forward to making further progress in making a difference in the lives of cancer patients.”
In February 2022, Medigene and BioNTech entered into a global multi-target collaboration to discover and develop T cell receptor immunotherapies against multiple cancer targets including PRAME (PReferentially expressed Antigen in MElanoma). The agreement also included non-exclusive licenses to some of the proprietary technologies contained in Medigene’s End-to-End Platform including its PD1-41BB costimulatory switch protein.
About Medigene AG
Medigene AG (FSE: MDG1) is an immuno-oncology platform company dedicated to developing differentiated T cell therapies to effectively eliminate cancer. Its End-to-End Platform consists of multiple proprietary and exclusive technologies that generate optimal T cell receptors, armor and enhance these T cells to overcome the immunosuppressive tumor microenvironment (TME), and ensure the T cells drug product composition maximizes safety, efficacy and durability of response. This creates potential best-in-class, T cell receptor engineered T cell (TCR-T) therapies to treat multiple solid tumor indications for both its in-house product pipeline and partnering. Medigene’s lead TCR-T program MDG1015 is on track for IND filing in 3Q 2024 and CTA filing in 4Q 2024. For more information, please visit www.medigene.com
About Medigene’s End-to-End Platform
Medigene’s immunotherapies help activate the patient’s own defense mechanisms by harnessing T cells in the battle against cancer. Medigene’s End-to-End Platform combines multiple exclusive and proprietary technologies to create best-in-class, differentiated TCR-T therapies. The platform includes multiple TCR generation and optimization technologies (e.g., Allogeneic-HLA (Allo-HLA) TCR Priming), as well as product enhancement technologies (e.g., PD1-41BB and CD40L-CD28 Costimulatory Switch Proteins, iM-TCR) to address challenges in developing effective, durable and safe TCR-T therapies. Partnerships with multiple companies including BioNTech and Regeneron, continue to validate the platform’s assets and technologies.
About Medigene’s PD1-41BB Costimulatory Switch Protein
Checkpoint inhibition via PD-1/PD-L1 pathway:
Cells of solid tumors are sensitive to killing by activated T cells but can escape this killing activity by producing inhibitory molecules known as ‘checkpoint proteins’, such as the Programmed Death Ligand 1 (PD-L1), on their surface. When this occurs, activated T cells which express PD-1, the natural receptor for PD-L1, are inactivated. The expression of PD-L1 is an adaptive immune resistance mechanism for tumors that can help them survive and grow.
The 4-1BB (CD137) costimulatory signaling pathway:
Effective T cell immune responses to antigens typically require both a primary antigenic stimulation via the T cell receptor (TCR) and costimulatory signals. The intracellular signaling domains of the 4-1BB protein offer a well-characterized pathway to costimulation and enhanced T cell responses.
Medigene’s PD1-41BB switch receptor turns the tumor’s attempted self-defense mechanism against the tumor by substituting the inhibitory signaling domain of PD-1 with the activating signaling domain of 4-1BB. Therefore, instead of inactivating T cells, the switch receptor delivers an activating signal to TCR-T cells. PD1-41BB-modified TCR-T cells proliferate strongly in the presence of PD-L1-positive tumor cells and kill more tumor cells upon repeated exposure. Additionally, switch receptor signals enable TCR-T cells to function better with low levels of glucose or high levels of TGFß, two conditions characteristic of strongly hostile tumor microenvironments.
About PRAME
PRAME (PReferentially expressed Antigen in MElanoma) is a tumor antigen of the cancer-testis-antigen family which is over-expressed in various solid and blood cancers. Expression in healthy tissue is limited to the testis, which itself is an immuno-privileged tissue that usually cannot be attacked by the body’s own immune cells. This renders PRAME very suitable as a target antigen for TCR-T therapies.
This press release contains forward-looking statements representing the opinion of Medigene as of the date of this release. The actual results achieved by Medigene may differ significantly from the forward-looking statements made herein. Medigene is not bound to update any of these forward-looking statements. Medigene® is a registered trademark of Medigene AG. This trademark may be owned or licensed in select locations only.
Medigene AG
Pamela Keck
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