Immatics Announces Upcoming Oral Presentation at the Society for Melanoma Research Congress 2024

On September 6, 2024 Immatics N.V. (NASDAQ: IMTX, "Immatics" or the "Company"), a clinical-stage biopharmaceutical company active in the discovery and development of T cell-redirecting cancer immunotherapies, reported that updated clinical data on its lead cell therapy candidate, ACTengine IMA203 targeting PRAME, will be presented at the 21st International Congress of the Society for Melanoma Research (Press release, Immatics, SEP 6, 2024, View Source [SID1234646393]).

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Oral presentation

Date / Time: October 11, 2024 / 8:00 – 8:20 am Central Daylight Time
Session: Plenary Session 1 – Developmental Immunotherapy (Cellular Immunotherapy, Vaccines, and New Checkpoints)
Title: ACTengine IMA203 TCR-T targeting PRAME in PD1-refractory metastatic melanoma – Clinical Update
Presenter: Martin Wermke, M.D. (University Hospital Dresden, Germany)

About IMA203

ACTengine IMA203 T cells is an autologous T cell product with a genetically modified, pairing-enhanced TCR directed against an HLA-A*02-presented peptide derived from preferentially expressed antigen in melanoma (PRAME). This peptide is frequently expressed in a large variety of solid cancers, thereby supporting the program’s potential to address a broad cancer patient population. Immatics’ PRAME peptide is present at a high copy number per tumor cell and is homogeneously and specifically expressed in tumor tissue. The peptide has been identified and characterized by Immatics’ proprietary mass spectrometry-based target discovery platform, XPRESIDENT. Through its proprietary TCR discovery and engineering platform XCEPTOR, Immatics has generated a highly specific T cell receptor (TCR) against this target for its TCR-based cell therapy approach, ACTengine IMA203.

ACTengine IMA203 TCR-T is currently being evaluated in a Phase 1 trial as IMA203 monotherapy, and as a second-generation IMA203CD8 (GEN2) monotherapy, where IMA203-engineered T cells are co-transduced with a CD8αβ co-receptor, thereby leveraging the power of both CD4+ and CD8+ T cells. As previously reported, IMA203 in combination with an immune checkpoint inhibitor has been deprioritized.