The FAP × CD3 bispecific antibody OMTX305 induces T cell–mediated antitumor effects in patient-derived ex vivo models of solid tumors

Within solid tumors, stromal barriers and immune exclusion limit the success of immunotherapies. Thus, novel therapeutic approaches are required to remodel the tumor-supportive microenvironment and enhance therapeutic responses. We developed a bispecific, trivalent Fab-eIg T cell engager (OMTX305) targeting fibroblast activation protein (FAP), a marker of tumor-promoting cancer-associated fibroblasts. The translational potential of OMTX305 was investigated in 2D and 3D patient-derived preclinical models, with a focus on precision-cut tumor slices (PCTSs) of lung and ovarian cancer cocultured with autologous PBMCs. By combining spatial biology with cytokine and transcriptomic analysis, we show that OMTX305 treatment eliminated FAP-expressing fibroblasts, induced interferon responses and extracellular matrix remodeling, ultimately triggering bystander killing of adjacent tumor cells. Distinct immune phenotypes and PD-L1 expression patterns appeared to be associated with differential treatment responses, suggesting their potential as biomarkers for patient stratification. Our findings highlight the clinical potential of targeting stromal elements as a cancer therapy and establish PCTS as a powerful preclinical platform for personalized immunotherapy assessment.

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Publication Details

Journal
Science Advances
Published
2026-09-11
DOI
https://doi.org/10.1126/sciadv.aee2124
Primary Topic
Peptidase Inhibition and Analysis
Type
article
Field-Weighted Citation Impact
0.00

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article

The FAP × CD3 bispecific antibody OMTX305 induces T cell–mediated antitumor effects in patient-derived ex vivo models of solid tumors

Katrin S. Kurz, Laureano Simón, Oliver Seifert, Lennart Kühl et al.
Science Advances
Peptidase Inhibition and Analysis
article

The FAP × CD3 bispecific antibody OMTX305 induces T cell–mediated antitumor effects in patient-derived ex vivo models of solid tumors

Katrin S. Kurz, Laureano Simón, Oliver Seifert, Lennart Kühl, Chunguang Liang, Adrian Kneer, Annelie K. Schäfer, Jan Schlegel, Gerhard Preißler, Monilola A. Olayioye, Thomas E. Mürdter, Walter E. Aulitzky, Matthias Schwab, Isabel Egaña, Roland E. Kontermann, Julia Thiel, Meng Dong, Myriam Fabre, German Ott, Sascha Dreher
article en

Abstract

Within solid tumors, stromal barriers and immune exclusion limit the success of immunotherapies. Thus, novel therapeutic approaches are required to remodel the tumor-supportive microenvironment and enhance therapeutic responses. We developed a bispecific, trivalent Fab-eIg T cell engager (OMTX305) targeting fibroblast activation protein (FAP), a marker of tumor-promoting cancer-associated fibroblasts. The translational potential of OMTX305 was investigated in 2D and 3D patient-derived preclinical models, with a focus on precision-cut tumor slices (PCTSs) of lung and ovarian cancer cocultured with autologous PBMCs. By combining spatial biology with cytokine and transcriptomic analysis, we show that OMTX305 treatment eliminated FAP-expressing fibroblasts, induced interferon responses and extracellular matrix remodeling, ultimately triggering bystander killing of adjacent tumor cells. Distinct immune phenotypes and PD-L1 expression patterns appeared to be associated with differential treatment responses, suggesting their potential as biomarkers for patient stratification. Our findings highlight the clinical potential of targeting stromal elements as a cancer therapy and establish PCTS as a powerful preclinical platform for personalized immunotherapy assessment.

Science AdvancesVol. 12(37)
University of Stuttgart (DE), German Cancer Research Center (DE), Heidelberg University (DE), University of Würzburg (DE), Robert Bosch Hospital (DE), Oncomatryx (Spain) (ES), Dr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology (DE), Research Institute for Work, Technology and Culture (DE), Jena University Hospital (DE), University Hospital Ulm (DE), Friedrich Schiller University Jena (DE), University of Tübingen (DE)
Berthold Leibinger Stiftung, Robert Bosch Stiftung, Deutsche Forschungsgemeinschaft, Ministerium für Wissenschaft, Forschung und Kunst Baden-Württemberg, Bundesministerium für Forschung und Technologie
Reduced inequalities
Openalex Percentile: Top 14%
Peptidase Inhibition and Analysis
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