MiNK Therapeutics Presents Preclinical Cancer Data For iNKT Cell Therapy Platform At SITC 2026

• Colorectal cancer: in a human liver-metastasis organoid model resistant to botensilimab and balstilimab alone, the addition of agenT-797 supported immune reprogramming and tumor-cell killing, reinforcing the rationale for an ongoing Phase 2 combination study
• Senolytic activity: agenT-797 and FAP-targeted MiNK-215 cleared senescent cells left behind after chemotherapy; cells linked to relapse and to fibrotic disease, and FAP targeting extended MiNK-215's killing into the tumor's supporting stroma
• Pulmonary development: findings highlight immune mechanisms relevant to acute inflammation, cellular senescence and tissue remodeling, supporting further investigation in MiNK's randomized Phase 2 trial in acute hypoxemic respiratory failure/ARDS
• Off-the-shelf platform: MiNK's allogeneic iNKT platform combines a clinical-stage unmodified cell therapy with next-generation engineered candidates, designed for scalable, cryopreserved delivery without patient-specific manufacturing

NEW YORK, Nov. 06, 2026 (GLOBE NEWSWIRE) -- MiNK Therapeutics, Inc. (NASDAQ:INKT), a clinical-stage biopharmaceutical company pioneering allogeneic invariant natural killer T (iNKT) cell therapies, today announced preclinical findings from two studies presented at the 41st Annual Meeting of the Society for Immunotherapy of Cancer (SITC) in Phoenix, Arizona. The studies address two distinct mechanisms by which tumors resist treatment: immune-suppressive metastatic environments that limit checkpoint blockade, and senescent cells that persist after therapy. Together they show how one foundational iNKT biology, in unmodified and engineered form, can be directed against both through tumor-cell killing, immune modulation and engineered targeting.

In one study, agenT-797 shifted suppressive immune populations toward an immune-stimulatory phenotype in a human organoid model of colorectal cancer liver metastases. Further, agenT-797, in combination with antigen-specific T cells and BOT+BAL, also increased tumor-cell killing.

In a second study, conducted in collaboration with Dr. Jesús Gil and his laboratory at the MRC London Institute of Medical Sciences, Imperial College London, both unmodified agenT-797 and MiNK-215, MiNK’s FAP-targeted, IL-15-armored CAR-iNKT candidate, killed senescent tumor cells. FAP-CAR engineering additionally enabled MiNK-215 to kill FAP-expressing fibroblasts, extending the platform's reach into the tumor stroma. These concordant findings reinforce the scientific foundation of MiNK’s pipeline and add to the growing body of evidence supporting iNKT cell therapy across cancer indications.