MiNK Therapeutics New Data Highlights Its Off-the-Shelf iNKT Cell Therapy Targets Two Key Mechanisms of Tumor Resistance Presented at the Society of Immunotherapy of Cancer (SITC 2026)
Key Highlights
- ➤AgenT-797 plus BOT+BAL restored tumor killing in checkpoint-resistant colorectal liver-metastasis organoids
- ➤MiNK-215 killed FAP-expressing fibroblasts, extending activity into tumor-supporting stroma
- ➤AgenT-797 and MiNK-215 eliminated therapy-induced senescent breast cancer cells
- ➤MiNK advances agenT-797 in randomized Phase 2 trial for acute hypoxemic respiratory failure
- ➤Allogeneic iNKT platform offers scalable, cryopreserved, off-the-shelf cell therapies
Expert Statements
Jennifer Buell, Ph.D., President and Chief Executive Officer of MiNK Therapeutics
“These findings demonstrate the breadth of our iNKT platform and its potential to address distinct mechanisms of immune dysfunction. In colorectal cancer, agenT-797 reprograms the tumor environment to support T-cell-mediated killing, providing a mechanistic rationale for our ongoing Phase 2 combination study. In parallel, our engineered iNKT platform expands our ability to target senescent and stromal cells implicated in persistent inflammation and tissue remodeling. This biology is also relevant to acute lung injury, where dysregulated inflammation can lead to lasting pulmonary damage and fibrosis. With agenT-797 advancing in a randomized Phase 2 study in acute respiratory failure, we are focused on translating these insights into clinical outcomes across serious diseases”
Jesús Gil, Professor of Cell Proliferation, MRC London Institute of Medical Sciences, Imperial College London, and corresponding author of the study
“The different responses across these models show that senescence does not create a single uniform immune target. Observing the signals associated with sensitivity and resistance will help us define where iNKT-based approaches are most useful”
* 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.
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