On November 6, 2026 MiNK Therapeutics, Inc. (NASDAQ: INKT), a clinical-stage biopharmaceutical company pioneering allogeneic invariant natural killer T (iNKT) cell therapies, reported preclinical findings from two studies presented at the 41st Annual Meeting of the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) 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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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.

"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," said Jennifer Buell, Ph.D., President and Chief Executive Officer of MiNK Therapeutics.

SITC 2026 Poster Presentations

Poster #270: "AgenT-797, An Allogeneic iNKT Cell Therapy, Enables Tumor-cell Killing In A Human Organoid Model of Immune Checkpoint Inhibitor-refractory Colorectal Cancer Liver Metastases."
Presenter: Shanmugarajan Krishnan, Ph.D.; Saturday, November 7, 2026; 10:00 a.m.–2:00 p.m. and 6:00–8:10 p.m. MST.

Poster #177: "Native and engineered allogenic invariant natural killer T (iNKT) cells eliminate senescent tumor cells and fibroblasts in oncogenic in vitro models."
Presenter: Jing Fang, Ph.D.; Friday, November 6, 2026; 12:15–1:45 p.m. and 6:40–8:10 p.m. MST.
Location: Phoenix Convention Center, North Building, Lower Level, Exhibition Halls 4–6, Phoenix, Arizona.

Reprogramming Immune Resistance in Colorectal Cancer Liver Metastases

Patients with microsatellite-stable (MSS) colorectal cancer and liver metastases represent a substantial unmet need with no approved immunotherapy option: the immune-suppressive metastatic environment limits the activity of existing therapies, and liver involvement is associated with resistance to checkpoint blockade.

In a human organoid model incorporating colorectal cancer, liver-associated and immune cells, agenT-797 shifted suppressive immune populations toward a more immune-stimulatory phenotype, depleting CD206+ M2-like macrophages and increasing CD86+/HLA-DR+ antigen-presenting cells. When combined with antigen-specific T cells and botensilimab (BOT), an Fc-enhanced anti-CTLA-4 antibody, plus balstilimab (BAL), an anti-PD-1 antibody, the triple combination increased CD8 T-cell density, raised granzyme B, IFN-γ, TNF-α, CXCL-9, CCL3 and IL-8, reduced EpCAM+ tumor-cell content and increased tumor-cell apoptosis. Critically, the model was refractory to BOT+BAL alone, which produced no statistically significant tumor-cell killing. Adding agenT-797 unlocked killing, and the full effect required all three components.

These findings provide a mechanistic rationale for the ongoing Phase 2 study of agenT-797 with BOT+BAL in previously treated microsatellite stable (MSS) colorectal cancer with liver metastases (CRC LM) (NCT07550088; funded by Scripps Institute, PI Darren Sigal).

Eliminating Senescent Cells with Unmodified and Engineered iNKT Therapies

Senescent cells can accumulate after cancer treatment or other cellular stress. Although they stop dividing, they can release signals that contribute to inflammation, tissue remodeling and immune escape. Dr. Jesús Gil and his team evaluated whether unmodified and engineered iNKT cell therapies could recognize and eliminate these cells and identified the cellular factors and resistance mechanisms that determine whether iNKT killing succeeds.

MiNK-215 is an allogeneic CAR-iNKT cell engineered to target fibroblast activation protein (FAP), which is expressed on cancer-associated and senescent fibroblasts — they support cells that surround tumors — and armored with IL-15 to support persistence and immune activation.

In this model, three findings emerged. First, both unmodified agenT-797 and MiNK-215 killed therapy-induced senescent breast cancer cells, which carried high levels of the NKG2D stress ligands MICA/B and ULBP2/5/6 and low checkpoint-ligand expression. Second, FAP-CAR engineering enabled MiNK-215 to kill non-senescent, FAP-high lung fibroblasts that unmodified agenT-797 did not; a targeting capability conferred by the CAR. Third, senescent lung fibroblasts resisted both therapies and carried elevated PD-L1, PD-L2 and CD155 — making checkpoint-ligand upregulation a defined, addressable obstacle that the next generation of engineered iNKT therapies can be built to overcome.

Loading the lipid antigen α-galactosylceramide (α-GalCer) restored unmodified agenT-797 killing of the less-sensitive senescent fibroblasts, indicating that this resistance can be overcome through antigen presentation and informing engineering and combination strategies. Because cellular senescence and fibroblast activation contribute to persistent tissue remodeling in cancer and fibrotic diseases, these findings provide a rationale for further investigation of engineered iNKT therapies in fibroinflammatory conditions.

"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," said Jesús Gil, Professor of Cell Proliferation, MRC London Institute of Medical Sciences, Imperial College London, and corresponding author of the study.

Extending iNKT Biology from Acute Inflammation to Tissue Remodeling and Fibrosis

MiNK is advancing agenT-797 in C-1300-02, a randomized, placebo-controlled Phase 2 trial in acute hypoxemic respiratory failure, including ARDS (NCT07615010), evaluating acute clinical outcomes. Severe acute lung injury involves dysregulated immune responses, epithelial and endothelial damage, and persistent inflammation that, in some patients, progresses to abnormal tissue repair and pulmonary fibrosis.

The SITC (Free SITC Whitepaper) findings highlight complementary mechanisms relevant to this continuum: agenT-797’s ability to reprogram suppressive immune environments, and the capacity of unmodified and engineered iNKT cells to recognize selected senescent and FAP-expressing cells involved in tissue remodeling. These observations extend the potential of MiNK’s pulmonary strategy, from intervening during acute inflammatory injury to exploring engineered iNKT approaches for persistent fibroinflammatory disease.

(Press release, MiNK Therapeutics, NOV 6, 2026, View Source [SID1234674428])