MiNK Therapeutics, Inc. (NASDAQ: INKT) released preclinical data for its next‑generation invariant natural killer T (iNKT) cell therapy, MiNK‑215, in the peer‑reviewed journal Cancer Immunology Research on November 20 2025. The study demonstrates that MiNK‑215 remodels the tumor stroma by targeting fibroblast‑activation protein (FAP)–positive cancer‑associated fibroblasts while simultaneously secreting interleukin‑15 (IL‑15) to enhance immune persistence and activation.
The dual mechanism of MiNK‑215 addresses two major barriers that limit the effectiveness of current checkpoint‑based immunotherapies in solid tumors. By depleting FAP‑positive CAFs, the therapy dismantles the dense, immunosuppressive stroma that blocks immune cell infiltration. The IL‑15 secretion then boosts the activity and longevity of natural killer and T cells, creating a broader immune response that can attack tumor cells more effectively.
MiNK‑215 is an off‑the‑shelf, allogeneic product that can be manufactured at scale and delivered on demand, positioning it as a potentially scalable and immediate therapeutic option for patients who have limited effective treatments. The company’s pipeline also includes its lead clinical candidate, agenT‑797, which is in trials for multiple indications, suggesting that MiNK‑215 could complement and accelerate the overall development strategy.
CEO Jennifer Buell said the findings “underscore the real potential of MiNK‑215 to reshape how we treat solid tumors that have resisted immunotherapy for decades. By dismantling the fibroblast barriers that shield these cancers and activating multiple arms of the immune system, MiNK‑215 goes beyond traditional checkpoint approaches.”
The preclinical data reinforce MiNK’s position in the competitive iNKT therapy landscape, where few products combine stromal remodeling with cytokine‑mediated immune activation. If the therapy translates into clinical benefit, it could provide a new avenue for patients with checkpoint‑resistant solid tumors and expand the company’s commercial prospects beyond its current clinical pipeline.
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