MiNK Therapeutics reports new data on agenT-797 at ATS 2026

MiNK Therapeutics (INKT) announced new clinical and translational data presented at the American Thoracic Society International Conference 2026 and the simultaneous publication in Clinical Immunology Communications1 describing the use of sequential immunotherapy with MiNK’s off-the-shelf iNKT cell therapy, agenT-797 and N-803, an IL-15 superagonist, in a critically ill patient with unresolving disseminated Coccidioides immitis infection, severe acute respiratory distress syndrome, and concurrent hospital-acquired Pseudomonas aeruginosa pneumonia. The poster, titled ‘Novel Invariant Natural Killer T Cell and Interleukin-15 Superagonist Combination Immunotherapy for Unresolving Coccidioides immitis Infection with Concurrent ARDS,’ was presented by Terese C. Hammond, M.D., Head of Inflammatory and Pulmonary Diseases at MiNK Therapeutics, and describes a sequential immunotherapy regimen pairing agenT-797, MiNK’s investigational off-the-shelf iNKT cell therapy, with Anktiva, an FDA-approved IL-15 superagonist developed by ImmunityBio, reflecting a combination strategy built on two clinically validated immune mechanisms. The patient was critically ill, facing a convergence of severe threats: disseminated Coccidioides immitis fungal infection, severe acute respiratory distress syndrome, and concurrent hospital-acquired Pseudomonas aeruginosa bacterial pneumonia, all after standard-of-care antifungal, antibacterial, and supportive therapies had failed to halt clinical decline. Following sequential treatment with Anktiva and agenT-797, investigators observed: Suppression of both fungal and bacterial pathogens; Active immune cell recruitment into the lung; Reduced early inflammatory signaling; Activation of tissue repair and immune regulatory pathways. Immune profiling revealed a coherent biological sequence: Anktiva triggered early immune activation, followed by agenT-797-driven changes consistent with iNKT cell engagement, pathogen control, and a transition from inflammation toward resolution and repair. The pattern suggests the treatment sequence may have helped restore coordinated immune function in a patient whose infection and respiratory failure had continued to progress despite intensive intervention. The patient’s family ultimately pivoted to comfort care due to recurrent cardiac decompensation in the setting of pre-existing mitral valve disease, acute mitral regurgitation and cardiogenic shock. The authors further supported this rationale in the ATS poster presentation, when chest imaging, clinical data including real time pulmonary arterial catheter and cardiac echocardiography data augmented post-mortem cytokine and biomarker results to prioritize acute heart failure rather than cytokine release or infectious contributions as the most likely mechanism.