MiNK Therapeutics, Inc. (NASDAQ: INKT), a clinical-stage biopharmaceutical company pioneering allogeneic, off-the-shelf invariant natural killer T (iNKT) cell therapies, has been awarded a prestigious grant from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH). The non-dilutive funding will support development of MiNK's allo-iNKT cell therapy platform for the prevention and treatment of graft-versus-host disease (GvHD) following hematopoietic stem cell transplantation (HSCT), in collaboration with the University of Wisconsin.
Addressing Critical Unmet Medical Need
The grant targets a significant clinical challenge, as nearly 50% of patients undergoing allogeneic stem cell transplants are at risk for GvHD, a serious and potentially life-threatening complication. GvHD is a severe immune complication that can occur after allogeneic HSCT, often leading to multi-organ damage and high mortality.
"This non-dilutive funding from NIAID underscores the growing recognition of iNKT cells as a unique and powerful modality in immune regulation," said Jennifer Buell, PhD, President and Chief Executive Officer of MiNK Therapeutics. "Through our preclinical and clinical collaboration, we aim to address the needs of the nearly 50% of patients undergoing allogeneic stem cell transplants who are at risk for this serious and potentially life-threatening complication."
Unique Therapeutic Approach
iNKT cells are uniquely suited for preventing GvHD due to their natural ability to regulate immune responses, promote tissue repair, and suppress inflammatory pathways. The collaboration leverages research insights from Dr. Jenny E. Gumperz and her team at the University of Wisconsin, who have provided important mechanistic insights into how allo-iNKT cells may not only prevent GvHD but also improve the success of engraftment.
"iNKT cells can calm the destructive allo-immune response that drives GvHD, while preserving the patient's ability to fight infection—a balance current therapies struggle to achieve," said Jenny E. Gumperz, PhD, Professor of Medical Microbiology & Immunology, University of Wisconsin School of Medicine and Public Health. "NIAID's support allows us to speed this science toward the clinic and, ultimately, give transplant patients a safer path to long-term survival."
Clinical Development Pipeline
MiNK's lead asset, AGENT-797, is an off-the-shelf, allogeneic iNKT cell therapy currently in clinical development for the treatment of graft-versus-host disease, solid tumors, and critical pulmonary immune collapse. The company's proprietary platform is designed to restore immune balance and drive cytotoxic immune responses across cancer, immune-mediated diseases, and pulmonary immune failure.
The company is also advancing a pipeline of T cell receptor (TCR)-based therapies and neoantigen discovery tools that enable tumor- and tissue-specific immune activation with broad potential application. With a scalable, cryopreserved manufacturing process and a differentiated mechanism that bridges innate and adaptive immunity, MiNK is developing next-generation immune reconstitution therapies designed to be accessible, durable, and applicable across a wide range of indications.
Strategic Collaboration
The partnership with the University of Wisconsin unites MiNK's cutting-edge iNKT manufacturing capabilities with the university's deep expertise in transplant immunology. This collaboration is expected to accelerate the development of iNKT cell therapy in what Buell described as "a high-priority area of unmet medical need."
The NIAID grant both validates the promise of MiNK's iNKT platform and provides crucial non-dilutive funding to advance development in this critical therapeutic area. The award underscores the growing recognition of iNKT cells as a unique and powerful modality in immune regulation, particularly in the challenging context of stem cell transplantation where balancing immune suppression and preservation of infection-fighting capabilities remains a significant clinical challenge.
