Precision car-NK therapy for VK4-1 autoreactive b cells in autoimmune diseases: advancing treatment with preserved immune function

The National Institute of Allergy and Infectious Diseases awarded Celdara Medical, LLC $320,863 on September 1, 2026, under the Allergy and Infectious Diseases Research program (CFDA 93.855) to develop precision chimeric antigen receptor (CAR) natural killer cell therapy targeting VK4-1-overexpressing autoreactive B cells in systemic lupus erythematosus. The Phase I SBIR project seeks to selectively remove disease-causing B cells while preserving non-pathogenic immune function, using humanized monoclonal antibodies and optimized CAR-NK cell platforms to address limitations of current immunosuppressive therapies such as corticosteroids, hydroxychloroquine, and biologics. Work is performed in Lebanon, New Hampshire, with a period of performance from September 1, 2026, through August 31, 2027. Celdara is a self-certified small disadvantaged business operating exclusively as a prime recipient on federal research grants, with an established portfolio of biomedical research awards from the National Institutes of Health across multiple disease areas including cancer immunotherapy, neurological disorders, and metabolic conditions.

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by widespread immune dysregulation, leading to multi-organ inflammation and significant morbidity. Current therapies, including corticosteroids, hydroxychloroquine, and biologics such as belimumab and anifrolumab, have limitations related to efficacy and safety. Broad immunosuppression increases the risk of severe infections and long-term immune depletion, necessitating more selective immune modulation approaches. This phase i sbir project seeks to address this critical unmet need by developing a precision- targeted therapeutic approach to selectively remove autoreactive b cells in lupus while preserving the non-pathogenic immune system. Our approach leverages monoclonal antibodies targeting VK4-1, a b cell receptor that is over-represented on pathogenic b cells, humanized for therapeutic application, and chimeric antigen receptor (car) NK-cell therapy optimized for efficacy and safety. Our innovative approach holds the potential to revolutionize SLE treatment by selectively removing disease causing b cells without inducing broad immunosuppression, ultimately improving long-term patient outcomes. Internal