Sasanka Ramanadham, Ph.D.Sasanka Ramanadham, Ph.D., professor in the UAB Department of Cell, Developmental and Integrative Biology and Senior Scientist in the UAB Comprehensive Diabetes Center, was among seven inventors awarded funding through the Harbert Institute for Innovation and Entrepreneurship (HIIE) Blazer Bridge Fund in 2026.
The Blazer Bridge Fund is intended to identify and assist in the development of promising ideas, discoveries, innovations and/or technologies from UAB faculty and staff that have commercial potential.
This year, HIIE received 40 applications, representing 54 inventors in 37 academic departments and divisions across seven UAB schools and Southern Research.
Ramanadham was selected for his innovative method of targeting select lipid signaling to counter Type 1 diabetes (T1D).
T1D develops as a consequence of autoimmune destruction of insulin-producing pancreatic beta-cells, resulting in insulin deficiency and elevated blood glucose levels. Ramanadham’s studies have identified select lipid signaling pathways that contribute to beta-cell injury, inflammation, and T1D development.
“Our unique approach focuses on modulating these pathways to reduce inflammation, preserve beta-cell function and survival, and prevent or delay T1D onset,” Ramanadham said. “We are evaluating complementary strategies, including pharmacological inhibitors, CRISPR/Cas9-mediated gene targeting, and immunotherapeutic approaches, to identify effective regimens that maximally reduce T1D incidence. This strategy offers the potential to intervene in disease-promoting lipid signaling without broadly suppressing normal immune function.”
Ramanadham said the appearance of multiple islet autoantibodies signals ongoing beta-cell autoimmunity and an increased likelihood of progressing to clinical T1D. Thus, strategies to prevent or delay disease onset would provide substantial benefit to individuals at high risk for developing T1D.
“Although our studies have primarily used mouse models of T1D, we have identified a similar lipid signature in euglycemic individuals at high risk for developing the disease, supporting the translational relevance of our findings,” he said. “Our results suggest that targeting select lipid signaling pathways represents a feasible and potentially safe and effective therapeutic approach to prevent or delay T1D onset. Importantly, this strategy may modulate inflammatory responses without directly targeting immune cells, potentially reducing the risk of broadly disrupting normal immune function.”