Eighty-five percent of the human proteome already has at least one monoclonal antibody built against it. Decades of biomedical research produced that library. Almost none of it works where a large share of the disease actually occurs, inside the cell.
A team at the University of Essex reported that the obstacle is more mundane than anyone had pinned down: electrical charge. Their paper, published January 31 in Nature Communications and pushed back into circulation by a fresh press cycle this month, describes a design rule plus AI-driven protein redesign that let them computationally reformat 672 antibodies as intrabodies, fragments built to fold and function in the cytoplasm.
