Adaptive immune responses contribute significantly to the progression of acute myocarditis, where overactivation of cytotoxic lymphocytes leads to myocardial injury and eventual heart failure. Targeting immune receptors such as CD160, which is selectively upregulated on activated natural killer (NK) cells and CD8+ T cells during inflammation, presents a promising therapeutic strategy. Antibody-based approaches that deplete these pathogenic populations may reduce cardiac damage and improve clinical outcomes. However, existing antibody therapeutics are often limited by immunogenicity, poor control of effector functions, and inconsistent manufacturing quality, posing challenges for safety, efficacy, and large-scale production.
This platform features humanized anti-CD160 antibodies and derived fragments engineered from mouse hybridoma clones using BioPhi and CUMab computational design tools. These antibodies retain high-affinity binding to CD160 while replacing murine framework regions with human germline-like sequences to reduce immunogenicity. Fc regions are selectively mutated to control glycosylation, antibody-dependent cellular cytotoxicity (ADCC), complement activation, and half-life. The technology supports diverse formats including full-length IgGs, scFvs, Fab and F(ab′)2 fragments, bispecific antibodies (BiTEs, DOCK-AND-LOCK™), and antibody–drug conjugates. These antibodies are validated using flow cytometry, ELISA, epitope mapping, and biophysical assays, and are suitable for both parenteral delivery and diagnostic applications.
US Provisional filed 06/18/2025