A fully human monoclonal antibody (VAY736) targeting the BAFF receptor (BAFF‑R; TNFRSF13C). Administered subcutaneously to block BAFF/BAFF‑R signaling and deplete B cells via ADCC, aiming to reduce autoreactive B cells and autoantibody production in SLE.
Fully human monoclonal antibody targeting the BAFF receptor (BAFF-R/TNFRSF13C); blocks BAFF–BAFF-R interaction and downstream NF-kB survival signaling, and depletes BAFF-R+ B cells via ADCC, reducing autoreactive B cells and autoantibody production.
Anti-BAFF-R IgG binds BAFF-R+ cells and recruits FcγR-bearing effector cells to induce ADCC (± CDC); BAFF-R signaling blockade can also promote apoptosis.
Antibody–drug conjugate targeting TROP2; after binding, it is internalized and releases a camptothecin/topoisomerase I inhibitor payload that induces DNA damage and apoptosis.
Humanized anti-TROP2 monoclonal antibody linked via a cleavable linker to the camptothecin/topoisomerase I inhibitor tirumotecan. After binding TROP2 on tumor cells and internalization (and/or extracellular pH-sensitive cleavage), the payload is released to inhibit topoisomerase I, causing DNA damage, replication arrest, and apoptosis, with a bystander effect on neighboring tumor cells.
The anti-TROP2 ADC binds TROP2, is internalized (and/or cleaved extracellularly), releasing the topoisomerase I inhibitor tirumotecan that causes DNA damage, replication arrest, and apoptosis; bystander killing can also occur.
Antibody–drug conjugate targeting Tissue Factor (TF) and delivering the microtubule inhibitor MMAE.
Anti–tissue factor (TF) monoclonal antibody linked via a protease‑cleavable linker to the microtubule inhibitor monomethyl auristatin E (MMAE). After binding TF on tumor cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; TF binding may also interfere with TF–FVIIa signaling, contributing antiangiogenic/anticoagulant effects.
ADC binds Tissue Factor on target cells, is internalized, and releases MMAE via protease cleavage; MMAE inhibits tubulin polymerization causing G2/M arrest and apoptosis of the TF-expressing cell.
Autologous dual-target BCMA/CD19 chimeric antigen receptor T-cell (CAR-T) therapy produced via lentiviral transduction; single IV infusion to deplete CD19+ B cells and BCMA+ plasma cells in autoimmune kidney disease.
Autologous T cells are lentivirally engineered to express dual chimeric antigen receptors targeting CD19 and BCMA. On engagement with these antigens on B cells and plasma cells, the CAR-T cells become activated and kill targets via perforin/granzyme and death receptor pathways, depleting CD19+ B cells and BCMA+ plasmablasts/plasma cells to reduce pathogenic autoantibody production in autoimmune kidney disease.
CAR-T cells bind CD19 via the CAR, become activated, and kill CD19+ cells through perforin/granzyme release and death receptor–mediated apoptosis.
Autologous dual-target BCMA/CD19 chimeric antigen receptor T-cell (CAR-T) therapy produced via lentiviral transduction; single IV infusion to deplete CD19+ B cells and BCMA+ plasma cells in autoimmune kidney disease.
Autologous T cells are lentivirally engineered to express dual chimeric antigen receptors targeting CD19 and BCMA. On engagement with these antigens on B cells and plasma cells, the CAR-T cells become activated and kill targets via perforin/granzyme and death receptor pathways, depleting CD19+ B cells and BCMA+ plasmablasts/plasma cells to reduce pathogenic autoantibody production in autoimmune kidney disease.
BCMA-directed CAR-T cells bind BCMA on target cells and kill them via T-cell cytotoxicity (perforin/granzyme release and death receptor pathways).