Anti-TROP2 antibody–drug conjugate delivering a topoisomerase I inhibitor payload (deruxtecan).
Datopotamab deruxtecan is an anti‑TROP2 antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases the membrane‑permeable topoisomerase I inhibitor payload deruxtecan via a cleavable linker in lysosomes. The released payload inhibits Topo I, causing DNA damage and tumor cell death, with potential bystander killing of adjacent cells.
ADC binds TROP2 on target cells, is internalized, and releases the deruxtecan topoisomerase I inhibitor via lysosomal linker cleavage, causing DNA damage and apoptosis; membrane-permeable payload can also produce bystander killing.
Type II glycoengineered anti-CD20 monoclonal antibody that induces potent ADCC and direct B-cell death with reduced reliance on complement.
Glycoengineered humanized anti-CD20 IgG1 that binds CD20 on B cells and depletes them via enhanced FcγRIIIa-mediated ADCC and potent type II, caspase‑independent direct B‑cell death, with reduced reliance on complement.
Obinutuzumab binds CD20 on B cells and induces killing via enhanced Fc-gamma RIIIa–mediated ADCC (NK cells/monocytes), antibody-dependent phagocytosis, and direct type II, caspase-independent B-cell death, with minimal reliance on complement.
Humanized Fc-engineered anti-CD19 monoclonal antibody that enhances ADCC/ADCP and can induce direct apoptosis of B cells.
Humanized Fc-engineered anti-CD19 monoclonal antibody that binds CD19 on B cells and enhances Fc-gamma receptor–mediated ADCC and ADCP, leading to depletion of CD19+ malignant B cells; can also induce direct apoptosis.
Binds CD19 on B cells and recruits FcγR-bearing effector cells to mediate ADCC/ADCP; can also trigger direct apoptosis of CD19+ cells.
Monoclonal IgG1 antibody targeting B7-H3 (CD276) on tumor cells; engages NK cells via Fc to drive antibody-dependent cellular cytotoxicity (ADCC).
Humanized, Fc‑engineered IgG1 monoclonal antibody targeting B7‑H3 (CD276) on tumor cells; binding flags tumor cells for immune elimination by engaging FcγRIIIa (CD16) on NK cells to drive potent antibody‑dependent cellular cytotoxicity (ADCC), with additional Fc‑mediated effector functions (e.g., macrophage engagement) possible. No payload; primary effect is target‑specific immune‑mediated cytotoxicity.
Enoblituzumab binds B7-H3 on target cells and engages NK cells via Fc-gamma receptor (CD16) to trigger antibody-dependent cellular cytotoxicity (perforin/granzyme); additional Fc-mediated effector functions (e.g., macrophage phagocytosis) may contribute.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy; patient T cells are gene-modified to express a CD19-targeted CAR that, upon antigen engagement, activates T-cell cytotoxicity to eliminate CD19-positive B-cell malignancies and induce B-cell aplasia.
Autologous T cells are gene‑modified to express an anti‑CD19 chimeric antigen receptor; binding to CD19 on B cells activates CAR signaling and T‑cell cytotoxicity, leading to elimination of CD19‑positive malignant B cells and on‑target B‑cell aplasia.
Anti-CD19 CAR T cells bind CD19 on target B cells and kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis and Fas–FasL signaling).