Type II, glycoengineered humanized anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via enhanced antibody-dependent cellular cytotoxicity/phagocytosis and direct cell death, with limited complement activation.
Type II, glycoengineered humanized anti‑CD20 IgG1 that binds CD20 on B cells; afucosylated Fc increases FcγRIIIa affinity to enhance antibody‑dependent cellular cytotoxicity and phagocytosis, and it triggers direct, caspase‑independent cell death with minimal complement activation, leading to depletion of CD20+ B cells.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages CD16a (Fc gamma receptor IIIa) on NK cells/macrophages to trigger ADCC and phagocytosis, killing CD20+ cells (and also induces direct caspase-independent death of CD20+ cells). CD16a-expressing cells are effectors, not killed.
Antibody-drug conjugate targeting Trop-2; a humanized anti–Trop-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor) to deliver cytotoxic payload to Trop-2–expressing tumor cells, causing DNA damage and bystander killing.
Humanized anti–Trop-2 monoclonal antibody conjugated to SN-38 (topoisomerase I inhibitor). After binding Trop-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which stabilizes topo I–DNA complexes, causing DNA strand breaks, cell-cycle arrest, and apoptosis; the membrane-permeable payload can also produce bystander killing.
YES
DIRECT
ADC binds TROP2, is internalized, and releases SN-38 (topoisomerase I inhibitor) that stabilizes topo I–DNA complexes, causing DNA damage, cell-cycle arrest, and apoptosis; the membrane-permeable payload can also cause bystander killing.
Type II, glycoengineered humanized anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via enhanced antibody-dependent cellular cytotoxicity/phagocytosis and direct cell death, with limited complement activation.
Type II, glycoengineered humanized anti‑CD20 IgG1 that binds CD20 on B cells; afucosylated Fc increases FcγRIIIa affinity to enhance antibody‑dependent cellular cytotoxicity and phagocytosis, and it triggers direct, caspase‑independent cell death with minimal complement activation, leading to depletion of CD20+ B cells.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages CD16b on neutrophils to mediate ADCC/ADCP against CD20+ cells. CD16b-expressing cells are not targeted or killed.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy in which a patient’s T cells are genetically engineered to express a CD19-specific scFv linked to CD28 costimulatory and CD3ζ activation domains; upon engagement with CD19 on malignant B cells, engineered T cells activate, expand, and mediate cytotoxicity.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor with CD28 costimulatory and CD3zeta activation domains; binding to CD19 on malignant B cells activates and expands the T cells and induces perforin/granzyme-mediated cytotoxicity, depleting CD19-positive tumor cells.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells, activate, form an immune synapse, and kill via perforin/granzyme-mediated cytotoxicity (and Fas–FasL apoptosis).
An anti-FOLR1 human IgG1 antibody-drug conjugate with a cleavable hemiasterlin payload (SC209); after FOLR1 binding and internalization, the payload inhibits tubulin polymerization, causing mitotic arrest and cell death.
Anti-FOLR1 human IgG1 antibody-drug conjugate that binds FOLR1 on tumor cells, is internalized, and releases a cleavable hemiasterlin payload (SC209) that inhibits tubulin polymerization, inducing mitotic arrest and cell death in FOLR1-expressing cells.
YES
DIRECT
An anti-FOLR1 ADC binds FOLR1 on target cells, is internalized, and releases a hemiasterlin payload (SC209) that inhibits tubulin polymerization, causing mitotic arrest and apoptosis of FOLR1-expressing cells.