Anti-CLDN18.2 monoclonal antibody that binds claudin 18.2 on tumor cells and mediates immune cytotoxicity (ADCC/CDC).
ASKB589 is an anti-CLDN18.2 monoclonal antibody that binds claudin 18.2 on tumor cells and promotes immune-mediated killing via antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), leading to lysis of CLDN18.2-positive cancer cells.
YES
DIRECT
Anti-CLDN18.2 antibody binds CLDN18.2 on tumor cells and triggers Fc-mediated ADCC by effector cells and complement-dependent cytotoxicity (CDC), leading to lysis of CLDN18.2-positive cells.
Type II, glycoengineered anti-CD20 monoclonal antibody that induces direct cell death and potent ADCC/ADCP against CD20+ B cells.
Type II, glycoengineered anti-CD20 IgG1 that binds CD20 on B cells and, via enhanced FcγRIIIa affinity (afucosylated Fc), drives potent antibody-dependent cellular cytotoxicity and phagocytosis (ADCC/ADCP) and induces direct, caspase-independent cell death, leading to depletion of CD20+ malignant B cells.
YES
DIRECT
Binds CD20 on B cells; afucosylated Fc engages FcγRIIIa on effector cells to mediate potent ADCC and ADCP, and the antibody itself induces direct, caspase‑independent cell death of CD20+ cells.
Type II, glycoengineered anti-CD20 monoclonal antibody that induces direct cell death and potent ADCC/ADCP against CD20+ B cells.
Type II, glycoengineered anti-CD20 IgG1 that binds CD20 on B cells and, via enhanced FcγRIIIa affinity (afucosylated Fc), drives potent antibody-dependent cellular cytotoxicity and phagocytosis (ADCC/ADCP) and induces direct, caspase-independent cell death, leading to depletion of CD20+ malignant B cells.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages FcγRIIIa (CD16a) on NK cells/macrophages to drive ADCC/ADCP, killing CD20+ B cells. CD16a-expressing cells act as effectors and are not killed by the drug.
B7-H3 (CD276)–targeted chimeric antigen receptor gamma-delta T cell (CAR-γδ T) therapy; autologous engineered γδ T cells designed to mediate MHC-independent cytotoxicity against B7-H3–expressing solid tumors. Administered as a single infusion with dose escalation (1×10^8–1×10^9 CAR+ γδ T cells).
Autologous gamma-delta T cells are engineered to express a chimeric antigen receptor specific for B7-H3 (CD276). Upon binding B7-H3 on tumor cells, CAR signaling activates the γδ T cells to mediate MHC-independent cytotoxicity, leading to tumor cell killing via perforin/granzyme release and cytokine secretion, with expansion and persistence driven by CAR costimulatory/ζ signaling.
YES
DIRECT
CAR γδ T cells bind B7‑H3 on target cells and, upon CAR activation, directly kill them via cytotoxic degranulation (perforin/granzyme) leading to apoptosis/lysis, with supportive cytokine effects.
Antibody-drug conjugate targeting a tumor-associated cell-surface antigen; internalizes and releases a cytotoxic payload (e.g., topoisomerase I or microtubule-targeting warhead) to kill cancer cells.
HER2-directed antibody-drug conjugate (trastuzumab rezetecan). The trastuzumab antibody binds HER2 on tumor cells, is internalized, and a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor that stabilizes Topo I-DNA complexes, causing DNA strand breaks, blocking DNA replication, and inducing apoptosis in HER2-expressing cancer cells.
NO
INDIRECT
This ADC binds HER2 (not topoisomerase I) on tumor cells, is internalized, and releases a topoisomerase I–inhibiting payload that causes DNA damage and apoptosis. Topoisomerase I is the intracellular enzymatic target of the payload, not the cell-surface antigen used for targeting.