An antibody–drug conjugate comprising a humanized anti-HER2 monoclonal antibody linked via a cleavable linker to deruxtecan, a topoisomerase I inhibitor. It binds HER2 (including HER2-low), is internalized, and releases deruxtecan in lysosomes to inhibit topoisomerase I, causing DNA damage and apoptosis; the membrane-permeable payload enables a bystander effect and the Fc region may mediate ADCC.
Humanized anti‑HER2 monoclonal antibody linked via a cleavable linker to deruxtecan (topoisomerase I inhibitor). Binds HER2 (including HER2‑low), is internalized, and releases deruxtecan in lysosomes to inhibit Topo I, causing DNA damage, cell‑cycle arrest, and apoptosis; membrane‑permeable payload enables a bystander effect, and the Fc region can mediate ADCC.
NO
INDIRECT
The ADC binds HER2 on the cell surface, is internalized, and releases deruxtecan that inhibits topoisomerase I to cause DNA damage and apoptosis (with bystander effect). Cells are targeted based on HER2, not on expression of topoisomerase I itself.
Autologous CD19-directed CAR T-cell therapy; engineered T cells target CD19+ B cells (naive, memory, plasmablasts) to deplete autoreactive B-cell compartments and reduce autoantibody production.
Autologous T cells are engineered to express a chimeric antigen receptor targeting CD19, enabling recognition and cytotoxic elimination of CD19+ B cells (naive, memory, plasmablasts). This depletes autoreactive B-cell compartments, reduces autoantibody production, and dampens B cell–driven immune inflammation.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target cells, triggering T-cell activation and cytotoxic killing via perforin/granzyme release and death-receptor pathways, inducing apoptosis of CD19+ cells.
A human anti-EphA5 monoclonal antibody–drug conjugate that binds EphA5 on tumor cells, is internalized, and releases the cytotoxic payload MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in advanced solid tumors.
Human anti-EphA5 IgG1 antibody linked via a protease-cleavable linker to MMAE. After binding EphA5 on tumor cells and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis in EphA5-expressing cancer cells.
YES
DIRECT
Anti-EphA5 ADC binds EphA5, is internalized, linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis of EphA5-expressing cells.
A human anti-EphA5 monoclonal antibody–drug conjugate that binds EphA5 on tumor cells, is internalized, and releases the cytotoxic payload MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in advanced solid tumors.
Human anti-EphA5 IgG1 antibody linked via a protease-cleavable linker to MMAE. After binding EphA5 on tumor cells and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis in EphA5-expressing cancer cells.
NO
INDIRECT
MBRC-101 binds EphA5 on tumor cells, is internalized, and releases MMAE that inhibits beta-tubulin polymerization, causing G2/M arrest and apoptosis; beta-tubulin expression itself is not the cell-surface target for delivery.
Fully human anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity and ADCC to reduce pathogenic autoantibodies in pemphigus vulgaris.
Fully human anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20+ B cells via complement-dependent cytotoxicity and antibody-dependent cell-mediated cytotoxicity, thereby reducing pathogenic autoantibody production.
YES
DIRECT
Ofatumumab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC (e.g., by NK cells), leading to lysis of CD20+ cells.