A Trop-2–targeted antibody–drug conjugate consisting of a humanized anti–Trop-2 monoclonal antibody linked via a hydrolyzable linker to SN-38 (the active metabolite of irinotecan). After binding Trop-2 on tumor cells and internalization, it releases SN-38 to inhibit topoisomerase I, causing DNA damage, S-phase arrest, and apoptosis, with potential bystander effect.
Humanized anti-Trop-2 monoclonal antibody linked via a hydrolyzable linker to SN-38. After binding Trop-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which inhibits topoisomerase I by stabilizing topo I-DNA complexes, leading to DNA damage, S-phase arrest, and apoptosis, with potential bystander killing of neighboring cells.
NO
INDIRECT
The ADC binds Trop-2 on tumor cells, is internalized, and releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis. Topoisomerase I is the payload’s enzymatic target, not the cell-surface antigen selected by the drug, so topo I–expressing cells are not directly targeted for killing.
An anti-HER2 antibody–drug conjugate (also known as RC48-ADC) consisting of a humanized IgG1 anti-HER2 antibody linked via a valine–citrulline linker to the cytotoxic payload monomethyl auristatin E (MMAE). It binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing mitotic arrest and apoptosis; may also exert Fc-mediated effects.
Anti-HER2 IgG1 antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, is internalized, and—via a protease-cleavable valine–citrulline linker—releases monomethyl auristatin E (MMAE), which inhibits tubulin polymerization to induce G2/M arrest and apoptosis; the IgG1 may also engage Fc-mediated effector functions (e.g., ADCC).
YES
DIRECT
The ADC binds HER2 on tumor cells, is internalized, and releases MMAE via a cleavable linker to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the IgG1 Fc can also mediate ADCC against HER2+ cells.
An anti-HER2 antibody–drug conjugate (also known as RC48-ADC) consisting of a humanized IgG1 anti-HER2 antibody linked via a valine–citrulline linker to the cytotoxic payload monomethyl auristatin E (MMAE). It binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing mitotic arrest and apoptosis; may also exert Fc-mediated effects.
Anti-HER2 IgG1 antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, is internalized, and—via a protease-cleavable valine–citrulline linker—releases monomethyl auristatin E (MMAE), which inhibits tubulin polymerization to induce G2/M arrest and apoptosis; the IgG1 may also engage Fc-mediated effector functions (e.g., ADCC).
NO
INDIRECT
Disitamab vedotin targets HER2 on the cell surface, is internalized, and releases MMAE, which binds beta-tubulin (vinca domain) to block microtubule polymerization and induce G2/M arrest and apoptosis. Killing depends on HER2-directed delivery, not on beta-tubulin expression alone.
Autologous, fully human anti-CD19 chimeric antigen receptor T-cell (CAR-T) therapy that targets and depletes CD19+ B-lineage cells to reduce pathogenic autoantibodies and B cell–driven inflammation.
Autologous T cells are lentivirally engineered to express a fully human anti‑CD19 CAR (CD8α hinge/transmembrane, CD28 costimulatory, CD3ζ signaling). After infusion, the CAR-T cells recognize CD19 on B-lineage cells, become activated, expand, and mediate cytolytic killing, depleting CD19+ B cells to reduce pathogenic autoantibodies and B cell–driven inflammation.
YES
DIRECT
Anti-CD19 CAR-T cells bind CD19 on B-lineage cells, become activated, and kill targets via T-cell cytolytic pathways (perforin/granzyme-mediated apoptosis and Fas–FasL), leading to lysis of CD19+ cells.
Human IgG1κ anti-CD38 monoclonal antibody for multiple myeloma; binds CD38 on malignant plasma cells to trigger complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity and phagocytosis (ADCC/ADCP), direct apoptosis, and depletion of CD38+ immunosuppressive cells.
Human IgG1kappa anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells to trigger complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity and phagocytosis (ADCC/ADCP), and direct apoptosis; also depletes CD38+ immunosuppressive cells (e.g., Tregs, Bregs, MDSCs) to enhance antitumor immunity.
YES
DIRECT
Binds CD38 on target cells and triggers complement-dependent cytotoxicity (CDC), Fc-mediated ADCC and ADCP, and can induce direct apoptosis of CD38+ cells.