A bispecific T‑cell engager (BiTE) antibody that binds CD19 on B‑lymphoblasts and CD3 on T cells to redirect and activate cytotoxic T cells against CD19+ leukemia.
A BiTE antibody that binds CD19 on B cells and CD3 on T cells, juxtaposing and activating T cells to form an immune synapse and induce perforin/granzyme-mediated lysis of CD19-positive leukemia cells.
YES
DIRECT
Blinatumomab links CD3 on T cells to CD19 on target cells, activating T cells to form an immune synapse and kill CD19+ cells via perforin/granzyme-mediated cytolysis/apoptosis.
A bispecific T‑cell engager (BiTE) antibody that binds CD19 on B‑lymphoblasts and CD3 on T cells to redirect and activate cytotoxic T cells against CD19+ leukemia.
A BiTE antibody that binds CD19 on B cells and CD3 on T cells, juxtaposing and activating T cells to form an immune synapse and induce perforin/granzyme-mediated lysis of CD19-positive leukemia cells.
NO
INDIRECT
Blinatumomab engages CD3 on T cells to redirect them to CD19+ cells; activated T cells kill the CD19-expressing targets via perforin/granzyme, while CD3+ T cells are effectors, not the killed cells.
An anti–PD-L1 antibody–drug conjugate administered IV every 3 weeks. The monoclonal antibody blocks the PD-1/PD-L1 immune checkpoint to restore T-cell antitumor activity and, after PD-L1–mediated internalization, releases a DNA topoisomerase I inhibitor payload that induces DNA damage, replication stress, and apoptosis in PD-L1–expressing cells.
HLX43 is an anti-PD-L1 IgG1 antibody–drug conjugate that both blocks the PD-1/PD-L1 immune checkpoint to restore T-cell antitumor activity and, after PD-L1–mediated internalization and linker cleavage, releases a camptothecin-based topoisomerase I inhibitor payload that causes DNA damage, replication stress, and apoptosis in PD-L1–expressing cells (with potential bystander killing).
YES
DIRECT
ADC binds PD-L1 on target cells, is internalized, and releases a camptothecin-based topoisomerase I inhibitor that causes DNA damage and apoptosis (with potential bystander killing).
An anti–PD-L1 antibody–drug conjugate administered IV every 3 weeks. The monoclonal antibody blocks the PD-1/PD-L1 immune checkpoint to restore T-cell antitumor activity and, after PD-L1–mediated internalization, releases a DNA topoisomerase I inhibitor payload that induces DNA damage, replication stress, and apoptosis in PD-L1–expressing cells.
HLX43 is an anti-PD-L1 IgG1 antibody–drug conjugate that both blocks the PD-1/PD-L1 immune checkpoint to restore T-cell antitumor activity and, after PD-L1–mediated internalization and linker cleavage, releases a camptothecin-based topoisomerase I inhibitor payload that causes DNA damage, replication stress, and apoptosis in PD-L1–expressing cells (with potential bystander killing).
NO
INDIRECT
HLX43 targets PD-L1, is internalized, and releases a camptothecin-based topoisomerase I inhibitor that induces DNA damage and apoptosis in PD-L1–positive (and some bystander) cells. DNA topoisomerase I is the intracellular payload target, not the cell-surface antigen used for targeting.
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.
YES
DIRECT
The anti-HER2 antibody–drug conjugate binds HER2, is internalized, and releases the topoisomerase I inhibitor deruxtecan in lysosomes, causing DNA damage, cell-cycle arrest, and apoptosis; Fc-mediated ADCC and a bystander effect can also contribute.