An antibody–drug conjugate comprising a humanized anti–Trop-2 IgG monoclonal antibody linked to SN-38 (the active metabolite of irinotecan), a topoisomerase I inhibitor; after binding Trop-2 on tumor cells, it is internalized and releases SN-38 to induce DNA damage and apoptosis, with a hydrolyzable linker enabling bystander killing.
Humanized anti-Trop-2 IgG monoclonal antibody linked via a hydrolyzable linker to SN-38 (topoisomerase I inhibitor). After binding Trop-2 on tumor cells and internalization, SN-38 is released, stabilizes Topo I-DNA complexes, induces DNA damage and replication stress, leading to cell death; the linker enables bystander killing.
YES
DIRECT
Anti-TROP2 ADC binds TROP2 and is internalized; the linker is cleaved to release SN-38, a topoisomerase I inhibitor that stabilizes Topo I–DNA complexes, causing DNA damage and apoptosis (with additional bystander killing).
An antibody–drug conjugate comprising a humanized anti–Trop-2 IgG monoclonal antibody linked to SN-38 (the active metabolite of irinotecan), a topoisomerase I inhibitor; after binding Trop-2 on tumor cells, it is internalized and releases SN-38 to induce DNA damage and apoptosis, with a hydrolyzable linker enabling bystander killing.
Humanized anti-Trop-2 IgG monoclonal antibody linked via a hydrolyzable linker to SN-38 (topoisomerase I inhibitor). After binding Trop-2 on tumor cells and internalization, SN-38 is released, stabilizes Topo I-DNA complexes, induces DNA damage and replication stress, leading to cell death; the linker enables bystander killing.
NO
INDIRECT
The ADC binds Trop-2 on tumor cells, is internalized, and releases SN-38, which poisons topoisomerase I to cause DNA damage and cell death (with bystander effect). Top1 is the intracellular payload target, not the antigen recognized by the ADC.
Autologous gene-modified T lymphocytes expressing a chimeric antigen receptor targeting Fc receptor–like 5 (FcRL5/CD307e) on multiple myeloma cells to mediate antigen-directed cytotoxicity.
Autologous T cells engineered to express a chimeric antigen receptor that binds FcRL5 (CD307e) on multiple myeloma cells; CAR engagement triggers CD3z/costimulatory signaling, leading to T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of FcRL5-positive plasma cells.
YES
DIRECT
CAR-T cells recognize FcRL5 on target cells; CAR engagement activates CD3ζ/costimulatory signaling, triggering perforin/granzyme-mediated cytolysis (and death receptor pathways) of FcRL5-positive cells.
Anti-HER2 IgG1 monoclonal antibody that blocks HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting HER2; binds the extracellular domain to block HER2 signaling and tumor cell proliferation, and recruits immune effector cells via Fc gamma receptors to mediate antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
HER2+ cells are killed via antibody-dependent cellular cytotoxicity (ADCC) when trastuzumab-bound cells are lysed by FcγR-expressing effector cells (e.g., NK cells); signaling blockade may also promote apoptosis.
Off-the-shelf allogeneic anti-EGFR–conjugated gamma delta T-cell therapy; healthy-donor γδ T cells conjugated to an anti-EGFR antibody to redirect cytotoxicity toward EGFR-expressing tumor cells; mediates killing via T-cell effector functions.
Off-the-shelf allogeneic gamma delta (gdT) T cells chemically conjugated to an anti-EGFR antibody; the antibody directs the gdT cells to EGFR-expressing tumor cells, enabling MHC-independent recognition and T-cell effector–mediated cytotoxicity (perforin/granzyme release and cytokine production).
YES
DIRECT
Anti-EGFR–conjugated gamma delta T cells bind EGFR on tumor cells and kill them via T-cell effector functions (immune synapse with perforin/granzyme-mediated cytolysis and cytokine release), MHC-independent.