An antibody-drug conjugate (Trodelvy) composed of a humanized anti–TROP-2 monoclonal antibody linked to SN-38, the active metabolite of irinotecan. It binds TROP-2 on tumor cells, is internalized, and releases SN-38 to inhibit topoisomerase I, causing DNA damage and tumor cell death.
Humanized anti–TROP-2 monoclonal antibody linked to SN-38. After binding TROP-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which inhibits topoisomerase I, stabilizes Topo I–DNA complexes, induces DNA breaks, and triggers tumor cell death; the membrane-permeable payload can produce a bystander effect.
YES
DIRECT
The ADC binds TROP-2 on tumor cells, is internalized, and releases SN-38; SN-38 inhibits topoisomerase I, causing DNA damage and apoptosis. The membrane-permeable payload can also create a bystander effect.
Autologous cellular immunotherapy using ex vivo–generated dendritic cells pulsed with patient-specific tumor neoantigen peptides to prime/expand neoantigen-specific CD8+ and CD4+ T cells.
Autologous dendritic cells are generated ex vivo and pulsed with patient-specific tumor neoantigen peptides. After infusion, the DCs migrate to lymphoid tissues and present these neoantigens on HLA class I and II, providing costimulation (e.g., CD80/CD86) and cytokines to prime and expand neoantigen-specific CD8+ cytotoxic T cells and CD4+ helper T cells, thereby promoting tumor-specific immune responses and immunologic memory.
NO
INDIRECT
CD80/CD86 on the infused dendritic cells provide costimulation to prime neoantigen-specific T cells; the resulting T cells kill tumor cells presenting the neoantigen via MHC, not the CD80/CD86-expressing dendritic cells.
An antibody-drug conjugate (Trodelvy) composed of a humanized anti–TROP-2 monoclonal antibody linked to SN-38, the active metabolite of irinotecan. It binds TROP-2 on tumor cells, is internalized, and releases SN-38 to inhibit topoisomerase I, causing DNA damage and tumor cell death.
Humanized anti–TROP-2 monoclonal antibody linked to SN-38. After binding TROP-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which inhibits topoisomerase I, stabilizes Topo I–DNA complexes, induces DNA breaks, and triggers tumor cell death; the membrane-permeable payload can produce a bystander effect.
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 death. Topoisomerase I is not the targeted antigen, so its expression alone does not make cells specifically killed by the drug.
HER2-targeted antibody-drug conjugate delivering a topoisomerase I inhibitor payload to HER2-expressing tumor cells.
HER2-targeted monoclonal antibody (trastuzumab) linked to a topoisomerase I inhibitor payload (deruxtecan, DXd). After binding HER2 and internalization, DXd is released to inhibit Top1-DNA complexes, leading to DNA replication arrest and apoptosis; the antibody also mediates ADCC and the membrane-permeable payload enables bystander killing.
YES
DIRECT
The ADC binds HER2 on target cells, is internalized, and releases the topoisomerase I inhibitor deruxtecan (DXd), causing Top1-mediated DNA damage/replication arrest and apoptosis; the antibody Fc can also trigger ADCC, with some bystander killing.
HER2-targeted antibody-drug conjugate delivering a topoisomerase I inhibitor payload to HER2-expressing tumor cells.
HER2-targeted monoclonal antibody (trastuzumab) linked to a topoisomerase I inhibitor payload (deruxtecan, DXd). After binding HER2 and internalization, DXd is released to inhibit Top1-DNA complexes, leading to DNA replication arrest and apoptosis; the antibody also mediates ADCC and the membrane-permeable payload enables bystander killing.
NO
INDIRECT
Trastuzumab deruxtecan targets HER2 on tumor cells, is internalized, and releases deruxtecan, which inhibits topoisomerase I to induce DNA damage and apoptosis; killing depends on HER2-mediated delivery (with possible bystander effect), not on expression of topoisomerase I itself.