Antibody–drug conjugate targeting HER2; trastuzumab linked via a cleavable linker to a topoisomerase I inhibitor payload (DXd). Binds HER2, internalizes, releases DXd to induce DNA damage, also blocks HER2 signaling and mediates ADCC with bystander killing.
HER2-directed monoclonal antibody (trastuzumab) linked via a cleavable linker to a membrane-permeable topoisomerase I inhibitor payload (DXd). After HER2 binding and internalization, the linker is cleaved to release DXd, which inhibits Top1, causing DNA damage, replication arrest, and apoptosis. The antibody also blocks HER2 signaling and mediates Fc-dependent ADCC, with a bystander killing effect from the released payload.
YES
DIRECT
The ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptosis in HER2+ cells; Fc-mediated ADCC and a bystander effect can also contribute.
Antibody–drug conjugate targeting HER2; trastuzumab linked via a cleavable linker to a topoisomerase I inhibitor payload (DXd). Binds HER2, internalizes, releases DXd to induce DNA damage, also blocks HER2 signaling and mediates ADCC with bystander killing.
HER2-directed monoclonal antibody (trastuzumab) linked via a cleavable linker to a membrane-permeable topoisomerase I inhibitor payload (DXd). After HER2 binding and internalization, the linker is cleaved to release DXd, which inhibits Top1, causing DNA damage, replication arrest, and apoptosis. The antibody also blocks HER2 signaling and mediates Fc-dependent ADCC, with a bystander killing effect from the released payload.
YES
INDIRECT
After HER2 binding and internalization, the ADC releases the DXd payload, which inhibits DNA topoisomerase I in exposed cells, causing DNA damage, replication arrest, and apoptosis (including bystander killing). The drug does not bind Top1 directly as the targeting moiety.
A subcutaneously administered bispecific antibody immunotherapy that binds CD20 on malignant B cells and an additional immune-effector target to redirect immune cell–mediated cytotoxicity for B-cell depletion in relapsed/refractory CD20+ B-cell non-Hodgkin lymphoma.
Subcutaneously administered bispecific antibody that binds CD20 on malignant B cells and a T‑cell effector target to recruit and activate T cells, forming an immune synapse and redirecting T‑cell–mediated cytotoxicity to deplete CD20+ B cells in relapsed/refractory non‑Hodgkin lymphoma.
YES
DIRECT
The bispecific antibody binds CD20 on B cells and CD3 on T cells, forming an immune synapse and activating T cells to lyse CD20+ cells via perforin/granzyme-mediated cytotoxicity.
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
Neoantigen-pulsed dendritic cells present peptides on HLA I/II to prime neoantigen-specific T cells; the activated CTLs then kill tumor cells presenting the neoantigen–HLA I complexes via perforin/granzyme. Dendritic cells expressing HLA class I are not directly targeted or killed by the therapy.
A subcutaneously administered bispecific antibody immunotherapy that binds CD20 on malignant B cells and an additional immune-effector target to redirect immune cell–mediated cytotoxicity for B-cell depletion in relapsed/refractory CD20+ B-cell non-Hodgkin lymphoma.
Subcutaneously administered bispecific antibody that binds CD20 on malignant B cells and a T‑cell effector target to recruit and activate T cells, forming an immune synapse and redirecting T‑cell–mediated cytotoxicity to deplete CD20+ B cells in relapsed/refractory non‑Hodgkin lymphoma.
NO
INDIRECT
The bispecific engages CD3 on T cells to activate and redirect them to kill CD20+ B cells via immune synapse formation and perforin/granzyme-mediated cytotoxicity; CD3+ T cells themselves are not targeted for killing.