Antibody–drug conjugate targeting HER2 that delivers DXd, a membrane-permeable topoisomerase I inhibitor via a cathepsin-cleavable linker; enables receptor-mediated internalization and bystander effect.
HER2-targeted monoclonal antibody (trastuzumab) linked via a cathepsin-cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. Binding to HER2 triggers receptor-mediated internalization; linker cleavage releases DXd, which stabilizes Top1–DNA complexes, inhibiting DNA replication and inducing apoptosis. Also mediates bystander killing and antibody-dependent cell-mediated cytotoxicity (ADCC).
YES
DIRECT
The ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor deruxtecan (DXd) after linker cleavage, causing DNA replication inhibition and apoptosis; it can also trigger ADCC and bystander killing.
Antibody–drug conjugate targeting HER2 that delivers DXd, a membrane-permeable topoisomerase I inhibitor via a cathepsin-cleavable linker; enables receptor-mediated internalization and bystander effect.
HER2-targeted monoclonal antibody (trastuzumab) linked via a cathepsin-cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. Binding to HER2 triggers receptor-mediated internalization; linker cleavage releases DXd, which stabilizes Top1–DNA complexes, inhibiting DNA replication and inducing apoptosis. Also mediates bystander killing and antibody-dependent cell-mediated cytotoxicity (ADCC).
YES
INDIRECT
After HER2 binding and internalization, the linker is cleaved to release deruxtecan, which inhibits DNA topoisomerase I in exposed cells, causing DNA damage and apoptosis; the payload’s membrane permeability enables bystander killing.
Autologous patient T cells genetically engineered to express a chimeric antigen receptor that co-recognizes CD38 and CS1 (SLAMF7) on myeloma cells, triggering T-cell cytotoxicity to treat relapsed/refractory multiple myeloma.
Autologous T cells are engineered to express a dual-target chimeric antigen receptor that co-recognizes CD38 and CS1 (SLAMF7) on myeloma cells; antigen binding activates CAR signaling (CD3zeta with costimulation), triggering perforin/granzyme release and cytokine-mediated killing of CD38+ and/or CS1+ malignant plasma cells, reducing antigen-loss escape.
YES
DIRECT
CAR T cells bind CD38 on target cells; CAR signaling triggers T‑cell degranulation with perforin/granzyme release (and death‑receptor/cytokine effects), causing apoptosis/lysis of CD38+ cells.
Autologous patient T cells genetically engineered to express a chimeric antigen receptor that co-recognizes CD38 and CS1 (SLAMF7) on myeloma cells, triggering T-cell cytotoxicity to treat relapsed/refractory multiple myeloma.
Autologous T cells are engineered to express a dual-target chimeric antigen receptor that co-recognizes CD38 and CS1 (SLAMF7) on myeloma cells; antigen binding activates CAR signaling (CD3zeta with costimulation), triggering perforin/granzyme release and cytokine-mediated killing of CD38+ and/or CS1+ malignant plasma cells, reducing antigen-loss escape.
YES
DIRECT
CAR T cells recognize CS1 (SLAMF7) on target cells; CAR signaling activates T-cell cytotoxicity with perforin/granzyme release (and cytokine-mediated apoptosis), killing CS1+ cells.
HER2-directed antibody–drug conjugate (IgG1 trastuzumab linked via a cleavable linker to the deruxtecan [DXd] topoisomerase I inhibitor). Binds HER2, internalizes, releases DXd in lysosomes to inhibit TOP1 causing DNA damage; trastuzumab component can inhibit HER2 signaling and mediate ADCC; payload can exert a bystander effect.
HER2-directed antibody-drug conjugate: trastuzumab (IgG1) linked via a cleavable linker to deruxtecan (DXd), a topoisomerase I inhibitor. After HER2 binding and internalization, lysosomal cleavage releases DXd to inhibit TOP1, causing DNA damage and tumor cell death. The trastuzumab component also blocks HER2 signaling and mediates ADCC; the membrane-permeable payload can produce a bystander effect.
YES
DIRECT
ADC binds HER2, is internalized, and releases the TOP1 inhibitor deruxtecan in lysosomes, causing DNA damage and tumor cell death; Fc can also mediate ADCC, with a membrane-permeable payload enabling bystander killing.