Autologous T cells engineered with a retroviral vector to express a single bispecific chimeric antigen receptor targeting CD19 and CD22, enabling TCR-independent activation, expansion, cytokine release, and cytotoxic killing of B-lineage leukemia; used to eradicate MRD and induce B-cell aplasia.
Autologous T cells are retrovirally engineered to express a single tandem (bispecific) CAR that recognizes CD19 and CD22 on B-lineage cells. Antigen binding triggers TCR-independent CD3ζ/costimulatory signaling, leading to T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD19+/CD22+ leukemia, resulting in MRD clearance and B-cell aplasia.
YES
DIRECT
CAR recognition of CD19 activates engineered T cells via CD3ζ/costimulatory signaling, inducing perforin/granzyme-mediated lysis of CD19+ cells (with associated cytokine release).
Anti-SLAMF7 monoclonal antibody that activates NK cells and mediates ADCC against SLAMF7+ myeloma cells.
Humanized anti‑SLAMF7 (CS1) monoclonal antibody that activates NK cells and induces Fc-mediated ADCC against SLAMF7-positive multiple myeloma cells, leading to targeted cytotoxicity with minimal effects on normal tissues.
YES
DIRECT
Elotuzumab binds SLAMF7 on target cells and engages NK cells via its Fc (FcγRIIIa), triggering antibody-dependent cellular cytotoxicity; it also activates NK cells, leading to killing of SLAMF7+ cells.
HER2-targeted antibody-drug conjugate (anti-HER2 IgG1 linked to the topoisomerase I inhibitor DXd); binds HER2 (including HER2-low), is internalized, releases DXd to cause DNA damage; also inhibits HER2 signaling and can mediate ADCC.
HER2-directed IgG1 antibody linked to a topoisomerase I inhibitor (DXd); binds HER2 (including HER2-low), is internalized, and releases DXd to inhibit Topo I–DNA complexes, causing DNA damage, cell-cycle arrest, and apoptosis; also inhibits HER2 signaling, mediates ADCC, and exerts a bystander killing effect.
YES
DIRECT
The HER2-targeted ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage, cell-cycle arrest, and apoptosis in HER2+ cells; it can also mediate Fc-dependent ADCC and a bystander effect.
HER2-targeted antibody-drug conjugate (anti-HER2 IgG1 linked to the topoisomerase I inhibitor DXd); binds HER2 (including HER2-low), is internalized, releases DXd to cause DNA damage; also inhibits HER2 signaling and can mediate ADCC.
HER2-directed IgG1 antibody linked to a topoisomerase I inhibitor (DXd); binds HER2 (including HER2-low), is internalized, and releases DXd to inhibit Topo I–DNA complexes, causing DNA damage, cell-cycle arrest, and apoptosis; also inhibits HER2 signaling, mediates ADCC, and exerts a bystander killing effect.
YES
INDIRECT
The ADC targets HER2 for uptake, then releases the DXd payload inside cells; DXd inhibits DNA topoisomerase I, trapping Top1-DNA complexes and causing DNA damage, cell-cycle arrest, and apoptosis (with possible bystander effect).
Engineered autologous T cells expressing a chimeric antigen receptor targeting B7-H3 (CD276), infused intravenously after lymphodepletion to mediate antigen-directed T-cell activation and cytotoxic killing of tumor cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes B7-H3 (CD276) on tumor cells. CAR engagement triggers CD3ζ/co-stimulatory signaling to activate, expand, and induce cytokine release and perforin/granzyme-mediated cytotoxic killing of target cells in an MHC-independent manner.
YES
DIRECT
CAR T cells bind B7-H3 on target cells, triggering T-cell activation and degranulation (perforin/granzymes) and death-receptor signaling, leading to apoptosis/lysis of antigen-positive cells.