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.
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.
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.
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.
Autologous BCMA-directed CAR T-cell therapy; patient T cells are engineered to express a CAR targeting BCMA to eliminate BCMA+ plasmablasts/long-lived plasma cells and reduce autoantibody-mediated platelet destruction.
Autologous T cells are genetically modified to express a chimeric antigen receptor targeting BCMA; after infusion they recognize and kill BCMA-positive plasmablasts and long-lived plasma cells, depleting autoantibody-producing cells and reducing platelet-directed autoimmunity.
BCMA-directed CAR T cells recognize BCMA on plasmablasts/plasma cells and induce T-cell cytolysis (perforin/granzyme-mediated apoptosis, with possible Fas–FasL contribution).
Intravenous anti-EGFR IgG1 monoclonal antibody that blocks ligand-dependent EGFR activation, reduces downstream RAS/MAPK signaling, and can induce antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream RAS/MAPK (and PI3K/AKT) signaling. Its Fc can engage ADCC against EGFR-expressing tumor cells.
Cetuximab’s IgG1 Fc engages Fcγ receptors on NK cells and other effectors to trigger ADCC (and some complement-mediated lysis), killing EGFR-expressing cells; EGFR blockade itself is primarily cytostatic.
Autologous, second-generation anti-CD19 CAR T-cell therapy. Patient T cells are gene-modified to express a CD19-targeted chimeric antigen receptor with CD3zeta signaling plus a costimulatory domain, driving activation, expansion, cytokine release, and cytotoxic killing of CD19-positive B-cell malignancies.
Autologous T cells are genetically engineered to express a second‑generation anti‑CD19 chimeric antigen receptor with CD3ζ signaling plus a costimulatory domain. Upon binding CD19 on B‑cell malignancies, the CAR triggers T‑cell activation, expansion, cytokine release, and cytotoxic killing of CD19‑positive cells, often resulting in depletion of normal B cells (B‑cell aplasia).
Anti-CD19 CAR T cells bind CD19 on target B cells, activating T-cell cytotoxicity (perforin/granzyme release and death-receptor pathways) to induce apoptosis of CD19-positive cells.