Autologous patient T cells engineered to express a chimeric antigen receptor targeting CD19 on B cells; CAR engagement activates cytotoxic T-cell responses (activation, expansion, cytokine release, perforin/granzyme-mediated killing) to eliminate CD19+ malignant B cells and can cause on-target B-cell aplasia in pediatric r/r B-ALL.
Autologous patient T cells are engineered to express a chimeric antigen receptor that recognizes CD19 on B cells. CAR engagement triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD19-positive malignant B cells, often leading to on-target B-cell aplasia.
CAR T cells bind CD19 on target cells and directly kill them via immunologic-synapse–mediated perforin/granzyme cytotoxicity (and death-receptor pathways), leading to apoptosis of CD19+ cells.
HER3-DXd; an antibody-drug conjugate composed of patritumab, a fully human anti-HER3 (ERBB3) IgG1 monoclonal antibody, linked via a cleavable tetrapeptide to deruxtecan (DXd), a membrane-permeable exatecan-derived topoisomerase I inhibitor. It binds HER3 on tumor cells, is internalized, and releases DXd in lysosomes to induce DNA single-strand breaks and apoptosis, with a bystander effect.
Fully human anti-HER3 (ERBB3) IgG1 antibody linked via a cleavable tetrapeptide to the topoisomerase I inhibitor DXd. Binds HER3 on tumor cells, is internalized, and releases DXd in lysosomes to inhibit topo I, causing DNA single-strand breaks and apoptosis, with a membrane-permeable bystander killing effect.
The anti-HER3 ADC binds HER3, is internalized, and releases the topoisomerase I inhibitor DXd in lysosomes, causing DNA damage and apoptosis in the target cell, with additional bystander killing from the membrane-permeable payload.
Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
ATG contains antibodies that bind CD25 on T cells, triggering complement-dependent cytotoxicity and Fc-mediated ADCC, with additional apoptosis, leading to depletion of CD25+ cells.
Humanized anti-EGFR IgG1 monoclonal antibody that blocks EGFR ligand binding/activation, suppresses MAPK/ERK and PI3K/AKT signaling, and mediates ADCC.
Humanized IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor activation, suppressing MAPK/ERK and PI3K/AKT signaling, inhibiting proliferation and survival of EGFR-overexpressing tumor cells, and engaging Fc-mediated ADCC.
Anti-EGFR IgG1 binds EGFR and its Fc engages FcγR+ immune effectors to mediate ADCC (NK/macrophage killing); may also trigger CDC. EGFR signaling blockade is cytostatic.
Bispecific antibody-drug conjugate targeting EGFR and HER3; after internalization, releases a topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific ADC that binds EGFR and HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor payload brengitecan to induce DNA damage and tumor cell death.
The bispecific ADC binds EGFR on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and cell death.