Autologous CAR-T cells targeting CD22 on B-lineage cells; CAR activation induces T-cell effector functions to kill CD22-positive malignant B cells, potentially causing B-cell aplasia.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds CD22 on B-lineage cells. Antigen engagement activates CAR signaling (CD3zeta with co-stimulatory domains), leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated killing of CD22-positive malignant B cells, with potential on-target B-cell aplasia.
CD22-specific CAR-T cells bind CD22 on B cells; CAR signaling activates T-cell effector functions leading to perforin/granzyme-mediated lysis of CD22-positive cells.
Intravenous chimeric IgG1 monoclonal antibody against EGFR that blocks ligand binding, promotes receptor downregulation, and mediates ADCC.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization, promoting receptor internalization/downregulation, and thereby inhibiting downstream MAPK/ERK and PI3K/AKT signaling and tumor cell proliferation; its Fc region also mediates antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells/macrophages to induce ADCC (and some CDC), leading to target-cell lysis/apoptosis; it also blocks EGFR signaling (antiproliferative).
Selective HER2 (ERBB2) tyrosine-kinase inhibitor that binds the HER2 kinase domain, blocks receptor autophosphorylation and signaling (including HER2 homodimers and HER2/EGFR heterodimers), suppresses downstream MAPK/ERK and PI3K/AKT pathways, and inhibits proliferation and survival of HER2-driven tumor cells.
Selective inhibition of HER2 kinase blocks autophosphorylation and MAPK/PI3K-AKT signaling, causing growth arrest and apoptosis of HER2-dependent tumor cells.
An antibody–drug conjugate targeting HER2: the trastuzumab antibody binds HER2, inhibits signaling and can trigger ADCC; after internalization it releases the DXd payload, a membrane-permeable topoisomerase I inhibitor that induces DNA damage and bystander killing.
Trastuzumab deruxtecan is an anti-HER2 antibody–drug conjugate: trastuzumab binds HER2, inhibits signaling and can trigger ADCC; after internalization a cleavable linker releases the DXd payload, a membrane-permeable topoisomerase I inhibitor that causes DNA damage and cell death with a bystander effect.
The anti-HER2 ADC binds HER2, is internalized, and a cleavable linker releases the DXd topoisomerase I inhibitor that induces DNA damage and cell death (with additional ADCC and bystander effects).