Chimeric IgG1 anti-EGFR monoclonal antibody that blocks ligand binding and downstream MAPK/ERK and PI3K/AKT signaling and can induce ADCC against EGFR-expressing tumor cells.
Cetuximab is a chimeric IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocking ligand binding and receptor dimerization, thereby inhibiting downstream MAPK/ERK and PI3K/AKT signaling; its Fc can also engage immune effector cells to mediate ADCC against EGFR-expressing tumor cells.
IgG1 Fc engages FcγR-bearing effector cells to mediate ADCC (and some CDC/ADCP), leading to lysis/phagocytosis of EGFR-expressing cells; signaling blockade is antiproliferative rather than cytotoxic.
Autologous BCMA-targeted chimeric antigen receptor T-cell (CAR-T) therapy; patient T cells are gene-modified to express a CAR recognizing BCMA (TNFRSF17) to eliminate BCMA+ plasmablasts/plasma cells and some memory B cells, reducing pathogenic autoantibody production.
Autologous T cells are engineered to express a CAR targeting BCMA (TNFRSF17). Upon binding BCMA on plasmablasts/plasma cells (and some memory B cells), the CAR T cells activate and kill these cells, depleting antibody-secreting populations and reducing pathogenic autoantibody production.
BCMA-targeted CAR T cells bind BCMA on plasmablasts/plasma cells, become activated, and induce cytotoxicity via perforin/granzyme-mediated apoptosis (and Fas/FasL signaling).
An antibody–drug conjugate (Blenrep; belantamab mafodotin-blmf) consisting of a humanized anti-BCMA IgG1 linked to mafodotin (MMAF). It binds BCMA on malignant plasma cells, is internalized, and releases MMAF to disrupt microtubules and induce apoptosis; the afucosylated IgG1 can mediate ADCC/ADCP.
Afucosylated anti-BCMA IgG1 antibody–drug conjugate that binds BCMA (TNFRSF17) on malignant plasma cells, is internalized, and releases the microtubule inhibitor MMAF to disrupt tubulin, leading to G2/M arrest and apoptosis; the afucosylated Fc also enhances ADCC/ADCP.
The ADC binds BCMA on target cells, is internalized, and releases the microtubule inhibitor MMAF, causing G2/M arrest and apoptosis; its afucosylated Fc also enhances ADCC/ADCP against BCMA-expressing cells.
Subcutaneous CD20xCD3 bispecific T-cell–engaging antibody that redirects patient T cells via CD3 to lyse CD20-positive B-cell lymphoma; administered with step-up dosing.
Humanized CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to form an immune synapse and activate T-cell cytotoxicity to lyse CD20-positive malignant B cells.
The bispecific antibody crosslinks CD3 on T cells with CD20 on B cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme-mediated lysis) to kill CD20-positive cells.
TROP2-targeting antibody–drug conjugate composed of a humanized monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor; binds TROP2 on tumor cells, internalizes, and releases the topo‑I payload to cause DNA damage and cell death (with potential bystander effect).
TROP2-targeting IgG1k antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and via a cleavable linker releases the topoisomerase I inhibitor tirumotecan, inhibiting topo I to cause DNA damage, replication arrest, and apoptosis, with a potential bystander effect.
ADC binds TROP2, is internalized, and releases a topoisomerase I inhibitor (tirumotecan) that causes DNA damage, replication arrest, and apoptosis in TROP2-expressing cells (with possible bystander effect).