Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream RAS/RAF/MEK/ERK signaling, thereby reducing tumor cell proliferation and survival; IgG1 Fc may also trigger ADCC.
Cetuximab opsonizes EGFR+ cells and engages FcγR-bearing effector cells (e.g., NK cells) to mediate ADCC (with some CDC possible); EGFR signaling blockade is mainly cytostatic.
Anti-BCMA monoclonal antibody–drug conjugate that binds BCMA on malignant plasma cells, internalizes, and delivers the microtubule inhibitor MMAF to induce cytotoxicity (with potential Fc-mediated effector functions).
Afucosylated anti-BCMA monoclonal antibody conjugated to the microtubule inhibitor MMAF. Binds BCMA on malignant plasma cells, is internalized, and delivers MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc engineering also enhances ADCC.
ADC binds BCMA, is internalized, and delivers MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; afucosylated Fc can also trigger ADCC.
HER2-directed antibody-drug conjugate composed of a humanized anti-HER2 monoclonal antibody linked to a microtubule-inhibiting auristatin/Amberstatin analog; binds HER2 on tumor cells, is internalized, and releases its cytotoxic payload via lysosomal processing to disrupt tubulin, causing mitotic arrest and apoptosis.
HER2-directed antibody-drug conjugate: a humanized anti-HER2 monoclonal antibody is site-specifically linked via a stable linker to an auristatin (opadotin/MMAF analog). After binding HER2 and internalization, lysosomal processing releases the payload, which inhibits tubulin polymerization, leading to G2/M arrest and apoptosis in HER2-expressing tumor cells.
The ADC binds HER2, is internalized, and releases an auristatin (MMAF/opadotin) payload that inhibits tubulin polymerization, causing G2/M arrest and apoptosis in HER2-expressing cells.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy; patient T cells are engineered to express a CD19-targeting CAR with CD3ζ and costimulatory domains and are infused after lymphodepletion to treat relapsed/refractory CD19+ B-cell lymphomas.
Autologous T cells are genetically engineered to express a CD19-targeted chimeric antigen receptor with CD3ζ and costimulatory domains. Upon binding CD19 on malignant B cells, the CAR triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, leading to depletion of CD19+ tumor cells (and on-target depletion of normal B cells) after lymphodepletion.
Anti-CD19 CAR T cells bind CD19 on target cells and directly kill them via immune-synapse formation with perforin/granzyme-mediated cytotoxicity (and Fas–FasL apoptosis).
Investigational bispecific antibody immunotherapy that engages two antitumor targets to enhance immune-mediated tumor killing.
Bispecific antibody designed to simultaneously bind a tumor-associated antigen and CD3 on T cells, recruiting and activating cytotoxic T cells to form an immune synapse and drive targeted tumor cell lysis.
The bispecific binds the tumor-associated antigen on target cells and CD3 on T cells, forming an immune synapse; engaged T cells kill antigen-positive cells via perforin/granzyme-mediated cytotoxicity.