Anti-EGFR IgG1 monoclonal antibody that blocks EGFR signaling and mediates antibody-dependent cellular cytotoxicity.
Cetuximab is an anti-EGFR IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream signaling (e.g., RAS/RAF/MEK/ERK and PI3K/AKT), resulting in anti-proliferative effects; as an IgG1 it also mediates NK cell–driven antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells to trigger ADCC (and possibly CDC), leading to lysis of EGFR-expressing cells.
A NECTIN-4–targeted antibody–drug conjugate delivering MMAE, a microtubule inhibitor that causes cell-cycle arrest and apoptosis.
Nectin-4–targeted monoclonal antibody–drug conjugate that binds Nectin-4 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE after linker cleavage, leading to tubulin depolymerization, G2/M cell-cycle arrest, and apoptosis in Nectin-4–expressing cancer cells.
YES
DIRECT
ADC binds Nectin-4 on target cells, is internalized, linker is cleaved to release MMAE, which depolymerizes microtubules causing G2/M arrest and apoptosis of the Nectin-4–expressing cells.
Anti-HER2 antibody–drug conjugate delivering the microtubule inhibitor MMAE to HER2 (ERBB2)-expressing tumor cells, leading to internalization and microtubule disruption.
Disitamab vedotin is an anti-HER2 (ERBB2) antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE via a cleavable linker. Released MMAE disrupts tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander killing of adjacent tumor cells.
YES
DIRECT
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits microtubule polymerization causing G2/M arrest and apoptosis (with possible bystander killing).
Anti-HER2 antibody–drug conjugate delivering the microtubule inhibitor MMAE to HER2 (ERBB2)-expressing tumor cells, leading to internalization and microtubule disruption.
Disitamab vedotin is an anti-HER2 (ERBB2) antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE via a cleavable linker. Released MMAE disrupts tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander killing of adjacent tumor cells.
NO
INDIRECT
The ADC binds HER2 (not beta-tubulin), is internalized, and releases MMAE, which inhibits beta-tubulin polymerization to cause G2/M arrest and apoptosis; killing is driven by HER2 targeting (with possible bystander effect), not by beta-tubulin expression itself.
Autologous T lymphocytes genetically modified ex vivo (typically via retroviral or lentiviral vectors) to express a chimeric antigen receptor targeting tumor antigens; adoptively transferred for durable in vivo persistence and anti-cancer activity.
Autologous T cells are genetically modified ex vivo (commonly via retroviral or lentiviral vectors) to express a chimeric antigen receptor that binds tumor surface antigens independent of MHC; CAR signaling (CD3ζ with costimulatory domains such as CD28 or 4-1BB) activates T cells to proliferate, persist, release cytokines, and mediate cytotoxic killing of tumor cells.
YES
DIRECT
CAR T cells bind the target antigen via the CAR and directly lyse antigen-expressing cells through perforin/granzyme release and death receptor (e.g., Fas/FasL) pathways.