Chimeric IgG1 anti-EGFR monoclonal antibody that inhibits EGFR signaling (MAPK and PI3K/AKT pathways) and induces antibody-dependent cellular cytotoxicity.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream MAPK and PI3K/AKT signaling, and engages Fc receptors to induce antibody-dependent cellular cytotoxicity (ADCC).
NO
INDIRECT
Cetuximab binds EGFR on tumor cells; its Fc engages CD16a on NK cells to trigger ADCC, killing EGFR-expressing cells, not the CD16a-expressing effector cells.
Chimeric IgG1 monoclonal antibody targeting TNF-α; binds soluble and transmembrane TNF-α to block TNFR1/TNFR2 signaling, suppress NF-κB–mediated pro-inflammatory cytokines, and can induce apoptosis and CDC/ADCC of TNF-expressing cells. Includes subcutaneous biosimilar CT-P13.
Chimeric IgG1 monoclonal antibody that binds and neutralizes soluble and transmembrane TNF-alpha, blocking TNFR1/TNFR2 signaling, reducing NF-kappaB-driven pro-inflammatory cytokines and leukocyte recruitment; can induce apoptosis and CDC/ADCC of TNF-expressing cells. Includes subcutaneous biosimilar CT-P13.
YES
DIRECT
Infliximab binds transmembrane TNF on cells and elicits Fc-mediated ADCC/CDC, and can trigger reverse-signaling–mediated apoptosis, killing tmTNF-expressing cells.
An intraperitoneal recombinant human–mouse chimeric bispecific T‑cell–engaging antibody (anti‑EpCAM × anti‑CD3) that binds EpCAM on tumor cells and CD3 on T cells to activate TCR/CD3 signaling and redirect cytotoxic T‑cell killing of EpCAM‑positive tumor cells for control of peritoneal tumor burden and ascites.
Bispecific antibody that binds EpCAM on tumor cells and CD3 on T cells, bringing them into proximity to activate TCR/CD3 signaling and redirect cytotoxic T-cell killing (perforin/granzyme and cytokine release) of EpCAM-positive tumor cells.
YES
DIRECT
M701 bridges EpCAM on tumor cells to CD3 on T cells, activating TCR signaling and inducing cytotoxic T‑cell killing (immune synapse formation, perforin/granzyme release and cytokine‑mediated lysis) of EpCAM‑positive cells.
An anti-HER2 antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, internalizes, and releases the cytotoxic payload MMAE to inhibit microtubules, causing G2/M arrest and apoptosis, with potential bystander killing.
Anti-HER2 (ERBB2) antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to disrupt tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander killing.
YES
DIRECT
The anti-HER2 ADC binds HER2 on target cells, is internalized, and releases MMAE intracellularly to inhibit microtubules, causing G2/M arrest and apoptosis (with possible bystander effect).
An anti-HER2 antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, internalizes, and releases the cytotoxic payload MMAE to inhibit microtubules, causing G2/M arrest and apoptosis, with potential bystander killing.
Anti-HER2 (ERBB2) antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to disrupt tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander killing.
NO
INDIRECT
The ADC binds HER2 (not beta-tubulin), is internalized, and releases MMAE, which binds beta-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; possible bystander killing.