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).
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on immune effectors (e.g., NK cells) to trigger ADCC, leading to lysis of EGFR-expressing cells; EGFR signaling blockade is mainly cytostatic.
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.
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.
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.
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).
A bispecific T-cell–engaging antibody that binds BCMA on myeloma plasma cells and CD3 on T cells, redirecting T cells to kill BCMA-positive tumor cells.
Humanized bispecific antibody that binds BCMA on myeloma plasma cells and CD3 on T cells, crosslinking them to form an immune synapse and redirect cytotoxic T-cell activity to kill BCMA-positive tumor cells.
Teclistamab bridges CD3 on T cells to BCMA on target cells, forming an immune synapse and triggering T‑cell–mediated killing via perforin/granzyme-induced apoptosis of BCMA+ cells.