Anti-EGFR IgG1 monoclonal antibody that blocks EGFR signaling and opsonizes tumor cells to trigger ADCC.
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream EGFR signaling and tumor proliferation, while Fc-mediated opsonization induces ADCC (and CDC) against EGFR-expressing tumor cells.
YES
DIRECT
Cetuximab opsonizes EGFR-expressing cells and recruits immune effectors via its IgG1 Fc to trigger NK cell–mediated ADCC and complement-dependent cytotoxicity, leading to lysis of EGFR+ cells (while also blocking EGFR signaling).
Anti-EGFR IgG1 monoclonal antibody that blocks EGFR signaling and opsonizes tumor cells to trigger ADCC.
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream EGFR signaling and tumor proliferation, while Fc-mediated opsonization induces ADCC (and CDC) against EGFR-expressing tumor cells.
NO
INDIRECT
Cetuximab binds EGFR on tumor cells; its Fc engages CD16a on NK cells to trigger ADCC against EGFR+ cells. CD16a-expressing cells are not killed by the drug.
Autologous gene‑engineered T cells expressing a mesothelin‑targeted CAR and providing local anti‑PD‑1 activity to block PD‑1/PD‑L1 signaling, enhancing T‑cell activation, cytotoxicity, and persistence in PD‑L1–positive, mesothelin‑expressing tumors.
Autologous T cells engineered to express a mesothelin-targeted chimeric antigen receptor that recognizes and kills mesothelin-positive tumor cells, while concurrently delivering local anti–PD-1 activity to block PD-1/PD-L1 signaling, enhancing T-cell activation, cytotoxicity, and persistence in the tumor microenvironment.
YES
DIRECT
MSLN-targeted CAR T cells bind mesothelin on tumor cells, activating T-cell killing via perforin/granzyme release and death-receptor pathways; PD-1 blockade locally enhances this cytotoxic response.
Autologous gene‑engineered T cells expressing a mesothelin‑targeted CAR and providing local anti‑PD‑1 activity to block PD‑1/PD‑L1 signaling, enhancing T‑cell activation, cytotoxicity, and persistence in PD‑L1–positive, mesothelin‑expressing tumors.
Autologous T cells engineered to express a mesothelin-targeted chimeric antigen receptor that recognizes and kills mesothelin-positive tumor cells, while concurrently delivering local anti–PD-1 activity to block PD-1/PD-L1 signaling, enhancing T-cell activation, cytotoxicity, and persistence in the tumor microenvironment.
NO
INDIRECT
PD-1 is blocked on T cells to relieve inhibition, enhancing CAR T activity; killing is directed at mesothelin-positive cells via CAR-mediated cytolysis (perforin/granzyme), not at PD-1–expressing cells.
Type II, glycoengineered humanized anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via enhanced antibody-dependent cellular cytotoxicity/phagocytosis and direct cell death, with limited complement activation.
Type II, glycoengineered humanized anti‑CD20 IgG1 that binds CD20 on B cells; afucosylated Fc increases FcγRIIIa affinity to enhance antibody‑dependent cellular cytotoxicity and phagocytosis, and it triggers direct, caspase‑independent cell death with minimal complement activation, leading to depletion of CD20+ B cells.
YES
DIRECT
Obinutuzumab binds CD20 on B cells and kills via enhanced Fc gamma RIIIa (CD16a)-mediated ADCC by NK cells and antibody-dependent phagocytosis, plus direct caspase-independent cell death; complement involvement is minimal.