Humanized anti-HER2 monoclonal antibody that inhibits HER2 signaling/dimerization and mediates ADCC.
Humanized anti-HER2 (ERBB2) IgG1 monoclonal antibody that binds the HER2 extracellular domain, blocks receptor activation and dimerization, downregulates HER2 signaling, and engages Fcγ-mediated antibody-dependent cellular cytotoxicity (ADCC), leading to tumor cell death.
Trastuzumab binds HER2 on target cells and engages Fcγ receptor–bearing immune effectors (e.g., NK cells) to mediate ADCC, killing the cells; it also inhibits HER2 signaling, promoting apoptosis.
Autologous TCR-engineered T cells (TCR-T) expressing an NY-ESO-1–specific, HLA-A2–restricted T-cell receptor to recognize NY-ESO-1 peptides on HLA-A2 and kill tumor cells via TCR-mediated cytotoxicity.
Autologous T cells are genetically engineered to express an NY-ESO-1–specific, HLA-A2–restricted T-cell receptor. They recognize NY-ESO-1 peptide presented on HLA-A2 on tumor cells and, upon TCR engagement, activate and kill target cells via perforin/granzyme-mediated cytotoxicity and associated effector functions.
Engineered TCR-T cells recognize the NY-ESO-1(157–165) peptide presented on HLA-A*02 and kill target cells via TCR-triggered perforin/granzyme-mediated cytotoxicity.
Autologous TCR-engineered T cells (TCR-T) expressing an NY-ESO-1–specific, HLA-A2–restricted T-cell receptor to recognize NY-ESO-1 peptides on HLA-A2 and kill tumor cells via TCR-mediated cytotoxicity.
Autologous T cells are genetically engineered to express an NY-ESO-1–specific, HLA-A2–restricted T-cell receptor. They recognize NY-ESO-1 peptide presented on HLA-A2 on tumor cells and, upon TCR engagement, activate and kill target cells via perforin/granzyme-mediated cytotoxicity and associated effector functions.
Engineered TCR-T cells recognize the NY-ESO-1 peptide presented by HLA-A2 and kill target cells via TCR-triggered perforin/granzyme-mediated cytotoxicity (apoptosis).
Humanized anti-EGFR IgG1 monoclonal antibody that blocks EGFR signaling and can mediate ADCC.
Humanized IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocking ligand binding, receptor activation/dimerization, and downstream MAPK/PI3K signaling to inhibit tumor cell proliferation and survival; its Fc region can engage immune effector cells to mediate ADCC. May enhance radiosensitivity.
IgG1 anti‑EGFR antibody binds EGFR on tumor cells and its Fc engages Fcγ receptors on immune effectors (e.g., NK cells) to trigger ADCC, killing EGFR+ cells; EGFR blockade mainly inhibits proliferation.
Anti-CD20 monoclonal antibody mediating complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity; used for CD20+ tumors.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and induces B-cell depletion primarily via complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP), with potential direct apoptotic signaling; used to target CD20-positive tumors.
Rituximab binds CD20 on B cells and kills via complement-dependent cytotoxicity (MAC-mediated lysis) and Fcγ receptor–mediated ADCC/ADCP by NK cells and macrophages; it may also trigger direct apoptotic signaling.