Chimeric IgG1 anti‑EGFR monoclonal antibody that blocks ligand binding to EGFR, inhibiting downstream RAS‑RAF‑MEK‑ERK and PI3K‑AKT signaling; also mediates ADCC.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor activation/dimerization, thereby inhibiting downstream RAS–RAF–MEK–ERK and PI3K–AKT signaling; also mediates antibody-dependent cellular cytotoxicity (ADCC) against EGFR-expressing tumor cells.
Cetuximab binds EGFR on target cells and engages Fcγ receptors on immune effectors (e.g., NK cells) to induce antibody‑dependent cellular cytotoxicity (ADCC; with some CDC), leading to killing of EGFR+ cells.
Autologous, gene-modified T cells engineered to express a chimeric antigen receptor targeting GPRC5D on malignant plasma cells; CAR signaling (CD3ζ with costimulation) activates T cells to proliferate, release cytokines, and mediate perforin/granzyme cytotoxic killing.
Autologous T cells are gene-modified to express a chimeric antigen receptor targeting GPRC5D on malignant plasma cells. CAR engagement activates CD3zeta with costimulatory signaling, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of GPRC5D-positive cells.
GPRC5D-specific CAR-T cells bind GPRC5D on target cells, activate via CD3ζ/costimulation, and kill through perforin/granzyme-mediated cytotoxicity.
Fc-engineered humanized IgG1 monoclonal antibody (also known as MGA271) targeting B7-H3 (CD276); given neoadjuvantly at 15 mg/kg IV every 2 weeks for 12 weeks. Mechanism: binds B7-H3 on tumor and stromal/vascular cells, engages Fcγ receptors to drive ADCC/ADCP (possible CDC), and may alleviate B7-H3–mediated immunosuppression to enhance T-cell activity.
Fc-engineered humanized IgG1 targeting B7-H3 (CD276) on tumor and stromal/vascular cells; enhances FcγR engagement to drive NK cell/macrophage-mediated ADCC and ADCP (with possible CDC), depleting B7-H3–expressing cells, and may relieve B7-H3–mediated immunosuppression to augment antitumor T‑cell responses.
Enoblituzumab binds B7-H3 on target cells and recruits Fc-gamma receptor–bearing effectors (NK cells/macrophages) to mediate ADCC and antibody-dependent phagocytosis; complement-dependent cytotoxicity may also contribute.
Autologous gene-engineered TCR-T cell therapy expressing an HLA-A*0201–restricted TCR specific for the H3.3K27M neoantigen; endogenous TCR is inhibited to reduce mispairing and off-target reactivity.
Autologous T cells genetically engineered to express an HLA-A*0201–restricted T-cell receptor specific for the H3.3K27M neoantigen on glioma cells. Upon recognition of the H3.3K27M peptide presented on MHC class I, the T cells activate and kill target cells via perforin/granzyme cytotoxicity and cytokine release. The endogenous TCR is inhibited to reduce mispairing and off-target reactivity; therapy relies on HLA-A*0201 restriction.
Engineered TCR-T cells recognize the H3.3K27M peptide presented by HLA-A*02:01 and directly kill target cells via perforin/granzyme-mediated cytolysis (with additional cytokine/Fas-FasL apoptotic effects).
Chimeric IgG1 monoclonal antibody targeting EGFR; blocks ligand binding and receptor activation and can mediate ADCC.
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain, blocks ligand binding and receptor activation/dimerization, suppressing downstream MAPK/PI3K signaling to inhibit tumor cell proliferation and survival; its Fc region can recruit immune effector cells to mediate antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptor–bearing effector cells to trigger antibody‑dependent cellular cytotoxicity (ADCC), with possible complement‑dependent cytotoxicity; EGFR signaling blockade is antiproliferative.