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.
YES
DIRECT
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.
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.
NO
INDIRECT
Enoblituzumab binds B7-H3 on tumor/stromal cells, then its Fc engages CD16A on NK cells/macrophages to drive ADCC/ADCP against B7-H3–positive targets. CD16A-expressing cells act as effectors and are not targeted or killed by the drug.
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.
NO
INDIRECT
Enoblituzumab binds B7-H3 on tumor cells; its Fc engages FcγRIIa (CD32A) on effector cells (e.g., macrophages) to mediate ADCC/ADCP against B7‑H3+ cells. CD32A+ cells are not killed; they mediate killing.
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.
YES
DIRECT
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).
YES
DIRECT
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.