A chimeric IgG1 anti-GD2 monoclonal antibody immunotherapy (brand: Qarziba) used as maintenance after response in relapsed/refractory high‑grade osteosarcoma. It binds the disialoganglioside GD2 on tumor cells and triggers immune effector killing via Fc-mediated ADCC and phagocytosis, and complement‑dependent cytotoxicity (CDC). Dosed as continuous IV 14 mg/m2/day on days 1–5 every 28 days for 5 cycles.
Chimeric IgG1 anti-GD2 monoclonal antibody that binds GD2 on tumor cells and elicits immune effector killing via Fcγ receptor–mediated ADCC and phagocytosis, and complement-dependent cytotoxicity (CDC).
NO
INDIRECT
Dinutuximab beta binds GD2 on tumor cells; its Fc engages Fcγ receptors (including CD16b/FCGR3B) on immune effector cells to trigger ADCC/phagocytosis and complement-mediated lysis of GD2+ cells. FCGR3B-expressing cells are not targeted or killed by the drug.
A chimeric IgG1 anti-GD2 monoclonal antibody immunotherapy (brand: Qarziba) used as maintenance after response in relapsed/refractory high‑grade osteosarcoma. It binds the disialoganglioside GD2 on tumor cells and triggers immune effector killing via Fc-mediated ADCC and phagocytosis, and complement‑dependent cytotoxicity (CDC). Dosed as continuous IV 14 mg/m2/day on days 1–5 every 28 days for 5 cycles.
Chimeric IgG1 anti-GD2 monoclonal antibody that binds GD2 on tumor cells and elicits immune effector killing via Fcγ receptor–mediated ADCC and phagocytosis, and complement-dependent cytotoxicity (CDC).
NO
INDIRECT
Dinutuximab beta binds GD2 on tumor cells and induces ADCC/phagocytosis and complement-dependent cytotoxicity. C1q binds the antibody Fc to activate complement but is not the antigen targeted; cells expressing C1q are not directly killed.
Chimeric anti-CD20 monoclonal antibody immunotherapy that binds CD20 on B cells and depletes malignant cells via antibody-dependent cellular cytotoxicity, complement-mediated cytotoxicity, and apoptosis; administered intralesionally in this trial.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis; in this trial administered intralesionally for local effect.
YES
DIRECT
Rituximab binds CD20 on B cells and kills them via Fc-mediated ADCC by immune effector cells, complement-dependent cytotoxicity, and antibody-induced apoptosis.
Partial HLA-matched multivirus-specific cytotoxic T lymphocytes administered by IV infusion to restore antiviral cellular immunity after allo-HSCT by HLA-restricted TCR recognition of CMV/EBV antigens and perforin/granzyme-mediated cytolysis.
Adoptive transfer of partial HLA-matched virus-specific cytotoxic T lymphocytes that use their endogenous, HLA-restricted TCRs to recognize CMV/EBV peptides on infected cells, expand in vivo, and mediate killing via perforin/granzyme and cytokine release, thereby clearing infected cells and restoring antiviral cellular immunity after allo-HSCT.
YES
DIRECT
Adoptively transferred CMV-specific T cells recognize CMV peptide–HLA complexes via their endogenous TCRs and directly kill infected cells through perforin/granzyme-mediated cytolysis (with cytokine support).
Partial HLA-matched multivirus-specific cytotoxic T lymphocytes administered by IV infusion to restore antiviral cellular immunity after allo-HSCT by HLA-restricted TCR recognition of CMV/EBV antigens and perforin/granzyme-mediated cytolysis.
Adoptive transfer of partial HLA-matched virus-specific cytotoxic T lymphocytes that use their endogenous, HLA-restricted TCRs to recognize CMV/EBV peptides on infected cells, expand in vivo, and mediate killing via perforin/granzyme and cytokine release, thereby clearing infected cells and restoring antiviral cellular immunity after allo-HSCT.
YES
DIRECT
Virus-specific T cells recognize EBV peptide–HLA complexes via their endogenous TCRs and kill the presenting cells by perforin/granzyme–mediated apoptosis (with possible Fas–FasL and cytokine-mediated effects).