Intravenous anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis; used when co-occurring B-cell lymphoproliferation is present.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers killing via Fc-mediated ADCC (e.g., NK cells/macrophages) and complement-dependent cytotoxicity (CDC), and can also induce apoptosis upon CD20 crosslinking.
Chimeric anti-CD20 IgG1 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity, and induction of apoptosis upon CD20 crosslinking.
Humanized monoclonal antibody that binds HER2 domain IV to inhibit HER2 signaling and mediate antibody-dependent cellular cytotoxicity (ADCC) via Fcγ receptors. Administered as part of PHESGO in this study.
Humanized IgG1 monoclonal antibody that binds HER2 (domain IV), inhibits HER2 signaling and receptor activation/heterodimerization, promotes receptor downregulation, and mediates Fcγ receptor–dependent ADCC against HER2-overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells, macrophages) to mediate ADCC, leading to perforin/granzyme-dependent killing; may also contribute some CDC and growth inhibition via HER2 blockade.
Humanized monoclonal antibody that binds HER2 domain IV to inhibit HER2 signaling and mediate antibody-dependent cellular cytotoxicity (ADCC) via Fcγ receptors. Administered as part of PHESGO in this study.
Humanized IgG1 monoclonal antibody that binds HER2 (domain IV), inhibits HER2 signaling and receptor activation/heterodimerization, promotes receptor downregulation, and mediates Fcγ receptor–dependent ADCC against HER2-overexpressing tumor cells.
NO
INDIRECT
Trastuzumab binds HER2 on tumor cells; its Fc engages CD16A on NK cells to trigger ADCC that kills HER2-positive cells. CD16A-expressing effector cells are not targeted or killed by the drug.
Autologous anti‑CD19 CAR T‑cell therapy with a 4‑1BB co‑stimulatory domain and CD3ζ signaling, engineered to recognize and kill CD19‑positive B cells.
Autologous T cells genetically engineered to express an anti‑CD19 chimeric antigen receptor with a 4‑1BB co‑stimulatory domain and CD3ζ signaling. Upon binding CD19 on B cells, the CAR activates T‑cell cytotoxicity, proliferation, and cytokine release to eliminate CD19‑positive malignant B cells and promote persistence.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on B cells, become activated via CD3ζ/4-1BB signaling, and directly kill target cells through perforin/granzyme-mediated lysis and death-receptor pathways.