Gene-modified autologous T cells expressing a CD19-specific CAR; includes metabolic armoring intended to enhance T-cell fitness, expansion, and persistence; targets CD19+ malignant B cells.
Autologous T cells are gene-modified to express a CD19-specific chimeric antigen receptor. Binding to CD19 on malignant B cells triggers CAR signaling, activating cytotoxic functions (e.g., perforin/granzyme release and cytokine production) to kill target cells. Metabolic armoring is included to enhance T-cell metabolic fitness, expansion, and persistence in the tumor microenvironment.
YES
DIRECT
CAR-T cells bind CD19 on target cells, triggering T-cell activation and immunologic synapse formation, leading to perforin/granzyme-mediated apoptosis (and related T-cell cytotoxic pathways).
Glycoengineered type II anti-CD20 IgG1 monoclonal antibody; induces potent ADCC and direct cell death.
Humanized, glycoengineered type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells; afucosylated Fc increases affinity for FcgammaRIIIa, driving potent antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis, and directly induces caspase-independent cell death, leading to depletion of malignant CD20+ B cells.
YES
DIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc strongly engages FcγRIIIa on NK cells and macrophages to drive ADCC and phagocytosis, and it also triggers direct, caspase-independent cell death of CD20+ cells.
Glycoengineered type II anti-CD20 IgG1 monoclonal antibody; induces potent ADCC and direct cell death.
Humanized, glycoengineered type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells; afucosylated Fc increases affinity for FcgammaRIIIa, driving potent antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis, and directly induces caspase-independent cell death, leading to depletion of malignant CD20+ B cells.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages CD16a (FcγRIIIa) on NK cells/macrophages to trigger ADCC/ADCP against CD20+ cells. CD16a-expressing effector cells are not killed by the drug.
Type I anti-CD20 monoclonal antibody; mediates ADCC and complement-dependent cytotoxicity.
Type I anti-CD20 chimeric IgG1 monoclonal antibody that binds CD20 on B cells and mediates antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and phagocytosis, resulting in depletion of CD20-positive B cells.
YES
DIRECT
Rituximab binds CD20 on B cells and recruits immune effectors to kill via ADCC and antibody-dependent phagocytosis, and activates complement for CDC, depleting CD20+ cells.
Anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric IgG1 monoclonal antibody targeting CD20 on B cells; induces B‑cell depletion via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and direct apoptosis.
YES
DIRECT
Anti‑CD20 antibody binding triggers complement-dependent cytotoxicity, Fc-mediated ADCC by NK cells/macrophages, and can induce apoptosis via CD20 crosslinking.