Humanized IgG1 monoclonal antibody targeting SLAMF7 (CS1) on myeloma and NK cells; enhances NK cell–mediated ADCC and immune activation.
Humanized IgG1 monoclonal antibody targeting SLAMF7 (CS1) on myeloma and NK cells; promotes antibody-dependent cellular cytotoxicity (ADCC) against SLAMF7+ myeloma cells via Fcγ receptor engagement and directly activates NK cells through SLAMF7 signaling to enhance immune-mediated tumor killing.
Elotuzumab binds SLAMF7 on myeloma cells and engages Fcγ receptors on NK cells to trigger ADCC; it also activates NK cells via SLAMF7 signaling, leading to immune-mediated killing of SLAMF7+ cells.
Gene-edited allogeneic universal CAR-T cell therapy using a CD94-based recognition domain to engage the CD94/HLA-E axis, designed to overcome immune evasion and enhance tumor killing.
Gene-edited allogeneic universal CAR-T cells engineered with a CD94-based recognition domain that engages the CD94/HLA-E axis on tumor cells, overcoming immune evasion and activating T-cell cytotoxicity to kill malignant cells.
CD94-based CAR-T cells recognize HLA-E on target cells, triggering immune-synapse formation and T-cell effector killing via perforin/granzyme release and death-receptor pathways.
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD19; after infusion they eliminate CD19+ B-lineage cells, producing deep and sustained B-cell depletion and a potential immune reset.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds CD19 on B-lineage cells. Upon CD19 engagement, the CAR T cells activate and kill target B cells and plasmablasts via perforin/granzyme and death-receptor pathways, causing deep and sustained B-cell depletion, suppression of autoantibody production, and a potential immune reset. Activity is MHC-independent.
CAR T cells bind CD19 on target B-lineage cells and kill them via T-cell cytotoxicity—perforin/granzyme-mediated lysis and death-receptor (e.g., Fas) apoptosis, MHC-independent.
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and recruits immune effectors via Fc to mediate ADCC, activates complement for CDC, and can induce apoptosis upon CD20 crosslinking.