An intravenous anti-CD38 IgG1 monoclonal antibody that binds CD38 on plasma cells and plasmablasts and depletes them via Fc-mediated cytotoxicity/phagocytosis and complement, reducing pathogenic autoantibody production; also known as HIB202, BIIB148, MOR202, and TJ202.
Fully human IgG1 anti-CD38 monoclonal antibody that binds CD38 on plasma cells/plasmablasts (and other CD38+ cells) and depletes them via Fc-mediated effector functions (ADCC/ADCP) and complement-dependent cytotoxicity, thereby reducing pathogenic autoantibody production; in oncology, induces lysis of CD38-expressing tumor cells.
Felzartamab binds CD38 on target cells and recruits immune effectors via its Fc to induce ADCC (NK cells), ADCP (phagocytes), and complement-dependent cytotoxicity, causing lysis of CD38+ cells.
Autologous gene-modified T cells engineered with a chimeric antigen receptor to redirect cytotoxicity against B-cell antigens.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds B-cell surface antigens (e.g., CD19), enabling antigen recognition and costimulation independent of HLA and triggering T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated lysis of malignant B cells.
CAR-T cells recognize CD19 on target cells via the CAR, triggering T-cell activation and perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via immune effector mechanisms.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, phagocytosis, and apoptosis, reducing CD20+ B-cell clones.
Anti-CD20 antibody binds CD20 on B cells and engages immune effectors via its Fc: NK cell–mediated ADCC, complement-dependent cytotoxicity (C1q activation/lysis), and macrophage phagocytosis; can also trigger apoptosis.
Anti-CD38 IgG1 monoclonal antibody that depletes CD38-positive clonal plasma cells via ADCC, CDC, ADCP, and apoptosis.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells and mediates cell killing via ADCC, CDC, and ADCP, with additional direct apoptotic effects; also depletes CD38+ immunosuppressive cells.
Daratumumab binds CD38 on target cells and induces killing via ADCC, complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and can trigger direct apoptosis.
Autologous genetically modified CAR T-cell therapy incorporating a chlorotoxin (CLTX) tumor-targeting domain that binds the MMP2 complex on glioblastoma, with CD28 costimulation, CD3ζ signaling, and a truncated CD19 selection tag; administered locally via intracavitary/intratumoral and intraventricular catheters.
Autologous T cells engineered with a chlorotoxin (CLTX)-based CAR that binds the MMP2-associated surface complex on glioblastoma. Antigen engagement triggers CD28 costimulation and CD3ζ signaling to activate T cells and mediate targeted cytotoxic killing of tumor cells. A truncated CD19 tag enables selection/tracking; cells are delivered locoregionally (intracavitary/intratumoral and intraventricular).
CLTX-based CAR on the T cells binds the MMP2-associated surface complex, triggering CD28/CD3zeta signaling and T-cell cytotoxicity via perforin/granzyme release (and Fas–FasL), killing the target cells.