Chimeric anti-CD20 monoclonal antibody (1 g IV on days 0 and 14, with optional retreatment at week 24) that depletes mature B cells via ADCC, complement-dependent cytotoxicity, and apoptosis, generally sparing long-lived plasma cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on mature B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, generally sparing long-lived plasma cells.
Anti-CD20 antibody binds CD20 on B cells and triggers killing via Fc-mediated ADCC (NK/macrophages), complement-dependent cytotoxicity, and CD20 ligation–induced apoptosis.
Off-the-shelf (allogeneic) CD7-directed chimeric antigen receptor T-cell (CAR-T) therapy; single intravenous dose of 2 x 10^8 CAR+ T cells engineered to express a CD7-binding CAR with CD3zeta/co-stimulatory signaling domains, inducing cytotoxic killing of CD7+ malignant T cells in relapsed/refractory T-ALL/LBL.
Off-the-shelf (allogeneic) T cells engineered to express a CD7-binding chimeric antigen receptor with CD3zeta and costimulatory signaling domains. Upon binding CD7 on malignant T cells, the CAR triggers T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxicity, leading to selective killing of CD7-positive leukemic/lymphoblastic cells.
CD7-directed CAR-T cells bind CD7 on target cells, become activated, and kill via perforin/granzyme-mediated cytotoxicity (and related T cell effector mechanisms).
Patient-derived T cells primed and expanded ex vivo against individualized tumor neoantigens using autologous antigen-presenting cells, then infused intravenously to mediate TCR-dependent cytotoxicity against neoantigen-expressing cancer cells.
Autologous T cells are primed and expanded ex vivo against patient-specific tumor neoantigens and, after infusion, use their endogenous TCRs to recognize neoantigen peptides presented by MHC on tumor cells, inducing cytotoxic killing via perforin/granzyme and antitumor cytokine release.
Neoantigen-specific TCRs recognize the patient-specific peptide–HLA class I complex on tumor cells, triggering cytotoxic T lymphocyte killing via perforin/granzyme (and Fas–FasL)–mediated apoptosis.
Patient-derived T cells primed and expanded ex vivo against individualized tumor neoantigens using autologous antigen-presenting cells, then infused intravenously to mediate TCR-dependent cytotoxicity against neoantigen-expressing cancer cells.
Autologous T cells are primed and expanded ex vivo against patient-specific tumor neoantigens and, after infusion, use their endogenous TCRs to recognize neoantigen peptides presented by MHC on tumor cells, inducing cytotoxic killing via perforin/granzyme and antitumor cytokine release.
Infused neoantigen-specific T cells use endogenous TCRs to recognize the neoantigen–HLA class II complex on target cells and kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL), inducing apoptosis.
Type II, glycoengineered anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC and direct cell death to suppress pathogenic humoral immunity.
Type II, glycoengineered anti-CD20 IgG1 that binds CD20 on B cells and, via enhanced FcγRIIIa engagement, induces potent antibody-dependent cellular cytotoxicity and direct (caspase-independent) cell death, depleting CD20+ B cells to suppress pathogenic humoral immunity.
Obinutuzumab binds CD20 on B cells; its Fc engages FcγRIIIa to trigger NK cell–mediated ADCC (and phagocytosis) and also induces direct, caspase-independent cell death; some complement-mediated lysis may occur.