Anti-CD20 monoclonal antibody that mediates ADCC, complement activation, and apoptosis of CD20-positive B cells.
Anti-CD20 monoclonal antibody that binds CD20 on B cells and induces their depletion via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Rituximab binds CD20 on B cells and triggers killing via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity (C1q activation), and direct apoptosis upon CD20 crosslinking.
Anti-HER2 antibody–drug conjugate (RC48) that binds HER2, is internalized, and releases the microtubule-disrupting payload MMAE; can also induce ADCC.
Anti-HER2 IgG1 antibody–drug conjugate that binds HER2, is internalized, and releases the cytotoxic payload monomethyl auristatin E (MMAE) to inhibit tubulin polymerization, leading to microtubule disruption, G2/M arrest, and apoptosis; the IgG1 Fc can also induce ADCC.
The HER2-binding ADC is internalized and releases MMAE, which inhibits tubulin polymerization leading to microtubule disruption, G2/M arrest, and apoptosis; IgG1 Fc can also mediate ADCC against HER2+ cells.
Autologous, gene-modified CAR T-cell therapy; patient T cells engineered to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD22) to induce targeted cytotoxicity.
Autologous T cells are gene-modified to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD22). Antigen binding activates the CAR signaling domains, driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells.
CAR T cells recognize CD19 on target cells, activate, and kill via perforin/granzyme-mediated cytolysis leading to apoptosis.
Autologous, gene-modified CAR T-cell therapy; patient T cells engineered to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD22) to induce targeted cytotoxicity.
Autologous T cells are gene-modified to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD22). Antigen binding activates the CAR signaling domains, driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells.
CAR T cells bind CD22 on target cells; CAR signaling activates T-cell cytotoxicity, leading to perforin/granzyme-mediated lysis and apoptosis of CD22+ cells.
Autologous, gene-modified CAR T-cell therapy; patient T cells engineered to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD20) to induce targeted cytotoxicity.
Autologous T cells are gene-modified to express a chimeric antigen receptor recognizing B-lineage antigens (e.g., CD19/CD20). Upon antigen binding, CAR signaling (CD3ζ with costimulatory domains) activates the T cells independently of MHC, inducing proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells.
CAR T cells recognize CD19 via the CAR and directly lyse target cells through perforin/granzyme-mediated cytotoxicity (and death-receptor signaling).