Autologous, gene-modified CD19-directed CAR T-cell therapy with metabolic armoring to enhance T-cell fitness and persistence; administered after lymphodepletion to treat CD19-positive B-cell malignancies.
Autologous gene‑modified T cells expressing a CD19‑targeted chimeric antigen receptor recognize CD19 on malignant B cells and, via CD3ζ/co‑stimulatory signaling, activate cytotoxic killing, proliferation, and cytokine release. Metabolic armoring enhances T‑cell metabolic fitness and persistence in the tumor microenvironment. Administered after lymphodepletion to promote CAR‑T expansion and engraftment.
CD19-directed CAR T cells bind CD19 on target B cells, activate via CD3ζ/co-stimulatory signaling, and kill through perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis), with cytokine release supporting cytotoxicity.
Bispecific T-cell–engaging monoclonal antibody (IgG, 2:1 format) targeting CD20 on B cells and CD3 on T cells to activate T cells and mediate cytotoxic killing of malignant B cells.
A 2:1 CD20×CD3 bispecific monoclonal antibody that simultaneously binds CD20 on B cells and CD3 on T cells, forming an immune synapse to activate TCR/CD3 signaling and redirect T-cell cytotoxicity (perforin/granzyme) to kill and deplete malignant CD20+ B cells.
Glofitamab bridges CD20 on B cells to CD3 on T cells, activating T cells to form an immune synapse and kill CD20+ cells via perforin/granzyme-mediated cytotoxicity.
Human IgG1 monoclonal antibody targeting PD-L1; immune checkpoint inhibitor that blocks PD-L1/PD-1 interaction to restore antitumor T-cell activity, with IgG1 Fc-mediated ADCC via NK cells.
Avelumab is a human IgG1 monoclonal antibody that binds PD-L1, blocking its interaction with PD-1 to relieve inhibitory checkpoint signaling and restore antitumor T-cell activity; its intact IgG1 Fc can also mediate antibody-dependent cellular cytotoxicity (ADCC) against PD-L1–expressing tumor cells.
Avelumab binds PD-L1 on target cells and, via its IgG1 Fc, engages Fcγ receptors on NK cells to trigger antibody-dependent cellular cytotoxicity (ADCC), killing PD-L1–expressing cells; it also blocks PD-1/PD-L1 to enhance T-cell killing (indirect).
Anti-CD79b antibody-drug conjugate delivering MMAE to B cells; microtubule toxin–mediated cytotoxicity.
Anti-CD79b antibody-drug conjugate that binds CD79b on B cells, is internalized, and releases the microtubule toxin MMAE via a protease-cleavable linker; MMAE inhibits tubulin polymerization, leading to G2/M arrest and apoptosis of malignant B cells.
ADC binds CD79B, is internalized, and releases MMAE; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of the target cell.
Anti-CD20 monoclonal antibody causing B-cell depletion via ADCC and complement activation.
Unconjugated anti-CD20 monoclonal antibody that binds CD20 on B cells and mediates cell depletion/killing via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct apoptosis, eliminating CD20-positive malignant and normal B cells.
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC by NK/macrophages, activates complement (CDC), and can directly induce apoptosis via CD20 signaling.