Off-the-shelf, gene-modified T cells from umbilical cord blood expressing chimeric antigen receptors against BCMA (TNFRSF17) and CD19; administered as a single IV infusion to induce T-cell mediated cytotoxicity against malignant plasma and B-lineage cells.
Off‑the‑shelf, umbilical cord blood–derived T cells engineered to express chimeric antigen receptors against BCMA and CD19. Upon binding either antigen on malignant plasma and B‑lineage cells, the CARs trigger T‑cell activation and perforin/granzyme‑mediated cytotoxicity independent of the native TCR, with dual targeting intended to reduce antigen escape.
BCMA-binding CAR on the T cells triggers activation and cytolytic killing of BCMA+ cells via perforin/granzyme release (and death receptor pathways).
Off-the-shelf, gene-modified T cells from umbilical cord blood expressing chimeric antigen receptors against BCMA (TNFRSF17) and CD19; administered as a single IV infusion to induce T-cell mediated cytotoxicity against malignant plasma and B-lineage cells.
Off‑the‑shelf, umbilical cord blood–derived T cells engineered to express chimeric antigen receptors against BCMA and CD19. Upon binding either antigen on malignant plasma and B‑lineage cells, the CARs trigger T‑cell activation and perforin/granzyme‑mediated cytotoxicity independent of the native TCR, with dual targeting intended to reduce antigen escape.
CAR-T cells bind CD19 on target cells, triggering T-cell activation and perforin/granzyme-mediated killing (apoptosis/lysis).
Autologous, gene-modified T cells expressing a mesothelin-specific CAR and engineered to secrete PD-1 nanobodies to enhance antitumor activity by CAR-mediated cytotoxicity and local PD-1/PD-L1 blockade.
Autologous T cells engineered to express a mesothelin-specific CAR mediate targeted tumor cell killing; the cells also secrete PD-1 nanobodies that locally block the PD-1/PD-L1 checkpoint to enhance CAR T activation, persistence, and antitumor efficacy in mesothelin-positive tumors.
Mesothelin-specific CAR T cells bind mesothelin on target cells and kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated apoptosis and Fas–FasL); PD-1 nanobody secretion enhances this activity.
A glycoengineered type II anti-CD20 IgG1 monoclonal antibody used as pre-treatment to debulk B cells and mitigate cytokine release syndrome; induces direct cell death and antibody-dependent cellular cytotoxicity (ADCC) of CD20+ B cells.
Obinutuzumab is a glycoengineered, humanized type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells; its afucosylated Fc increases affinity for Fc gamma RIII receptors to enhance antibody-dependent cellular cytotoxicity and it induces direct cell death, resulting in depletion of CD20+ B cells (used to debulk B cells and mitigate cytokine release syndrome risk).
Binds CD20 on B cells and kills via Fc-mediated ADCC (enhanced FcγRIIIa engagement; also ADCP) and type II antibody–induced direct cell death/caspase-independent apoptosis of CD20+ cells.
An anti-CD20 × anti-CD3 T-cell–redirecting bispecific monoclonal antibody that engages CD3+ T cells and CD20+ B cells to induce cytotoxicity in malignant B cells.
Bispecific anti-CD20×anti-CD3 antibody that simultaneously binds CD20 on B cells and CD3 on T cells, crosslinking them to form an immune synapse and activate T cells to kill CD20+ malignant B cells via redirected cytotoxicity (perforin/granzyme and cytokine-mediated effects).
Odronextamab crosslinks CD3 on T cells to CD20 on target B cells, forming an immune synapse that triggers T-cell–mediated killing via perforin/granzyme release and cytokine-dependent cytotoxicity of CD20+ cells.