Fc-engineered anti-CD19 monoclonal antibody that induces ADCC and ADCP leading to B-cell depletion.
Fc-engineered humanized anti-CD19 monoclonal antibody that binds CD19 on B cells and enhances Fc-gamma receptor engagement to induce ADCC and ADCP, resulting in depletion of CD19-positive B cells.
Binds CD19 on B cells and engages Fcγ receptors on immune effectors to trigger ADCC (NK cells) and ADCP (macrophages), leading to depletion of CD19+ cells.
PSMA-targeted radioimmunotherapy: a humanized anti-PSMA monoclonal antibody (rosopatamab) chelated via tetraxetan (DOTA) to beta-emitting lutetium-177 to deliver targeted radiation to PSMA-expressing prostate cancer cells, causing DNA double-strand breaks and cell death.
Humanized anti-PSMA monoclonal antibody (rosopatamab) chelated via tetraxetan (DOTA) to beta-emitting lutetium-177 binds PSMA on prostate cancer cells and delivers targeted ionizing radiation, inducing DNA double-strand breaks and tumor cell death.
Anti-PSMA antibody (rosopatamab) labeled with lutetium-177 binds PSMA on tumor cells and emits beta radiation at the cell surface, causing DNA double-strand breaks and lethal damage (apoptosis/mitotic catastrophe).
Autologous, gene-engineered T-cell therapy expressing chimeric antigen receptors that target CLDN18.2 and PD-L1 to enable antigen-specific tumor cell killing and counteract PD-1/PD-L1–mediated immunosuppression.
Autologous T cells engineered to express CARs that recognize CLDN18.2 and PD-L1 on tumor and stromal cells, inducing antigen-dependent T-cell activation and cytolytic killing; PD-L1 targeting also counters PD-1/PD-L1-mediated immunosuppression and may reduce antigen escape.
CAR-T cells bind CLDN18.2 on target cells, triggering T‑cell activation and cytolytic killing via perforin/granzyme release and/or Fas–FasL–mediated apoptosis.
Autologous, gene-engineered T-cell therapy expressing chimeric antigen receptors that target CLDN18.2 and PD-L1 to enable antigen-specific tumor cell killing and counteract PD-1/PD-L1–mediated immunosuppression.
Autologous T cells engineered to express CARs that recognize CLDN18.2 and PD-L1 on tumor and stromal cells, inducing antigen-dependent T-cell activation and cytolytic killing; PD-L1 targeting also counters PD-1/PD-L1-mediated immunosuppression and may reduce antigen escape.
CAR-T cells bind PD-L1 via the CAR, activating T-cell cytotoxicity and killing PD-L1–expressing cells through perforin/granzyme-mediated apoptosis.
Autologous, genetically engineered anti-CD19 CAR T-cell therapy with a 4-1BB costimulatory domain that targets CD19+ B cells to induce cytotoxic killing; may cause on-target B-cell aplasia.
Autologous T cells are genetically engineered to express an anti-CD19 chimeric antigen receptor with a CD3-zeta signaling domain and 4-1BB costimulatory domain. After infusion, the CAR T cells recognize CD19 on malignant and normal B cells in an HLA-independent manner, activate and proliferate, and induce cytotoxic killing, often leading to on-target B-cell aplasia.
Anti-CD19 CAR T cells recognize CD19 on target cells, become activated via CD3-zeta and 4-1BB costimulation, and kill through T-cell cytotoxic mechanisms (perforin/granzyme release and death-receptor signaling).