A first-in-human, intravenous bispecific antibody–drug conjugate that co-engages TROP2 and EGFR on tumor cells to enable receptor-mediated internalization and targeted delivery of a cytotoxic payload; administered every 3 weeks for advanced solid tumors.
Bispecific antibody–drug conjugate that co-binds TROP2 and EGFR on tumor cells, undergoes receptor-mediated internalization, and releases the cytotoxic payload MMAE via a protease-cleavable linker; MMAE binds tubulin, inhibits microtubule polymerization, and induces G2/M arrest and apoptosis in TROP2/EGFR-expressing tumors.
YES
INDIRECT
DM001 binds TROP2/EGFR on tumor cells, is internalized, and releases MMAE; MMAE binds beta-tubulin, blocks microtubule polymerization, causing G2/M arrest and apoptosis in the targeted cells.
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
CAR-T cells bind PD-L1 via the CAR, activating T-cell cytotoxicity and killing PD-L1–expressing cells through perforin/granzyme-mediated apoptosis.