Gene-modified autologous T cells engineered to express a chimeric antigen receptor that recognizes VEGFR1 and PD-L1; upon antigen engagement, the CAR T cells exert cytotoxic activity against VEGFR1+ and/or PD-L1+ cells, aiming to disrupt VEGF/VEGFR1-driven angiogenesis and overcome PD-L1–mediated immune suppression. Administered regionally into the pleural or peritoneal cavity.
Autologous T cells genetically engineered to express a chimeric antigen receptor recognizing VEGFR1 and PD-L1. Binding to either antigen triggers T‑cell activation, cytotoxicity, and cytokine release to kill VEGFR1+ vascular/endothelial cells and PD‑L1+ tumor and immunosuppressive stromal/immune cells, disrupting VEGF/VEGFR1‑driven angiogenesis and overcoming PD‑L1–mediated immune evasion. Administered regionally into the pleural or peritoneal cavity.
YES
DIRECT
CAR-T cells bind PD-L1 and are activated to kill PD-L1+ cells via perforin/granzyme-mediated cytolysis and apoptotic death ligand pathways, with cytokine release.
Donor-derived T lymphocytes engineered by CRISPR genome editing to disrupt the endogenous T-cell receptor (and potentially other loci) and to express a tumor antigen–specific chimeric antigen receptor; intended for off-the-shelf use to reduce graft-versus-host risk and mediate cytotoxic killing of antigen-expressing malignant cells via CAR signaling and T-cell effector pathways.
Donor-derived T lymphocytes are CRISPR-edited to disrupt the endogenous T-cell receptor (and potentially other loci) and engineered to express a tumor antigen–specific chimeric antigen receptor. The CAR redirects T cells to bind the target antigen and activate via CD3ζ/costimulatory signaling, leading to cytotoxic killing of antigen-expressing malignant cells through perforin/granzyme release and cytokine-mediated effects. TCR knockout enables off-the-shelf use and reduces graft-versus-host disease risk.
NO
INDIRECT
Not applicable for this target; CAR T cells kill only cells expressing the CAR-recognized antigen via T-cell cytotoxicity (perforin/granzyme and cytokine-mediated killing).
Recombinant humanized monoclonal antibody targeting Claudin 18.2 (CLDN18.2); promotes antitumor activity via direct tumor cell targeting and immune effector mechanisms such as ADCC and CDC.
Humanized monoclonal antibody targeting Claudin 18.2 on tumor cells; induces immune-mediated tumor cell killing via antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) after binding to CLDN18.2-expressing cells.
YES
DIRECT
Binds CLDN18.2 on tumor cells and recruits immune effector functions—Fc-mediated ADCC (e.g., NK cells) and complement-dependent cytotoxicity (CDC)—to lyse target-expressing cells.
Fully human bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and signaling, induces receptor internalization/degradation, and mediates Fc-dependent ADCC/ADCP.
Fully human bispecific IgG1 that binds EGFR and MET to block ligand binding and receptor phosphorylation, promotes receptor internalization/degradation, suppresses downstream RAS/MAPK and PI3K/AKT signaling, and mediates Fc-dependent ADCC/ADCP against tumor cells.
YES
DIRECT
Amivantamab binds MET on tumor cells and engages Fc receptors on immune effectors to mediate Fc-dependent ADCC and ADCP, leading to killing of MET-expressing cells.
Glycoengineered type II anti-CD20 monoclonal antibody that depletes B cells via direct cell death and antibody-dependent cytotoxicity/phagocytosis (ADCC/ADCP).
Glycoengineered type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them through enhanced Fc gamma receptor III (FcγRIII)-mediated ADCC/ADCP and direct, caspase-independent cell death.
YES
DIRECT
Binds CD20 on B cells, inducing direct caspase-independent cell death and recruiting FcγRIII+ effector cells (NK cells/macrophages) to mediate ADCC/ADCP, depleting CD20+ cells.