Investigational intravenous bispecific antibody immunotherapy (immune-cell engager) that binds Claudin-6 on tumor cells and an immune effector cell receptor to trigger immune-mediated killing of CLDN6-positive cancers.
ASP1893 is an investigational bispecific antibody that binds Claudin‑6 on tumor cells and a receptor on T cells (e.g., CD3), bringing T cells into close proximity to CLDN6‑positive tumor cells to trigger T‑cell activation and cytotoxic killing.
NO
INDIRECT
The bispecific binds CD3 on T cells to engage and activate them against CLDN6-positive tumor cells; activated T cells kill the CLDN6-expressing tumor cells (perforin/granzyme), not the CD3+ effector cells.
An anti-PSMA monoclonal antibody that binds prostate-specific membrane antigen (FOLH1) on prostate cancer cells; upon binding and internalization, it enables tumor-targeted uptake of the attached radionuclide for imaging and potential cytotoxicity.
NY108 is a PSMA (FOLH1)-targeted monoclonal antibody linked to lutetium-177. After binding PSMA on prostate cancer cells and being internalized, it delivers tumor-targeted beta radiation that can induce cytotoxic DNA damage, while its gamma emissions enable SPECT imaging of biodistribution.
YES
DIRECT
An anti-PSMA monoclonal antibody delivers lutetium-177 to PSMA-expressing cells; internalization concentrates beta radiation that induces DNA double-strand breaks leading to cell death (with some crossfire to nearby cells).
Patient-derived T cells genetically engineered to express a chimeric antigen receptor targeting CD19 on B-lineage cells; HLA-independent antigen binding triggers CD3ζ/co-stimulatory signaling to activate T cells, leading to proliferation, cytokine secretion, and perforin/granzyme-mediated killing of malignant B cells (with expected on-target B-cell aplasia).
Autologous T cells engineered to express a CD19-specific chimeric antigen receptor; HLA-independent binding to CD19 triggers CD3zeta and co-stimulatory signaling, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated lysis of CD19-positive malignant B cells, with expected on-target B-cell aplasia.
YES
DIRECT
CAR-T cells bind CD19 on target cells, triggering CD3zeta/co-stimulatory signaling and T-cell cytotoxicity (perforin/granzyme release and death-receptor pathways) that lyse CD19-positive cells.
A beta- and gamma-emitting radionuclide used as a radiopharmaceutical label; when conjugated to NY108, it enables SPECT imaging of biodistribution and delivers targeted beta radiation to PSMA-expressing tumor cells.
Lutetium-177, a beta- and gamma-emitting radionuclide, is chelated to the anti-PSMA monoclonal antibody NY108. After binding PSMA on tumor cells and being internalized, it delivers short-range beta radiation that induces DNA damage and tumor cell death, while gamma emissions enable SPECT imaging of biodistribution.
YES
DIRECT
An anti-PSMA antibody chelated to 177Lu binds PSMA and is internalized, delivering short-range beta radiation that induces DNA damage (e.g., double-strand breaks) and kills the PSMA-expressing cells.
Autologous peripheral blood mononuclear cells (primarily T cells) activated ex vivo with IL-2 and OKT3 and coated with OKT3 and elotuzumab to generate bispecific antibody–armed T cells targeting SLAMF7+ multiple myeloma.
Autologous PBMCs (primarily T cells) are activated ex vivo with IL-2/OKT3 and coated with OKT3 (anti‑CD3) plus elotuzumab (anti‑SLAMF7), creating bispecific antibody–armed T cells that bridge CD3 on T cells to SLAMF7 on myeloma cells, forming an immune synapse and redirecting T‑cell cytotoxicity against SLAMF7+ multiple myeloma.
YES
DIRECT
Bispecific antibody–armed autologous T cells are bridged to SLAMF7 on target cells via elotuzumab and to CD3 on T cells via OKT3, forming an immune synapse and inducing T‑cell cytotoxicity (perforin/granzyme-mediated lysis) of SLAMF7+ cells.