An intravenous antibody-drug conjugate targeting CDH3 (P-cadherin) that uses a cathepsin-cleavable Val-Cit linker to release the microtubule-disrupting payload MMAE, causing G2/M arrest and apoptosis with potential bystander effect.
Monoclonal antibody targets CDH3 (P‑cadherin) on tumor cells and is internalized; a cathepsin-cleavable Val‑Cit linker releases the MMAE payload, which inhibits tubulin polymerization, leading to G2/M mitotic arrest and apoptosis, with potential membrane-permeable bystander effect.
The ADC binds CDH3 on tumor cells, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis (with possible bystander killing).
Allogeneic anti-CD19 chimeric antigen receptor natural killer (CAR-NK) cell therapy designed to deplete CD19+ B-lineage cells in SLE.
Allogeneic NK cells engineered to express an anti-CD19 chimeric antigen receptor recognize CD19 on B-lineage cells and eliminate them via NK cytotoxic mechanisms (perforin/granzyme and death receptor signaling), depleting autoreactive B cells and plasmablasts to reduce autoantibody production in SLE.
Anti-CD19 CAR-NK cells bind CD19 on target cells and induce cytotoxicity via degranulation (perforin/granzyme) and death-receptor signaling, causing apoptosis of CD19+ cells.
Autologous, fully human anti-BCMA chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are engineered to express a CAR that binds BCMA; antigen engagement triggers CAR signaling leading to T-cell expansion, cytokine release, and perforin/granzyme-mediated cytotoxicity against BCMA-positive malignant plasma cells.
Autologous T cells are genetically engineered to express a fully human anti-BCMA chimeric antigen receptor. Upon binding BCMA on malignant plasma cells, CAR signaling activates and expands the T cells, inducing cytokine release and perforin/granzyme-mediated cytotoxicity to eliminate BCMA-positive multiple myeloma cells.
CAR T cells recognize BCMA on target cells and induce cytotoxicity via perforin/granzyme-mediated lysis and apoptosis, with cytokine-driven T-cell activation/expansion.
An investigational intravenous anticancer agent; the registry does not specify its drug class or precise mechanism of action.
An anti–nectin-4 (PVRL4) IgG1 antibody–drug conjugate. The antibody binds nectin-4 on tumor cells and is internalized; a cleavable linker then releases a topoisomerase-1 inhibitor payload that blocks Topo I–mediated DNA replication, leading to cell-cycle arrest and apoptosis in nectin-4–expressing cancer cells.
The anti–nectin-4 antibody-drug conjugate binds Nectin-4 on target cells, is internalized, and a cleavable linker releases a topoisomerase-1 inhibitor that blocks DNA replication, leading to cell-cycle arrest and apoptosis of Nectin-4–expressing cells.