Nectin-4-targeted antibody-drug conjugate (ASG-22CE) that delivers the microtubule-disrupting agent MMAE to tumor cells, causing apoptosis.
Nectin-4–targeted monoclonal antibody linked via a cleavable linker to the microtubule inhibitor MMAE; binding to Nectin-4 on tumor cells triggers internalization and linker cleavage, releasing MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in Nectin-4–expressing cancer cells.
YES
DIRECT
ADC binds Nectin-4 on the cell surface, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization causing G2/M arrest and apoptosis of the Nectin-4–expressing cell.
Nectin-4-targeted antibody-drug conjugate (ASG-22CE) that delivers the microtubule-disrupting agent MMAE to tumor cells, causing apoptosis.
Nectin-4–targeted monoclonal antibody linked via a cleavable linker to the microtubule inhibitor MMAE; binding to Nectin-4 on tumor cells triggers internalization and linker cleavage, releasing MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in Nectin-4–expressing cancer cells.
NO
INDIRECT
The ADC binds Nectin-4 on tumor cells, is internalized, and releases MMAE, which binds beta-tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis. Killing is directed by Nectin-4 expression, not by beta-tubulin expression itself.
Investigational biologic, likely a monoclonal antibody; the specific target and mechanism are not specified in the trial record.
Enoblituzumab (TJ271) is a humanized, Fc-optimized IgG1 monoclonal antibody targeting B7-H3 (CD276) on tumor cells and tumor vasculature. By blocking B7-H3-mediated inhibitory signaling and engaging Fc gamma receptor-expressing effector cells, it induces antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis to kill tumor cells.
YES
DIRECT
IgG1 antibody binds B7-H3 on tumor cells and engages FcγR-expressing effector cells (e.g., NK cells, macrophages) to induce ADCC and antibody-dependent cellular phagocytosis, killing target-expressing cells.
Lentiviral CAR T cells specific for CLL-1 (CLEC12A); IV infusion with dose escalation; intended to eliminate CLL-1+ myeloid leukemia stem cells and myeloid blasts via MHC-independent mechanisms.
Genetically engineered T cells (via lentiviral transduction) expressing a CAR that recognizes CLL‑1/CLEC12A on myeloid leukemia stem cells and blasts. Antigen binding activates T cells independent of MHC, inducing cytotoxicity (perforin/granzyme) and cytokine release to eliminate CLL‑1–positive malignant cells.
YES
DIRECT
CLL-1 (CLEC12A)-targeted CAR T cells bind CLEC12A on target cells and induce MHC-independent T-cell cytolysis via perforin/granzyme (and apoptotic pathways).
Chimeric anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, reducing auto/alloantibody production and germinal center activity.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, reducing auto/alloantibody production and germinal center activity.
YES
DIRECT
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC/ADCP), with possible direct apoptosis, depleting CD20+ cells.