An antibody–drug conjugate (iza-bren; izalontamab brengitecan; BMS-986507) administered IV every 3 weeks. The monoclonal antibody targets a tumor-associated cell-surface antigen on glioblastoma cells, is internalized, and releases a brengitecan topoisomerase I inhibitor payload causing DNA damage and apoptosis; Fc-mediated effector functions may also contribute.
Dual-targeting anti-EGFR/anti-HER3 antibody–drug conjugate that binds EGFR/HER3 on tumor cells, is internalized, and releases a brengitecan topoisomerase I inhibitor payload to cause DNA damage and apoptosis; Fc-mediated effector functions (e.g., ADCC/CDC) may also contribute.
NO
INDIRECT
BL-B01D1 binds EGFR/HER3 on tumor cells, is internalized, and releases a topoisomerase I–inhibiting payload that causes DNA damage and apoptosis. Topoisomerase I is not the binding target; it is the intracellular enzyme inhibited after delivery.
A CD123-directed antibody-drug conjugate administered intravenously weekly or twice weekly in dose escalation. An anti-CD123 monoclonal antibody binds IL-3 receptor alpha (CD123) on malignant cells, is internalized, and releases a potent cytotoxic payload via linker cleavage to induce targeted death of CD123+ cells in relapsed/refractory AML, B-ALL, and high-risk MDS.
Anti-CD123 monoclonal antibody binds IL-3 receptor alpha (CD123) on malignant cells, is internalized, and a legumain-cleavable linker releases a kinesin spindle protein (Eg5/KSP) inhibitor payload inside the cell, inhibiting mitotic spindle assembly and causing mitotic arrest and targeted death of CD123+ tumor cells.
YES
DIRECT
An anti-CD123 antibody-drug conjugate binds CD123, is internalized, and in lysosomes a legumain-cleavable linker releases a KSP (Eg5) inhibitor that blocks mitotic spindle assembly, causing mitotic arrest and death of CD123+ cells.
A CD123-directed antibody-drug conjugate administered intravenously weekly or twice weekly in dose escalation. An anti-CD123 monoclonal antibody binds IL-3 receptor alpha (CD123) on malignant cells, is internalized, and releases a potent cytotoxic payload via linker cleavage to induce targeted death of CD123+ cells in relapsed/refractory AML, B-ALL, and high-risk MDS.
Anti-CD123 monoclonal antibody binds IL-3 receptor alpha (CD123) on malignant cells, is internalized, and a legumain-cleavable linker releases a kinesin spindle protein (Eg5/KSP) inhibitor payload inside the cell, inhibiting mitotic spindle assembly and causing mitotic arrest and targeted death of CD123+ tumor cells.
NO
INDIRECT
VIP943 binds CD123, is internalized, and releases a KSP (Eg5) inhibitor that induces mitotic arrest and death in CD123+ cells. KSP expression alone is not targeted by the drug; only CD123-mediated uptake leads to cytotoxicity.
Anti-CD30 monoclonal antibody linked via a cleavable valine-citrulline linker to monomethyl auristatin E (MMAE). After binding CD30 and internalization by CD30-positive cells, the linker is proteolytically cleaved to release MMAE, which binds tubulin, blocks microtubule polymerization, causes G2/M arrest, and induces apoptosis.
YES
DIRECT
The ADC binds CD30, is internalized, then releases MMAE intracellularly; MMAE disrupts tubulin polymerization, causing G2/M arrest and apoptosis of CD30+ cells.
Autologous cellular immunotherapy using ex vivo–generated dendritic cells pulsed with patient-specific tumor neoantigen peptides to prime/expand neoantigen-specific CD8+ and CD4+ T cells.
Autologous dendritic cells are generated ex vivo and pulsed with patient-specific tumor neoantigen peptides. After infusion, the DCs migrate to lymphoid tissues and present these neoantigens on HLA class I and II, providing costimulation (e.g., CD80/CD86) and cytokines to prime and expand neoantigen-specific CD8+ cytotoxic T cells and CD4+ helper T cells, thereby promoting tumor-specific immune responses and immunologic memory.
NO
INDIRECT
Neoantigen-pulsed dendritic cells present peptides on HLA class I to prime neoantigen-specific CD8+ T cells; the resulting CTLs kill tumor cells presenting the same peptide–HLA complexes via perforin/granzyme or Fas–FasL, not the dendritic cells expressing HLA I.