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.
The ADC binds EGFR on tumor cells, is internalized, and releases a brengitecan topoisomerase I inhibitor that induces DNA damage and apoptosis; Fc-mediated ADCC/CDC may also contribute.
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.
The ADC binds HER3 on tumor cells, is internalized, and releases a brengitecan topoisomerase I inhibitor payload that causes DNA damage and apoptosis; Fc-mediated ADCC/CDC may also contribute.
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.
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.
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.
The ADC binds CD30, is internalized, then releases MMAE intracellularly; MMAE disrupts tubulin polymerization, causing G2/M arrest and apoptosis of CD30+ cells.
Autologous, genetically modified CAR T-cell therapy targeting GPRC5D. Patient T cells are engineered to express an anti-GPRC5D chimeric antigen receptor with CD3ζ and co-stimulatory signaling domains; CAR engagement activates T cells, inducing proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of GPRC5D-expressing malignant plasma cells.
Autologous T cells are genetically engineered to express an anti-GPRC5D chimeric antigen receptor with CD3ζ and co-stimulatory domains. Upon binding GPRC5D on malignant plasma cells, the CAR activates T-cell signaling, leading to expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of target cells.
CAR T cells bind GPRC5D on target cells, form an immunologic synapse, and kill via perforin/granzyme-mediated apoptosis (with T-cell activation and cytokine release).