Autologous, genetically engineered chimeric antigen receptor T-cell therapy targeting HLA-G; administered as a single intravenous infusion to redirect patient T cells to recognize and kill HLA-G–expressing tumor cells and overcome HLA-G–mediated immune evasion.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes HLA-G on tumor cells. CAR engagement activates T-cell cytotoxicity, cytokine release, and proliferation, enabling targeted killing of HLA-G–expressing tumors and overcoming HLA-G–mediated immune evasion.
YES
DIRECT
Anti–HLA-G CAR-T cells bind HLA-G on target cells and induce T-cell–mediated killing via perforin/granzyme release and Fas–FasL apoptosis.
An anti-mesothelin antibody–drug conjugate (ADC) that binds mesothelin on tumor cells; after internalization it releases a tubulysin cytotoxic payload to disrupt microtubules and induce cell death. Dosed 1.5–2.5 mg/kg IV every 3 weeks.
Mesothelin-targeted antibody–drug conjugate; after binding mesothelin on tumor cells and internalization, a cleavable linker releases a tubulysin microtubule-disrupting payload, causing microtubule depolymerization, G2/M arrest, and apoptosis in mesothelin-expressing cells.
YES
DIRECT
The ADC binds mesothelin on target cells, is internalized, and a cleavable linker releases a tubulysin microtubule-disrupting payload, causing microtubule depolymerization, G2/M arrest, and apoptosis.
An anti-mesothelin antibody–drug conjugate (ADC) that binds mesothelin on tumor cells; after internalization it releases a tubulysin cytotoxic payload to disrupt microtubules and induce cell death. Dosed 1.5–2.5 mg/kg IV every 3 weeks.
Mesothelin-targeted antibody–drug conjugate; after binding mesothelin on tumor cells and internalization, a cleavable linker releases a tubulysin microtubule-disrupting payload, causing microtubule depolymerization, G2/M arrest, and apoptosis in mesothelin-expressing cells.
NO
INDIRECT
RC88 targets mesothelin on tumor cells, is internalized, and releases a tubulysin payload that binds beta‑tubulin to disrupt microtubules, causing G2/M arrest and apoptosis. Beta‑tubulin expression alone does not direct targeting or killing.
Intravenous anti-MICA/MICB monoclonal antibody designed to maintain/restore MICA/B on the tumor surface and opsonize tumor cells, enhancing NKG2D-driven cytotoxicity and Fcγ receptor–mediated ADCC/ADCP by NK cells and macrophages.
Anti-MICA/MICB monoclonal antibody that maintains/restores MICA/B on tumor cells and opsonizes them, enhancing NKG2D-mediated recognition and Fcγ receptor–dependent ADCC/ADCP by NK cells and macrophages to promote tumor cell killing.
YES
DIRECT
The anti-MICA antibody binds MICA on tumor cells and opsonizes them; its Fc engages Fc gamma receptors on NK cells and macrophages to trigger ADCC/ADCP, and maintaining surface MICA enhances NKG2D-mediated killing.
Intravenous anti-MICA/MICB monoclonal antibody designed to maintain/restore MICA/B on the tumor surface and opsonize tumor cells, enhancing NKG2D-driven cytotoxicity and Fcγ receptor–mediated ADCC/ADCP by NK cells and macrophages.
Anti-MICA/MICB monoclonal antibody that maintains/restores MICA/B on tumor cells and opsonizes them, enhancing NKG2D-mediated recognition and Fcγ receptor–dependent ADCC/ADCP by NK cells and macrophages to promote tumor cell killing.
YES
DIRECT
The anti-MICB antibody opsonizes MICB+ tumor cells and directly engages Fcγ receptors on NK cells and macrophages to trigger ADCC/ADCP, while maintaining MICB enhances NKG2D-mediated cytotoxicity.