Autologous, genetically engineered T cells expressing a CD7-specific chimeric antigen receptor to recognize and eliminate CD7-positive malignant T cells.
Autologous T cells are genetically engineered to express a CD7-specific chimeric antigen receptor; upon binding CD7 on malignant T cells, CAR signaling activates the T cells to proliferate, release cytotoxic mediators, and lyse CD7-positive tumor cells independently of the native TCR.
CAR-T cells bind CD7 on target cells, become activated, and kill via perforin/granzyme release and death-receptor pathways, lysing CD7-positive cells.
Antibody-drug conjugate targeting MET (c-Met/HGFR); after internalization it releases a topoisomerase I inhibitor payload that causes DNA damage and tumor cell death.
Monoclonal antibody–drug conjugate targeting MET (c-Met/HGFR); after binding and internalization, it releases a topoisomerase I inhibitor payload that inhibits DNA replication, causing DNA damage and death of MET-expressing tumor cells.
The ADC binds MET on target cells, is internalized, and releases a topoisomerase I inhibitor payload that blocks DNA replication and causes DNA damage, leading to cell death.
An anti-CD38 human IgG1 monoclonal antibody given intravenously (16 mg/kg weekly for 8 weeks) to deplete CD38-expressing plasma cells via ADCC, CDC, ADCP and apoptosis, thereby reducing pathogenic autoantibodies driving Evans syndrome.
Anti-CD38 human IgG1 monoclonal antibody that binds CD38 on plasma cells and other CD38+ immune cells and mediates Fc-dependent cytotoxicity (ADCC, CDC, ADCP) and apoptosis, depleting CD38-expressing cells and reducing pathogenic autoantibodies.
Daratumumab binds CD38 on target cells and triggers immune effector killing via ADCC (NK cells), CDC (complement), ADCP (macrophages), and can induce apoptosis upon crosslinking.
An anti-GD2 antibody–drug conjugate (ADC) that binds the GD2 ganglioside on tumor cells, is internalized, and releases an exatecan-based topoisomerase I inhibitor payload, leading to TOP1 inhibition, DNA damage, replication stress, and tumor cell death. Evaluated in GD2-positive soft tissue sarcomas and IDH-wildtype glioblastoma to establish MTD/RP2D, safety, and preliminary activity.
Anti-GD2 monoclonal antibody–drug conjugate that binds the GD2 ganglioside on tumor cells, is internalized, and releases an exatecan-based topoisomerase I inhibitor payload, leading to TOP1 inhibition, DNA damage/replication stress, and tumor cell death.
ADC binds GD2 on tumor cells, is internalized, and releases an exatecan-based topoisomerase I inhibitor, causing DNA damage/replication stress and apoptosis.
Allogeneic, cord blood–derived CAR natural killer (NK) cell therapy engineered to express two CARs targeting CD19 and CD70; administered IV to induce MHC-independent NK cytotoxicity against B-cell malignancies and reduce antigen escape.
Allogeneic cord blood-derived NK cells engineered to express two chimeric antigen receptors targeting CD19 and CD70. Binding to either antigen activates NK cell signaling and MHC-independent cytotoxicity (perforin/granzyme-mediated lysis and cytokine release) against malignant B cells, with dual targeting designed to reduce antigen escape.
CAR-engineered NK cells bind CD19 on target cells, triggering NK activation and MHC-independent killing via perforin/granzyme-mediated cytolysis (with supportive cytokine/death-receptor pathways).