Anti-CD38 monoclonal antibody mediating ADCC, CDC, and apoptosis of CD38+ plasma cells.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on plasma cells and other immune cells, inducing tumor cell death via ADCC, ADCP, CDC, and direct apoptosis; also depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs), enhancing antitumor immunity.
Daratumumab binds CD38 on target cells and induces NK-cell ADCC, macrophage ADCP, complement-mediated CDC, and can trigger direct apoptosis, depleting CD38+ cells.
Bispecific TCR/CD3 ImmTAC that targets gp100/HLA-A*02:01 and engages CD3 to redirect T cells to gp100-positive melanoma cells.
ImmTAC consisting of a high‑affinity TCR specific for the gp100 peptide presented by HLA‑A*02:01 fused to an anti‑CD3 scFv; binds gp100/HLA‑A*02:01 on melanoma cells and CD3 on T cells to redirect and activate polyclonal T cells, leading to CTL-mediated killing of gp100‑positive tumor cells.
Tebentafusp binds gp100 peptide presented by HLA-A*02:01 on target cells and CD3 on T cells, recruiting and activating T cells to kill the bound cells via perforin/granzyme-mediated cytotoxicity (apoptosis).
Autologous genetically engineered T cells expressing a chimeric antigen receptor targeting CD19 to deplete CD19-positive B-lineage cells and reset autoreactive B-cell pools in autoimmune disease.
Autologous T cells are engineered to express a chimeric antigen receptor targeting CD19, enabling MHC-independent recognition and cytotoxic killing of CD19-positive B-lineage cells (naive and memory B cells, plasmablasts). Through T-cell activation and effector mechanisms (perforin/granzyme and cytokines), the therapy depletes B cells, reduces autoantibody production, and helps reset autoreactive B-cell pools in autoimmune disease.
CAR-T cells recognize CD19 via the CAR and kill target cells through T-cell effector mechanisms (perforin/granzyme-mediated cytolysis and apoptosis, ± death-receptor pathways).
Anti-CD123 antibody-drug conjugate (ADC) that binds IL-3Rα (CD123) on leukemic blasts and delivers an internalized DNA-alkylating cytotoxic payload.
Humanized anti‑CD123 (IL‑3Rα) IgG1 antibody–drug conjugate that binds CD123 on leukemic cells, is internalized, and via a cleavable linker releases an indolino‑benzodiazepine dimer DNA‑alkylating payload. The payload alkylates DNA (via an imine moiety), causing S‑phase arrest and apoptosis in CD123‑overexpressing cells.
The anti-CD123 ADC binds IL3RA on target cells, is internalized, and releases a DNA-alkylating indolino-benzodiazepine payload via a cleavable linker, leading to DNA damage, S-phase arrest, and apoptosis of CD123-expressing cells.
Autologous, genetically engineered T cells expressing a chimeric antigen receptor targeting MUC16 to recognize and kill MUC16-positive tumor cells.
Autologous T cells engineered to express a chimeric antigen receptor that binds MUC16 on tumor cells; CAR signaling activates the T cells to proliferate, release cytotoxic mediators, and lyse MUC16-positive cancer cells.
Anti-MUC16 CAR T cells recognize MUC16 on target cells, activate, and directly lyse them via T-cell cytotoxic pathways (perforin/granzyme release and Fas-FasL-mediated apoptosis).