Intravenous, Fc-engineered humanized anti-CD19 IgG1 monoclonal antibody that binds CD19 on B cells to induce antibody-dependent cellular cytotoxicity and phagocytosis and direct apoptosis, depleting tumor B cells.
Fc-engineered humanized anti-CD19 IgG1 monoclonal antibody that binds CD19 on B cells and enhances FcγR-mediated ADCC and ADCP, and can directly induce apoptosis, leading to depletion of malignant CD19+ B cells.
Anti-CD19 IgG1 binds CD19 on B cells; its Fc region engages FcγR on effector cells to trigger ADCC and ADCP, and it can also directly induce apoptosis of CD19+ cells.
Bispecific IgG-like T-cell–engaging antibody (ABBV-383) that binds BCMA on myeloma cells and CD3 on T cells to redirect T-cell cytotoxicity.
Human IgG4 bispecific antibody that binds BCMA on myeloma cells and CD3 on T cells, redirecting cytotoxic T lymphocytes to kill BCMA-expressing tumor cells; incorporates a low-activating CD3 arm to preferentially activate effector T cells and limit cytokine release.
The BCMA×CD3 bispecific antibody binds BCMA on target cells and CD3 on T cells, forming an immune synapse that activates T cells to release perforin/granzymes and kill BCMA-expressing cells.
Anti-SLAMF7 monoclonal antibody that activates NK cells and mediates ADCC against SLAMF7-positive myeloma cells.
Humanized anti-SLAMF7 (CS1) monoclonal antibody that binds SLAMF7 on myeloma and NK cells, activates NK-cell cytotoxicity, and induces Fc-dependent antibody-dependent cellular cytotoxicity (ADCC) against SLAMF7-positive myeloma cells.
Elotuzumab binds SLAMF7 on myeloma cells and its Fc engages FcγRIIIa on NK cells, triggering antibody-dependent cellular cytotoxicity (ADCC) with perforin/granzyme release; it also activates NK cells via SLAMF7 to enhance killing.
Chimeric IgG1 monoclonal antibody targeting soluble and transmembrane TNF-α; blocks TNFR1/2-mediated signaling to reduce NF-κB–driven inflammation (cytokines/chemokines, adhesion molecules, leukocyte trafficking) and can induce apoptosis of activated TNF-expressing immune cells.
Chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-alpha, neutralizing TNF and preventing TNFR1/2 signaling. This suppresses NF-kB–driven inflammatory pathways (proinflammatory cytokines/chemokines, adhesion molecules, leukocyte trafficking) and can induce apoptosis of activated TNF-expressing immune cells via Fc-mediated effects/reverse signaling.
Infliximab binds transmembrane TNF-α; antibody cross-linking induces reverse signaling–mediated apoptosis of TNF-expressing immune cells and its IgG1 Fc triggers ADCC and complement-dependent cytotoxicity against tmTNF+ cells.
Autologous T cells engineered to express a chimeric antigen receptor targeting CD19 to induce MHC-independent T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19-positive malignant B cells.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor bind CD19 on B cells, triggering MHC-independent activation via CD3z and costimulatory domains, leading to T-cell expansion, cytokine release, and cytotoxic killing of CD19-positive malignant B cells.
Anti-CD19 CAR T cells bind CD19 and, upon CAR signaling, directly kill CD19+ cells via perforin/granzyme cytolysis and Fas–FasL–mediated apoptosis, with associated cytokine release.