A BCMA×CD3 bispecific monoclonal antibody immunotherapy (brand: Elrexfio; PF-06863135) that redirects T cells to kill BCMA-expressing myeloma cells.
Elranatamab is a BCMA×CD3 bispecific antibody that binds CD3 on T cells and BCMA on malignant plasma cells, cross-linking them to form an immune synapse and redirect T-cell cytotoxicity and cytokine release to kill BCMA-expressing myeloma cells.
BCMAxCD3 bispecific links T cells to BCMA+ cells, forming an immune synapse and inducing T-cell cytotoxicity (perforin/granzyme apoptosis and cytokine-mediated killing).
Investigational antibody–drug conjugate administered IV; a tumor-targeting monoclonal antibody is internalized and releases the topoisomerase I inhibitor payload brengitecan, causing DNA damage and tumor cell death.
Tumor-targeting monoclonal antibody binds a surface antigen, is internalized, and releases the camptothecin-derived topoisomerase I inhibitor brengitecan, inducing DNA damage (replication-associated strand breaks) and tumor cell death.
An antibody–drug conjugate binds the tumor-associated surface antigen, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing replication-associated DNA damage and apoptosis of the antigen-expressing cells.
Autologous T cells genetically engineered to express a chimeric antigen receptor with two nanobody binding domains that recognize distinct BCMA epitopes, aiming to increase avidity, prevent antigen escape, and mediate cytotoxic killing of multiple myeloma cells.
Autologous T cells are engineered to express a chimeric antigen receptor with two nanobody binding domains recognizing distinct BCMA epitopes. Dual-epitope binding increases avidity and reduces antigen escape. Upon BCMA engagement, CAR signaling activates T-cell cytotoxicity (perforin/granzyme and cytokine release), leading to killing of BCMA-expressing multiple myeloma cells and depletion of normal BCMA+ plasma cells.
CAR-T cells bind BCMA on target cells, triggering T-cell activation and killing via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis), eliminating BCMA-expressing cells.
A BCMA×CD3 bispecific T‑cell–engaging monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells to redirect cytotoxic T‑cell killing in relapsed/refractory multiple myeloma.
Humanized bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, crosslinking them to form an immune synapse and activate T-cell cytotoxicity to kill BCMA-expressing myeloma cells.
Teclistamab bridges CD3+ T cells to BCMA+ cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme and Fas/FasL) to kill the BCMA-expressing cells.
A T-cell-engaging bispecific IgG antibody (CD20xCD3) that binds CD20 on B cells and CD3 on T cells to form an immune synapse, activating T cells to kill malignant B cells via cytotoxic granule release and cytokines.
Bispecific IgG antibody that binds CD3 on T cells and CD20 on B cells, forming an immune synapse that activates T cells to release cytotoxic granules and cytokines, resulting in targeted lysis of CD20+ malignant B cells.
Bispecific CD20xCD3 antibody crosslinks T cells to CD20+ cells, activating T cells to release perforin/granzymes and cytokines, causing targeted lysis/apoptosis of CD20-expressing cells.