Subcutaneous CD3-directed T-cell engager bispecific antibody that binds CD3 on T cells and a B-cell tumor antigen to redirect cytotoxic T cells against malignant B cells.
CD3-directed bispecific antibody (rezetamig) that binds CD3 on T cells and CD22 on B-lineage tumor cells, crosslinking them to form an immune synapse, activate TCR/CD3 signaling, and induce perforin/granzyme-mediated killing of CD22+ malignant B cells, with associated cytokine release.
CD3xCD22 bispecific antibody crosslinks T cells to CD22+ cells, activates TCR/CD3 signaling, and induces perforin/granzyme-mediated killing after immune synapse formation.
Antigen-specific T cells expanded ex vivo and reinfused to recognize tumor peptides on MHC class I via the TCR, mediating cytotoxicity through perforin/granzyme release and IFN-gamma-mediated effects.
Autologous antigen-specific CTLs expanded ex vivo are reinfused to recognize tumor peptides presented on MHC class I via their endogenous TCR, inducing tumor-cell killing via perforin/granzyme release and death-receptor pathways (FasL/TRAIL), along with IFN-γ secretion to enhance antitumor immune responses.
Antigen-specific CTLs recognize peptide–MHC I on targets, then kill via perforin/granzyme and by engaging DR4 with TRAIL to trigger extrinsic (caspase-mediated) apoptosis.
BCMA×CD3 bispecific T‑cell engager antibody given subcutaneously; binds BCMA on malignant plasma cells and CD3 on T cells to redirect T‑cell cytotoxicity and cytokine‑mediated killing of myeloma cells.
BCMA×CD3 bispecific monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to redirect T-cell cytotoxicity and cytokine-mediated killing of BCMA-expressing myeloma cells.
Bispecific T-cell engager binds BCMA on target cells and CD3 on T cells, cross-linking to activate cytotoxic T cells that kill BCMA+ cells via perforin/granzyme-mediated lysis and cytokine effects.
A T-cell–engaging bispecific monoclonal antibody (2:1 CD20:CD3) that binds CD20 on B cells and CD3 on T cells to activate cytotoxic T-cell killing of malignant B cells.
A 2:1 CD20:CD3 bispecific monoclonal antibody that co-binds CD20 on B cells and CD3 on T cells, cross-linking them to form an immunologic synapse and activate cytotoxic T-cell killing of CD20-positive malignant B cells.
Glofitamab bridges CD20 on B cells and CD3 on T cells, forming an immunologic synapse that activates T-cell cytotoxicity (perforin/granzyme and Fas–FasL) to lyse CD20-expressing cells.
An anti-CD79b antibody–drug conjugate that delivers the microtubule inhibitor MMAE to CD79b+ B cells, inducing mitotic arrest and apoptosis.
Anti-CD79b monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE. After binding CD79b on B cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in CD79b+ malignant B cells.
ADC binds CD79b on B cells, is internalized, linker cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis of CD79b+ cells.