A T-cell–engaging bispecific IgG monoclonal antibody (2:1 format) targeting CD20 on B cells and CD3 on T cells; bridges T cells to CD20+ malignant B cells to trigger TCR/CD3 activation, immunologic synapse formation, and cytotoxic killing.
CD20xCD3 bispecific IgG (2:1) that bridges T cells to CD20+ B cells, activating TCR/CD3 signaling and forming an immunologic synapse to drive CTL-mediated killing (perforin/granzyme, apoptosis) of malignant B cells, with associated cytokine release.
YES
DIRECT
Glofitamab bridges T cells to CD20+ cells via CD3 and CD20, triggering TCR activation and CTL-mediated killing through perforin/granzyme-induced apoptosis.
A T-cell–engaging bispecific IgG monoclonal antibody (2:1 format) targeting CD20 on B cells and CD3 on T cells; bridges T cells to CD20+ malignant B cells to trigger TCR/CD3 activation, immunologic synapse formation, and cytotoxic killing.
CD20xCD3 bispecific IgG (2:1) that bridges T cells to CD20+ B cells, activating TCR/CD3 signaling and forming an immunologic synapse to drive CTL-mediated killing (perforin/granzyme, apoptosis) of malignant B cells, with associated cytokine release.
NO
INDIRECT
The drug binds CD3 on T cells to activate them and bridge them to CD20+ B cells; T cells then kill the CD20+ targets via perforin/granzyme-mediated apoptosis. CD3+ cells are effectors, not killed.
Bispecific anti-HER2 monoclonal antibody that binds two non-overlapping HER2 epitopes to produce dual HER2 signaling blockade, inhibiting HER2-driven pathways such as MAPK and PI3K/AKT in tumor cells.
Bispecific anti-HER2 monoclonal antibody (derived from trastuzumab and pertuzumab) that binds two non-overlapping HER2 epitopes, blocks HER2 heterodimerization and downstream MAPK and PI3K/AKT signaling, and elicits ADCC against HER2-overexpressing tumor cells, leading to inhibited proliferation and apoptosis.
YES
DIRECT
Binds two HER2 epitopes on tumor cells, blocks HER2 dimerization/signaling causing apoptosis, and engages Fc receptors to elicit ADCC against HER2-expressing cells.
Bispecific anti-HER2 monoclonal antibody that binds two non-overlapping HER2 epitopes to produce dual HER2 signaling blockade, inhibiting HER2-driven pathways such as MAPK and PI3K/AKT in tumor cells.
Bispecific anti-HER2 monoclonal antibody (derived from trastuzumab and pertuzumab) that binds two non-overlapping HER2 epitopes, blocks HER2 heterodimerization and downstream MAPK and PI3K/AKT signaling, and elicits ADCC against HER2-overexpressing tumor cells, leading to inhibited proliferation and apoptosis.
YES
DIRECT
Binds HER2 on tumor cells and recruits FcγR+ effector cells to mediate ADCC (and ADCP), while dual-epitope blockade of HER2 signaling promotes apoptosis.
Autologous gamma delta T cells engineered with a chimeric antigen receptor targeting Prostate Stem Cell Antigen (PSCA), redirecting γδ T-cell activation and cytotoxicity against PSCA-positive tumor cells.
Autologous gamma delta T cells engineered with a PSCA-specific chimeric antigen receptor bind PSCA on tumor cells, triggering MHC-independent activation, cytokine release, and perforin/granzyme-mediated cytotoxicity against PSCA-positive cancer cells.
YES
DIRECT
PSCA-specific CAR-engineered gamma delta T cells bind PSCA on tumor cells and directly lyse them via immunologic synapse formation and perforin/granzyme-mediated cytotoxicity (MHC-independent).