A subcutaneous bispecific T‑cell–engaging monoclonal antibody (Lunsumio) that binds CD20 on B cells and CD3 on T cells to recruit and activate cytotoxic T cells against malignant B cells.
Humanized bispecific monoclonal antibody that simultaneously binds CD20 on B cells and CD3 on T cells, cross-linking T cells to malignant B cells to activate cytotoxic T-lymphocyte responses (immune synapse formation, perforin/granzyme release) and kill CD20-positive tumor cells.
YES
DIRECT
Mosunetuzumab bridges CD3+ T cells to CD20+ cells, forming an immune synapse that activates T cells to kill the CD20-expressing cells via perforin/granzyme-mediated apoptosis (and Fas/FasL pathways).
A subcutaneous bispecific T‑cell–engaging monoclonal antibody (Lunsumio) that binds CD20 on B cells and CD3 on T cells to recruit and activate cytotoxic T cells against malignant B cells.
Humanized bispecific monoclonal antibody that simultaneously binds CD20 on B cells and CD3 on T cells, cross-linking T cells to malignant B cells to activate cytotoxic T-lymphocyte responses (immune synapse formation, perforin/granzyme release) and kill CD20-positive tumor cells.
NO
INDIRECT
The drug binds CD3 on T cells to activate and recruit them; these T cells then kill CD20+ B cells via immune synapse formation and perforin/granzyme release. CD3+ cells are effectors, not killed.
An intravenous antibody‑drug conjugate (Polivy) targeting CD79b on B cells that delivers the microtubule inhibitor MMAE, leading to cell cycle 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 of malignant B cells.
YES
DIRECT
An anti-CD79b ADC binds CD79b, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD79b-positive cells.
An intravenous antibody‑drug conjugate (Polivy) targeting CD79b on B cells that delivers the microtubule inhibitor MMAE, leading to cell cycle 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 of malignant B cells.
NO
INDIRECT
Polatuzumab vedotin binds CD79b on B cells, is internalized, and releases MMAE, which binds beta-tubulin to inhibit microtubule polymerization causing G2/M arrest and apoptosis. Beta-tubulin expression alone does not lead to targeted killing.
Patient-derived T cells genetically engineered to express a T-cell receptor recognizing the TP53 R248Q mutant peptide presented by HLA-A*11:01; reinfused to mediate antigen-specific cytotoxicity against TP53 R248Q–positive tumor cells.
Autologous T cells are engineered to express an HLA-A*11:01–restricted T-cell receptor that recognizes the TP53 R248Q mutant peptide on MHC class I. Upon binding the mutant peptide–MHC complex on tumor cells, the T cells activate TCR signaling and mediate antigen-specific cytotoxicity via perforin/granzyme release and cytokine-driven killing, selectively targeting TP53 R248Q–positive cancer cells.
YES
DIRECT
Engineered TCR T cells recognize the TP53 R248Q peptide–HLA-A*11:01 complex and directly lyse target cells via TCR-activated perforin/granzyme cytotoxicity (and Fas–FasL pathways).