A subcutaneous bispecific T‑cell–engaging monoclonal antibody (CD20×CD3) that binds CD20 on malignant B cells and CD3 on T cells to form an immune synapse, activating T cells to kill CD20+ B-ALL blasts via cytotoxicity and cytokine release.
CD20×CD3 bispecific antibody that simultaneously binds CD20 on malignant B cells and CD3 on T cells, forming an immune synapse that activates T cells via CD3/TCR signaling to lyse CD20+ B cells through cytotoxicity and cytokine release.
NO
INDIRECT
Mosunetuzumab engages CD3 on T cells to activate and redirect them to kill CD20+ target cells via T‑cell cytotoxicity (perforin/granzyme and cytokines); CD3+ T cells themselves are not killed.
Genetically engineered autologous T-lymphocytes expressing a chimeric antigen receptor that recognizes CD44 and CD133 to target glioma and cancer stem-like cells; incorporates a truncated IL-7 receptor alpha intracellular signaling module to enhance T-cell survival, persistence, and activity. Administered locoregionally via Ommaya reservoir for recurrent glioblastoma.
Autologous T cells are genetically engineered to express a dual-target chimeric antigen receptor recognizing CD44 and CD133 on glioblastoma and cancer stem-like cells. CAR engagement activates T-cell cytotoxicity via CD3-zeta/co-stimulatory signaling, while an incorporated truncated IL-7Rα intracellular module enhances T-cell survival, persistence, and functional activity. Cells are delivered locoregionally via an Ommaya reservoir to maximize tumor exposure and reduce antigen escape through dual targeting.
YES
DIRECT
CAR T cells recognize CD44 on target cells, activating CD3ζ/co-stimulatory signaling and killing bound cells via perforin/granzyme release and death-receptor pathways.
Genetically engineered autologous T-lymphocytes expressing a chimeric antigen receptor that recognizes CD44 and CD133 to target glioma and cancer stem-like cells; incorporates a truncated IL-7 receptor alpha intracellular signaling module to enhance T-cell survival, persistence, and activity. Administered locoregionally via Ommaya reservoir for recurrent glioblastoma.
Autologous T cells are genetically engineered to express a dual-target chimeric antigen receptor recognizing CD44 and CD133 on glioblastoma and cancer stem-like cells. CAR engagement activates T-cell cytotoxicity via CD3-zeta/co-stimulatory signaling, while an incorporated truncated IL-7Rα intracellular module enhances T-cell survival, persistence, and functional activity. Cells are delivered locoregionally via an Ommaya reservoir to maximize tumor exposure and reduce antigen escape through dual targeting.
YES
DIRECT
CAR T cells bind CD133 via the CAR and directly lyse target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
HER2-targeted antibody-drug conjugate that binds HER2 (including low-expressing tumors), is internalized, and releases the microtubule inhibitor MMAE (monomethyl auristatin E) to induce cancer cell apoptosis.
HER2-targeted monoclonal antibody linked to monomethyl auristatin E (MMAE). After binding HER2 on tumor cells (including low expressers), the ADC is internalized and cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis; the membrane-permeable payload can also exert a bystander cytotoxic effect.
YES
DIRECT
The HER2-targeted ADC binds HER2, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; the membrane-permeable payload can also cause bystander killing.
HER2-targeted antibody-drug conjugate that binds HER2 (including low-expressing tumors), is internalized, and releases the microtubule inhibitor MMAE (monomethyl auristatin E) to induce cancer cell apoptosis.
HER2-targeted monoclonal antibody linked to monomethyl auristatin E (MMAE). After binding HER2 on tumor cells (including low expressers), the ADC is internalized and cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis; the membrane-permeable payload can also exert a bystander cytotoxic effect.
NO
INDIRECT
The ADC binds HER2 (not beta-tubulin), is internalized, and releases MMAE, which inhibits beta-tubulin polymerization to trigger G2/M arrest and apoptosis; membrane-permeable MMAE can also cause bystander killing. Beta-tubulin expression alone does not lead to targeted killing.