Half-life–extended bispecific T-cell engager antibody that binds DLL3 on SCLC cells and CD3 on T cells to redirect cytotoxic T-cell killing (immunotherapy).
Half-life–extended bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells, redirecting and activating cytotoxic T lymphocytes to kill DLL3-expressing cancer cells.
YES
DIRECT
Bispecific T‑cell engager links CD3 on T cells to DLL3 on target cells, activating CTLs to kill DLL3-expressing cells via perforin/granzyme-mediated cytotoxicity.
Half-life–extended bispecific T-cell engager antibody that binds DLL3 on SCLC cells and CD3 on T cells to redirect cytotoxic T-cell killing (immunotherapy).
Half-life–extended bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells, redirecting and activating cytotoxic T lymphocytes to kill DLL3-expressing cancer cells.
NO
INDIRECT
The drug binds CD3E on T cells to engage and activate them against DLL3-expressing tumor cells; T cells then kill DLL3+ cancer cells via perforin/granzyme-mediated cytotoxicity. CD3E+ T cells are not targeted for killing.
Third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor that covalently binds mutant EGFR (e.g., T790M, L858R, exon 19 deletions), suppressing EGFR signaling to inhibit proliferation and induce apoptosis, with relatively reduced activity on wild-type EGFR.
YES
DIRECT
Mutant‑selective, irreversible EGFR tyrosine kinase inhibition of EGFR T790M suppresses downstream signaling (e.g., MAPK/PI3K‑AKT), leading to growth inhibition and apoptosis of the mutant EGFR–expressing tumor cells.
A glycoengineered type II anti-CD20 IgG1 monoclonal antibody used as pre-treatment to debulk B cells and mitigate cytokine release syndrome; induces direct cell death and antibody-dependent cellular cytotoxicity (ADCC) of CD20+ B cells.
Obinutuzumab is a glycoengineered, humanized type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells; its afucosylated Fc increases affinity for Fc gamma RIII receptors to enhance antibody-dependent cellular cytotoxicity and it induces direct cell death, resulting in depletion of CD20+ B cells (used to debulk B cells and mitigate cytokine release syndrome risk).
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages FcγRIIIb (CD16b) on neutrophils to trigger ADCC/phagocytosis against CD20+ B cells. CD16b-expressing cells act as effectors and are not killed by the drug.