Oral third-generation irreversible EGFR tyrosine kinase inhibitor active against Exon 19 deletion/L858R and T790M mutations.
Oral third-generation irreversible EGFR tyrosine kinase inhibitor that selectively and covalently targets mutant EGFR (Exon 19 deletion, L858R, T790M), blocking downstream signaling and inducing death of EGFR-mutant tumor cells while sparing wild-type EGFR; penetrates the blood–brain barrier.
YES
DIRECT
Irreversible inhibition of mutant EGFR kinase (e.g., Exon 19 del, L858R, T790M) blocks downstream survival signaling (PI3K/AKT, MAPK), leading to growth arrest and apoptosis of EGFR-mutant tumor cells; minimal effect on wild-type EGFR.
A recombinant human broadly neutralizing monoclonal antibody that binds the HIV-1 Env gp120 CD4-binding site to block virus–CD4 interaction and entry; neutralizes diverse HIV-1 strains and can mediate Fc-dependent effector functions (ADCC/ADCP). The LS Fc mutations enhance FcRn binding and extend serum half-life.
Recombinant human broadly neutralizing monoclonal antibody that binds the HIV-1 Env gp120 CD4-binding site, blocking gp120–CD4 interaction and viral entry; neutralizes diverse HIV-1 strains and can engage Fc-dependent effector functions (ADCC/ADCP) against infected cells. LS Fc mutations enhance FcRn binding to extend serum half-life.
NO
INDIRECT
3BNC117-LS opsonizes HIV-1 Env on infected cells; its Fc binds CD16a on NK cells to trigger ADCC/ADCP that kills Env+ cells. CD16a-expressing cells act as effectors, not targets.
Bispecific monoclonal antibody (CD20×CD3) T‑cell engager that redirects T cells to kill CD20+ B cells.
Humanized bispecific CD20xCD3 monoclonal antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to activate TCR/CD3 signaling and form cytolytic synapses, leading to perforin/granzyme-mediated killing of CD20+ malignant B cells.
YES
DIRECT
Bispecific CD20xCD3 T‑cell engager redirects T cells to CD20+ cells, forming a cytolytic synapse and inducing perforin/granzyme-mediated killing.