Mutant-selective small-molecule EGFR tyrosine kinase inhibitor active against Ex19del/L858R and T790M with reduced activity on wild-type EGFR.
Third-generation, mutant-selective EGFR tyrosine kinase inhibitor that irreversibly binds mutant EGFR (e.g., Ex19del, L858R, T790M), blocking EGFR signaling with minimal activity on wild-type EGFR, leading to tumor cell death; penetrates the blood-brain barrier.
NO
DIRECT
Lazertinib is a mutant‑selective EGFR tyrosine kinase inhibitor with minimal activity on wild‑type EGFR, so wtEGFR-expressing cells are not directly inhibited or killed.
Investigational HER2-targeted monoclonal antibody administered IV every 3 weeks; likely inhibits HER2/ERBB2 signaling and mediates Fc-dependent cytotoxicity (ADCC/ADCP).
IAH0968 is a HER2-targeted monoclonal antibody that binds ERBB2 on tumor cells, inhibits HER2 receptor activation and downstream PI3K/AKT and RAS/MAPK signaling to reduce proliferation, and recruits FcγR-expressing immune cells to mediate ADCC and ADCP.
YES
DIRECT
Fc-mediated recruitment of immune effectors: NK cell ADCC and macrophage ADCP against HER2-expressing cells; signaling blockade may contribute to apoptosis.
HER2-targeted antibody–drug conjugate carrying MMAE; binds HER2 on tumor cells, is internalized, and releases MMAE to disrupt microtubules, leading to cell-cycle arrest and apoptosis (with potential bystander effect).
HER2-targeted antibody–drug conjugate: disitamab antibody binds HER2 on tumor cells, is internalized, and a cleavable linker releases the cytotoxic payload MMAE, which disrupts microtubules, causing G2/M cell-cycle arrest and apoptosis; the released payload can diffuse to nearby cells (bystander effect).
YES
DIRECT
The ADC binds HER2, is internalized, and releases the cytotoxic payload MMAE, which disrupts microtubules leading to G2/M arrest and apoptosis; released MMAE can also cause bystander killing of nearby cells.
Antibody–drug conjugate that binds a tumor-associated antigen, is internalized, and releases a topoisomerase I inhibitor payload to induce DNA damage and tumor cell death; potential bystander effect.
Nectin-4–targeted IgG1 antibody–drug conjugate; after binding and internalization, a cleavable linker releases a topoisomerase I inhibitor payload that inhibits topo I, causing DNA damage during replication and leading to cell-cycle arrest and apoptosis in antigen-expressing tumor cells, with potential bystander effect.
YES
DIRECT
The ADC binds nectin-4 on target cells, is internalized, and releases a topoisomerase I inhibitor via a cleavable linker, causing DNA damage during replication leading to cell-cycle arrest and apoptosis (with potential bystander effect).
HER2-targeted antibody–drug conjugate carrying MMAE; binds HER2 on tumor cells, is internalized, and releases MMAE to disrupt microtubules, leading to cell-cycle arrest and apoptosis (with potential bystander effect).
HER2-targeted antibody–drug conjugate: disitamab antibody binds HER2 on tumor cells, is internalized, and a cleavable linker releases the cytotoxic payload MMAE, which disrupts microtubules, causing G2/M cell-cycle arrest and apoptosis; the released payload can diffuse to nearby cells (bystander effect).
NO
INDIRECT
RC48 binds HER2 (not beta-tubulin), is internalized, and releases MMAE, which then binds the beta-tubulin vinca site to disrupt microtubules and trigger G2/M arrest and apoptosis; tubulin-expressing cells are killed only if they receive MMAE via HER2-mediated delivery or bystander diffusion.