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Only direct cytotoxic targets are shown
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Gene NCT ID Antigen/Ligand Binding Type Drug Name Drug NCI Concept Drug Category Drug Class Drug Description Drug Mechanism of Action Target Cytotoxicity Mechanism Disease Disease Type Tissue OncoTree Main Type OncoTree Name Annotation Status
MET NCT05299125 MET (c-MET/HGFR) antigen recognition Amivantamab C124993 INHIBITORY ANTIBODY Inhibitor Low-fucose, fully human IgG1 bispecific monoclonal antibody targeting EGFR and MET; inhibits EGFR/MET signaling and active against EGFR activating/resistance mutations (e.g., T790M/C797S) and MET pathway activation. Low-fucose, fully human IgG1 bispecific antibody that targets EGFR and MET (wild-type and mutant), blocks ligand binding and receptor phosphorylation, promotes receptor internalization/degradation, and mediates Fc-dependent ADCC; collectively shuts down EGFR/MET downstream signaling (e.g., MAPK, PI3K-AKT) and inhibits tumor cell proliferation, including in EGFR-activating/resistance and MET-driven settings. Amivantamab binds MET on target cells and engages Fcγ receptor–bearing effector cells to mediate Fc-dependent ADCC (and phagocytosis), leading to target-cell killing; it also induces receptor internalization/degradation and signaling blockade. Metastatic Non-Small Cell Lung Cancer CANCER Lung Non-Small Cell Lung Cancer Non-Small Cell Lung Cancer ai
EGFR NCT05299125 EGFR exon 19 deletion mutant (Del19) other Lazertinib C148147 SMALL MOLECULE DRUG Inhibitor 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. Mutant-selective EGFR TKI that irreversibly inhibits EGFR Del19 kinase activity, blocking downstream survival signaling (e.g., PI3K/AKT, MAPK) and inducing apoptosis of EGFR-mutant tumor cells. Metastatic Non-Small Cell Lung Cancer CANCER Lung Non-Small Cell Lung Cancer Non-Small Cell Lung Cancer ai
EGFR NCT05299125 EGFR L858R mutant other Lazertinib C148147 SMALL MOLECULE DRUG Inhibitor 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. Mutant-selective, irreversible inhibition of EGFR L858R blocks EGFR signaling (e.g., MAPK/PI3K), triggering apoptosis of EGFR-mutant tumor cells. Metastatic Non-Small Cell Lung Cancer CANCER Lung Non-Small Cell Lung Cancer Non-Small Cell Lung Cancer ai
EGFR NCT05299125 EGFR T790M resistance mutant other Lazertinib C148147 SMALL MOLECULE DRUG Inhibitor 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. Lazertinib irreversibly inhibits the EGFR T790M mutant kinase, blocking downstream survival signaling (e.g., PI3K/AKT, MAPK) and inducing apoptosis of EGFR-mutant tumor cells. Metastatic Non-Small Cell Lung Cancer CANCER Lung Non-Small Cell Lung Cancer Non-Small Cell Lung Cancer ai
ERBB2 NCT05991518 HER2 antigen recognition IAH0968 INHIBITORY ANTIBODY Inhibitor 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. Fc-mediated recruitment of immune effectors: NK cell ADCC and macrophage ADCP against HER2-expressing cells; signaling blockade may contribute to apoptosis. Cholangiocarcinoma CANCER Biliary Tract Cholangiocarcinoma Cholangiocarcinoma ai
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