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Gene NCT ID Antigen/Ligand Binding Type Drug Name Drug Type Drug NCI Concept Drug Category Drug Class Drug Description Drug Mechanism of Action Cytotoxicity Cytotoxicity Type Target Cytotoxicity Mechanism Disease Disease Type Tissue OncoTree Main Type OncoTree Name Annotation Status
EGFR NCT05816252 EGFR (T790M mutant) other Osimertinib RELEVANT_DRUG C116377 SMALL MOLECULE DRUG Inhibitor EGFR tyrosine kinase inhibitor targeting EGFR-mutant signaling in tumor cells. Third‑generation, oral, irreversible EGFR tyrosine kinase inhibitor that covalently binds mutant EGFR (e.g., T790M, L858R, exon 19 deletions) at Cys797, selectively blocking EGFR signaling (MAPK/PI3K pathways) to inhibit proliferation and induce tumor cell death, with reduced activity against wild‑type EGFR. YES DIRECT Osimertinib irreversibly binds the EGFR T790M-mutant kinase (Cys797), inhibits EGFR signaling (MAPK/PI3K-AKT), leading to growth arrest and apoptosis of EGFR-mutant tumor cells. Non-small Cell Lung Cancer CANCER Lung Non-Small Cell Lung Cancer Non-Small Cell Lung Cancer ai
EGFR NCT05816252 EGFR (L858R mutant) other Osimertinib RELEVANT_DRUG C116377 SMALL MOLECULE DRUG Inhibitor EGFR tyrosine kinase inhibitor targeting EGFR-mutant signaling in tumor cells. Third‑generation, oral, irreversible EGFR tyrosine kinase inhibitor that covalently binds mutant EGFR (e.g., T790M, L858R, exon 19 deletions) at Cys797, selectively blocking EGFR signaling (MAPK/PI3K pathways) to inhibit proliferation and induce tumor cell death, with reduced activity against wild‑type EGFR. YES DIRECT Osimertinib irreversibly inhibits mutant EGFR (L858R) kinase activity, blocking downstream MAPK/PI3K signaling and inducing apoptosis of EGFR-mutant tumor cells. Non-small Cell Lung Cancer CANCER Lung Non-Small Cell Lung Cancer Non-Small Cell Lung Cancer ai
TUBB NCT06483334 Tubulin (beta-tubulin; microtubules) other Enfortumab vedotin RELEVANT_DRUG C114500 ANTIBODY DRUG CONJUGATE Conjugate A NECTIN-4–targeted antibody–drug conjugate delivering MMAE, a microtubule inhibitor that causes cell-cycle arrest and apoptosis. Nectin-4–targeted monoclonal antibody–drug conjugate that binds Nectin-4 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE after linker cleavage, leading to tubulin depolymerization, G2/M cell-cycle arrest, and apoptosis in Nectin-4–expressing cancer cells. NO INDIRECT Enfortumab vedotin targets Nectin-4 on tumor cells; after internalization it releases MMAE, which binds tubulin to depolymerize microtubules and cause G2/M arrest and apoptosis. Tubulin is the intracellular effector, not the targeting antigen determining which cells are killed. Locally Advanced Urothelial Carcinoma CANCER Bladder/Urinary Tract Bladder Cancer Bladder Urothelial Carcinoma ai
EGFR NCT05816252 EGFR (exon 19 deletion mutants) other Osimertinib RELEVANT_DRUG C116377 SMALL MOLECULE DRUG Inhibitor EGFR tyrosine kinase inhibitor targeting EGFR-mutant signaling in tumor cells. Third‑generation, oral, irreversible EGFR tyrosine kinase inhibitor that covalently binds mutant EGFR (e.g., T790M, L858R, exon 19 deletions) at Cys797, selectively blocking EGFR signaling (MAPK/PI3K pathways) to inhibit proliferation and induce tumor cell death, with reduced activity against wild‑type EGFR. YES DIRECT Osimertinib irreversibly inhibits mutant EGFR (exon 19 deletions) kinase activity, shutting down MAPK/PI3K-AKT survival signaling and inducing apoptosis of the EGFR-mutant tumor cells. Non-small Cell Lung Cancer CANCER Lung Non-Small Cell Lung Cancer Non-Small Cell Lung Cancer ai
CD19 NCT06279923 CD19 antigen recognition CD19-BAFF-targeted CAR T cells RELEVANT_DRUG CAR T Cellular Therapy Autologous gene-modified T lymphocytes engineered to express a chimeric antigen receptor that recognizes CD19 and targets within the BAFF (BLyS) axis (e.g., BAFF-R/TACI/BCMA), enabling activation and cytolytic depletion of pathogenic B cells/plasmablasts to reduce BCR signaling, germinal center activity, and autoantibody production in refractory autoimmune disease. Autologous T cells engineered with a chimeric antigen receptor that recognizes CD19 and BAFF-axis receptors (BAFF-R/TACI/BCMA), leading to antigen-dependent activation and cytolytic elimination of B cells and plasmablasts. This depletes pathogenic B-lineage cells, disrupts BAFF-mediated survival signals, and reduces BCR signaling, germinal center activity, and autoantibody production in autoimmune disease. YES DIRECT CAR T cells recognize CD19 on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis). Neuromyelitis optica NON-CANCER CNS/Brain ai
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