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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
TOP1 NCT06670196 DNA topoisomerase I other SKB264 RELEVANT_DRUG C166409 ANTIBODY DRUG CONJUGATE Conjugate TROP2-targeting antibody–drug conjugate composed of a humanized monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor; binds TROP2 on tumor cells, internalizes, and releases the topo‑I payload to cause DNA damage and cell death (with potential bystander effect). TROP2-targeting IgG1k antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and via a cleavable linker releases the topoisomerase I inhibitor tirumotecan, inhibiting topo I to cause DNA damage, replication arrest, and apoptosis, with a potential bystander effect. NO INDIRECT The ADC binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor that causes DNA damage and apoptosis. Topoisomerase I is the intracellular enzymatic payload target; its expression alone is not sufficient for targeting or killing without TROP2-mediated delivery. Non-Small Cell Lung Cancer CANCER Lung Non-Small Cell Lung Cancer Non-Small Cell Lung Cancer ai
TOP1 NCT06649331 DNA topoisomerase I other SHR-A2102 RELEVANT_DRUG C200198 ANTIBODY DRUG CONJUGATE Conjugate Nectin-4–directed antibody–drug conjugate targeting PVRL4; binds to Nectin-4 on tumor cells, is internalized, and releases a cytotoxic payload. Nectin-4 (PVRL4)–targeted IgG1 antibody–drug conjugate. After binding Nectin-4 on tumor cells, the ADC is internalized and a cleavable linker releases a topoisomerase I inhibitor payload, blocking DNA replication and inducing cell cycle arrest and apoptosis in Nectin-4–expressing cells. NO INDIRECT SHR-A2102 targets Nectin-4 on the cell surface, is internalized, and releases a topoisomerase I inhibitor that blocks DNA replication and induces apoptosis. DNA topoisomerase I is the intracellular enzyme inhibited by the payload, not the antigen that directs cell killing. Breast Cancer CANCER Breast Breast Cancer Breast Cancer ai
EGFR NCT06670196 EGFR other Osimertinib RELEVANT_DRUG C116377 SMALL MOLECULE DRUG Inhibitor Third‑generation, irreversible small‑molecule EGFR tyrosine kinase inhibitor that targets mutant EGFR (exon 19 deletion/L858R ± T790M), suppressing downstream MAPK and PI3K/AKT signaling. Third‑generation, irreversible, mutant‑selective EGFR tyrosine kinase inhibitor that covalently inhibits mutant EGFR (exon 19 deletion, L858R, and T790M), blocking downstream MAPK and PI3K/AKT signaling to suppress tumor growth and induce cancer cell death. YES DIRECT Osimertinib covalently inhibits mutant EGFR kinase (e.g., exon 19 deletion, L858R, T790M), blocking MAPK and PI3K/AKT survival 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
UNKNOWN NCT05971589 Patient-specific tumor neoantigen peptide presented by HLA class I (peptide–MHC-I) antigen recognition LM103 RELEVANT_DRUG C187659 TUMOR INFILTRATING LYMPHOCYTES Unedited cells Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy composed of ex vivo–expanded patient CD8+/CD4+ TILs reinfused to mediate TCR-dependent recognition and cytotoxic killing of tumor antigen–bearing cells. Autologous, ex vivo–expanded CD8+/CD4+ tumor-infiltrating T lymphocytes are reinfused to recognize tumor antigen–bearing cells via native TCRs and mediate cytotoxic killing (e.g., perforin/granzyme), leading to antitumor immune responses; product is non–genetically engineered and activity is typically supported by lymphodepletion and IL-2. YES DIRECT Reinfused TILs recognize the neoantigen peptide–MHC-I via native TCRs and directly kill target cells through cytotoxic T-cell mechanisms (perforin/granzyme-mediated apoptosis, Fas–FasL). Solid Tumor CANCER Other Solid Tumors Solid Tumors manual_review_required
UNKNOWN NCT05971589 Shared/non-mutated tumor-associated antigen peptide presented by HLA class I (peptide–MHC-I) antigen recognition LM103 RELEVANT_DRUG C187659 TUMOR INFILTRATING LYMPHOCYTES Unedited cells Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy composed of ex vivo–expanded patient CD8+/CD4+ TILs reinfused to mediate TCR-dependent recognition and cytotoxic killing of tumor antigen–bearing cells. Autologous, ex vivo–expanded CD8+/CD4+ tumor-infiltrating T lymphocytes are reinfused to recognize tumor antigen–bearing cells via native TCRs and mediate cytotoxic killing (e.g., perforin/granzyme), leading to antitumor immune responses; product is non–genetically engineered and activity is typically supported by lymphodepletion and IL-2. YES DIRECT Autologous TILs recognize the shared tumor-associated antigen peptide presented on HLA class I via native TCRs and directly kill the presenting cells through perforin/granzyme cytolysis (and Fas–FasL apoptosis). Solid Tumor CANCER Other Solid Tumors Solid Tumors manual_review_required
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