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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 NCT06667076 EGFR other Lazertinib RELEVANT_DRUG C148147 SMALL MOLECULE DRUG Inhibitor Third-generation, irreversible, CNS-penetrant EGFR tyrosine kinase inhibitor targeting activating EGFR mutations (and T790M) with reduced inhibition of wild-type EGFR. Third-generation, irreversible, CNS-penetrant EGFR tyrosine kinase inhibitor that selectively and covalently targets mutant EGFR (e.g., T790M, exon 19 deletions, L858R) with minimal wild‑type EGFR activity, thereby blocking EGFR-mediated signaling (MAPK/PI3K-AKT) and inducing death of EGFR-mutant tumor cells. YES DIRECT Covalent inhibition of mutant EGFR kinase blocks MAPK/PI3K-AKT survival signaling, triggering apoptosis of EGFR‑mutant tumor cells. Carcinoma, Non-Small-Cell Lung CANCER Lung Non-Small Cell Lung Cancer Non-Small Cell Lung Cancer ai
HLA-A NCT06158828 HLA-A (MHC class I heavy chain) antigen recognition Rabbit anti-thymocyte globulin (rATG) RELEVANT_DRUG CYTOTOXIC ANTIBODY Inhibitor Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk. Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk. YES DIRECT rATG contains antibodies that bind HLA-A on target cells and mediate complement-dependent cytotoxicity and Fc-dependent ADCC/phagocytosis (and apoptosis), directly depleting those cells. Acute Myeloid Leukemia CANCER Myeloid Acute Myeloid Leukemia Acute Myeloid Leukemia manual_review_required
EGFR NCT06667076 EGFR other Lazertinib RELEVANT_DRUG C148147 SMALL MOLECULE DRUG Inhibitor Third-generation, irreversible, CNS-penetrant EGFR tyrosine kinase inhibitor targeting activating EGFR mutations (and T790M) with reduced inhibition of wild-type EGFR. Third-generation, irreversible, CNS-penetrant EGFR tyrosine kinase inhibitor that selectively and covalently targets mutant EGFR (e.g., T790M, exon 19 deletions, L858R) with minimal wild‑type EGFR activity, thereby blocking EGFR-mediated signaling (MAPK/PI3K-AKT) and inducing death of EGFR-mutant tumor cells. YES DIRECT Irreversible small‑molecule inhibition of mutant EGFR blocks MAPK/PI3K‑AKT signaling, causing apoptosis of EGFR‑mutant tumor cells (minimal effect on wild‑type EGFR). Carcinoma, Non-Small-Cell Lung CANCER Lung Non-Small Cell Lung Cancer Non-Small Cell Lung Cancer ai
EGFR NCT06616259 EGFR (epidermal growth factor receptor, HER1/ERBB1) antigen recognition Cetuximab RELEVANT_DRUG C1723 INHIBITORY ANTIBODY Inhibitor Chimeric IgG1 anti‑EGFR monoclonal antibody that blocks ligand binding to EGFR, inhibiting downstream RAS‑RAF‑MEK‑ERK and PI3K‑AKT signaling; also mediates ADCC. Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor activation/dimerization, thereby inhibiting downstream RAS–RAF–MEK–ERK and PI3K–AKT signaling; also mediates antibody-dependent cellular cytotoxicity (ADCC) against EGFR-expressing tumor cells. YES DIRECT Cetuximab binds EGFR on target cells and engages Fcγ receptors on immune effectors (e.g., NK cells) to induce antibody‑dependent cellular cytotoxicity (ADCC; with some CDC), leading to killing of EGFR+ cells. Colorectal Cancer (CRC) CANCER Bowel Colorectal Cancer Colorectal Cancer ai
GPRC5D NCT05838131 GPRC5D (G protein-coupled receptor class C group 5 member D) antigen recognition CT071 (autologous GPRC5D-directed CAR-T cells) RELEVANT_DRUG CAR T Cellular Therapy Autologous, gene-modified T cells engineered to express a chimeric antigen receptor targeting GPRC5D on malignant plasma cells; CAR signaling (CD3ζ with costimulation) activates T cells to proliferate, release cytokines, and mediate perforin/granzyme cytotoxic killing. Autologous T cells are gene-modified to express a chimeric antigen receptor targeting GPRC5D on malignant plasma cells. CAR engagement activates CD3zeta with costimulatory signaling, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of GPRC5D-positive cells. YES DIRECT GPRC5D-specific CAR-T cells bind GPRC5D on target cells, activate via CD3ζ/costimulation, and kill through perforin/granzyme-mediated cytotoxicity. Primary Plasma Cell Leukemia CANCER Lymphoid Non-Hodgkin Lymphoma, B Cell Plasma Cell Myeloma ai
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