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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
ULBP1 NCT06503497 ULBP1 receptor ligand recognition NKG2D CAR-NK cells CAR NK Cellular Therapy Natural killer cells genetically engineered to express a chimeric antigen receptor using the NKG2D ectodomain, enabling recognition of stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells and triggering NK activation, degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis. Administered as two IV infusions on days 2–3 after each chemotherapy cycle with dose escalation. Genetically engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells, triggering NK activation with degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis (e.g., TRAIL/Fas) to kill tumor cells. NKG2D CAR-NK cells bind ULBP1 via the NKG2D-based CAR, activating NK cytotoxicity with degranulation (perforin/granzyme) and death receptor pathways (e.g., TRAIL/FasL), leading to target cell lysis/apoptosis. Pancreatic Cancer CANCER Pancreas Pancreatic Cancer Pancreatic Cancer ai
ULBP2 NCT06503497 ULBP2 receptor ligand recognition NKG2D CAR-NK cells CAR NK Cellular Therapy Natural killer cells genetically engineered to express a chimeric antigen receptor using the NKG2D ectodomain, enabling recognition of stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells and triggering NK activation, degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis. Administered as two IV infusions on days 2–3 after each chemotherapy cycle with dose escalation. Genetically engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells, triggering NK activation with degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis (e.g., TRAIL/Fas) to kill tumor cells. NKG2D CAR–NK cells bind ULBP2 on target cells, triggering NK activation and killing via perforin/granzyme-mediated cytolysis and death receptor–mediated apoptosis (e.g., TRAIL/Fas). Pancreatic Cancer CANCER Pancreas Pancreatic Cancer Pancreatic Cancer ai
ULBP3 NCT06503497 ULBP3 receptor ligand recognition NKG2D CAR-NK cells CAR NK Cellular Therapy Natural killer cells genetically engineered to express a chimeric antigen receptor using the NKG2D ectodomain, enabling recognition of stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells and triggering NK activation, degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis. Administered as two IV infusions on days 2–3 after each chemotherapy cycle with dose escalation. Genetically engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells, triggering NK activation with degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis (e.g., TRAIL/Fas) to kill tumor cells. NKG2D CAR-NK cells recognize ULBP3, leading to NK activation and killing via perforin/granzyme degranulation and death receptor–mediated apoptosis (e.g., TRAIL/Fas). Pancreatic Cancer CANCER Pancreas Pancreatic Cancer Pancreatic Cancer ai
ULBP4 NCT06503497 ULBP4 receptor ligand recognition NKG2D CAR-NK cells CAR NK Cellular Therapy Natural killer cells genetically engineered to express a chimeric antigen receptor using the NKG2D ectodomain, enabling recognition of stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells and triggering NK activation, degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis. Administered as two IV infusions on days 2–3 after each chemotherapy cycle with dose escalation. Genetically engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells, triggering NK activation with degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis (e.g., TRAIL/Fas) to kill tumor cells. NKG2D CAR–NK cells recognize ULBP4 via the NKG2D ectodomain and directly kill target cells through NK degranulation (perforin/granzyme) and death receptor–mediated apoptosis (e.g., TRAIL/Fas). Pancreatic Cancer CANCER Pancreas Pancreatic Cancer Pancreatic Cancer ai
ULBP5 NCT06503497 ULBP5 receptor ligand recognition NKG2D CAR-NK cells CAR NK Cellular Therapy Natural killer cells genetically engineered to express a chimeric antigen receptor using the NKG2D ectodomain, enabling recognition of stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells and triggering NK activation, degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis. Administered as two IV infusions on days 2–3 after each chemotherapy cycle with dose escalation. Genetically engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind stress-induced ligands (MICA, MICB, ULBP1–6) on tumor cells, triggering NK activation with degranulation (perforin/granzyme), cytokine release, and death receptor–mediated apoptosis (e.g., TRAIL/Fas) to kill tumor cells. NKG2D CAR on NK cells binds ULBP5 on target cells, triggering NK activation and cytotoxicity via perforin/granzyme degranulation and death receptor–mediated apoptosis (e.g., TRAIL/Fas). Pancreatic Cancer CANCER Pancreas Pancreatic Cancer Pancreatic Cancer ai
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