Target Search | CytoTargetDB

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Gene

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antigen recognition (3404)

other (145)

receptor ligand recognition (192)

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ai (3167)

manual_review_required (574)

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CANCER (2959)

NON-CANCER (780)

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Gene	NCT ID	Antigen/Ligand	Binding Type	Drug Name	Drug Category	Drug Class	Drug Description	Drug Mechanism of Action	Target Cytotoxicity Mechanism	Disease	Disease Type	Tissue	OncoTree Main Type	OncoTree Name	Annotation Status
MICA	NCT05734898	MICA	antigen recognition	NKG2D CAR-NK cells	CAR NK	Cellular Therapy	Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.	Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.	NKG2D CAR–NK cells bind MICA on target cells and signal via DAP10/CD3ζ to activate NK degranulation, releasing perforin and granzymes that induce cytolysis/apoptosis.	Acute Myeloid Leukemia	CANCER	Myeloid	Acute Myeloid Leukemia	Acute Myeloid Leukemia	ai
MICB	NCT05734898	MICB	antigen recognition	NKG2D CAR-NK cells	CAR NK	Cellular Therapy	Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.	Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.	NKG2D CAR on NK cells binds MICB on target cells, activating DAP10/CD3ζ signaling and NK degranulation with perforin/granzyme-mediated lysis.	Acute Myeloid Leukemia	CANCER	Myeloid	Acute Myeloid Leukemia	Acute Myeloid Leukemia	ai
ULBP1	NCT05734898	ULBP1	antigen recognition	NKG2D CAR-NK cells	CAR NK	Cellular Therapy	Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.	Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.	NKG2D CAR on NK cells binds ULBP1 on target cells and signals via DAP10/CD3ζ, triggering NK degranulation (perforin/granzymes) and death receptor pathways to kill the ULBP1+ cells.	Acute Myeloid Leukemia	CANCER	Myeloid	Acute Myeloid Leukemia	Acute Myeloid Leukemia	ai
ULBP2	NCT05734898	ULBP2	antigen recognition	NKG2D CAR-NK cells	CAR NK	Cellular Therapy	Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.	Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.	NKG2D CAR on NK cells binds ULBP2 on target cells, signaling via DAP10/CD3ζ to activate NK degranulation and kill targets through perforin/granzyme-mediated cytolysis (and death receptor pathways).	Acute Myeloid Leukemia	CANCER	Myeloid	Acute Myeloid Leukemia	Acute Myeloid Leukemia	ai
ULBP3	NCT05734898	ULBP3	antigen recognition	NKG2D CAR-NK cells	CAR NK	Cellular Therapy	Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.	Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.	NKG2D CAR-NK cells bind ULBP3 on target cells, signal via DAP10/CD3ζ, and kill through NK degranulation (perforin/granzyme-mediated cytolysis; may also engage death receptor pathways).	Acute Myeloid Leukemia	CANCER	Myeloid	Acute Myeloid Leukemia	Acute Myeloid Leukemia	ai