Target Search | CytoTargetDB

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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	NCT06389305	MICA	receptor ligand recognition	Cytokine-induced killer (CIK) cells	CULTURED CELLS	Cellular Therapy	Autologous/allogeneic CD3+CD56+ NKT-like effector cells expanded ex vivo; provide MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) and killing through perforin/granzyme and Fas/FasL; used to target B-ALL blasts and support persistence/function of prior CAR-T cells.	Ex vivo–expanded CD3+CD56+ cytokine-induced killer (CIK) cells exert MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) on leukemia cells, mediating killing through perforin/granzyme release and Fas/FasL interactions; they also produce cytokines and can support the persistence and function of previously infused CAR-T cells.	CIK cells recognize MICA via NKG2D, triggering cytotoxic degranulation (perforin/granzyme) and Fas–FasL–mediated apoptosis of target cells.	Refractory Acute Lymphoid Leukemia	CANCER	Lymphoid	B-Lymphoblastic Leukemia/Lymphoma	B-Lymphoblastic Leukemia/Lymphoma, NOS	ai
MICB	NCT06389305	MICB	receptor ligand recognition	Cytokine-induced killer (CIK) cells	CULTURED CELLS	Cellular Therapy	Autologous/allogeneic CD3+CD56+ NKT-like effector cells expanded ex vivo; provide MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) and killing through perforin/granzyme and Fas/FasL; used to target B-ALL blasts and support persistence/function of prior CAR-T cells.	Ex vivo–expanded CD3+CD56+ cytokine-induced killer (CIK) cells exert MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) on leukemia cells, mediating killing through perforin/granzyme release and Fas/FasL interactions; they also produce cytokines and can support the persistence and function of previously infused CAR-T cells.	CIK cells recognize MICB via NKG2D, triggering direct tumor cell killing through perforin/granzyme release and Fas–FasL–mediated apoptosis.	Refractory Acute Lymphoid Leukemia	CANCER	Lymphoid	B-Lymphoblastic Leukemia/Lymphoma	B-Lymphoblastic Leukemia/Lymphoma, NOS	ai
ULBP1	NCT06389305	ULBP1	receptor ligand recognition	Cytokine-induced killer (CIK) cells	CULTURED CELLS	Cellular Therapy	Autologous/allogeneic CD3+CD56+ NKT-like effector cells expanded ex vivo; provide MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) and killing through perforin/granzyme and Fas/FasL; used to target B-ALL blasts and support persistence/function of prior CAR-T cells.	Ex vivo–expanded CD3+CD56+ cytokine-induced killer (CIK) cells exert MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) on leukemia cells, mediating killing through perforin/granzyme release and Fas/FasL interactions; they also produce cytokines and can support the persistence and function of previously infused CAR-T cells.	CIK cells recognize ULBP1 via NKG2D in an MHC-unrestricted manner, triggering cytotoxic granule (perforin/granzyme) release and Fas/FasL-mediated apoptosis of target cells.	Refractory Acute Lymphoid Leukemia	CANCER	Lymphoid	B-Lymphoblastic Leukemia/Lymphoma	B-Lymphoblastic Leukemia/Lymphoma, NOS	ai
ULBP2	NCT06389305	ULBP2	receptor ligand recognition	Cytokine-induced killer (CIK) cells	CULTURED CELLS	Cellular Therapy	Autologous/allogeneic CD3+CD56+ NKT-like effector cells expanded ex vivo; provide MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) and killing through perforin/granzyme and Fas/FasL; used to target B-ALL blasts and support persistence/function of prior CAR-T cells.	Ex vivo–expanded CD3+CD56+ cytokine-induced killer (CIK) cells exert MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) on leukemia cells, mediating killing through perforin/granzyme release and Fas/FasL interactions; they also produce cytokines and can support the persistence and function of previously infused CAR-T cells.	CIK cells express NKG2D, which binds ULBP2 on target cells and triggers cytotoxicity via perforin/granzyme release and Fas/FasL-mediated apoptosis.	Refractory Acute Lymphoid Leukemia	CANCER	Lymphoid	B-Lymphoblastic Leukemia/Lymphoma	B-Lymphoblastic Leukemia/Lymphoma, NOS	ai
ULBP3	NCT06389305	ULBP3	receptor ligand recognition	Cytokine-induced killer (CIK) cells	CULTURED CELLS	Cellular Therapy	Autologous/allogeneic CD3+CD56+ NKT-like effector cells expanded ex vivo; provide MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) and killing through perforin/granzyme and Fas/FasL; used to target B-ALL blasts and support persistence/function of prior CAR-T cells.	Ex vivo–expanded CD3+CD56+ cytokine-induced killer (CIK) cells exert MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) on leukemia cells, mediating killing through perforin/granzyme release and Fas/FasL interactions; they also produce cytokines and can support the persistence and function of previously infused CAR-T cells.	CIK cells express NKG2D, which binds ULBP3 on target cells, activating cytotoxicity via perforin/granzyme release and Fas/FasL-mediated apoptosis.	Refractory Acute Lymphoid Leukemia	CANCER	Lymphoid	B-Lymphoblastic Leukemia/Lymphoma	B-Lymphoblastic Leukemia/Lymphoma, NOS	ai