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	mRNA-modified CIK cells (mRNA-CIK)	OTHER ENGINEERED IMMUNE CELL	Cellular Therapy	CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.	mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.	CIK cells recognize MICA via NKG2D, triggering cytotoxic granule release (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	mRNA-modified CIK cells (mRNA-CIK)	OTHER ENGINEERED IMMUNE CELL	Cellular Therapy	CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.	mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.	CIK cells recognize MICB via NKG2D and directly kill target cells through perforin/granzyme-mediated lysis and Fas/FasL-induced apoptosis (MHC-unrestricted).	Refractory Acute Lymphoid Leukemia	CANCER	Lymphoid	B-Lymphoblastic Leukemia/Lymphoma	B-Lymphoblastic Leukemia/Lymphoma, NOS	ai
ULBP1	NCT06389305	ULBP1	receptor ligand recognition	mRNA-modified CIK cells (mRNA-CIK)	OTHER ENGINEERED IMMUNE CELL	Cellular Therapy	CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.	mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.	mRNA-CIK cells recognize ULBP1 via NKG2D and directly kill target cells through perforin/granzyme release and Fas–FasL signaling.	Refractory Acute Lymphoid Leukemia	CANCER	Lymphoid	B-Lymphoblastic Leukemia/Lymphoma	B-Lymphoblastic Leukemia/Lymphoma, NOS	ai
ULBP2	NCT06389305	ULBP2	receptor ligand recognition	mRNA-modified CIK cells (mRNA-CIK)	OTHER ENGINEERED IMMUNE CELL	Cellular Therapy	CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.	mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.	CIK cells recognize ULBP2 via NKG2D and directly kill target cells through perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.	Refractory Acute Lymphoid Leukemia	CANCER	Lymphoid	B-Lymphoblastic Leukemia/Lymphoma	B-Lymphoblastic Leukemia/Lymphoma, NOS	ai
ULBP3	NCT06389305	ULBP3	receptor ligand recognition	mRNA-modified CIK cells (mRNA-CIK)	OTHER ENGINEERED IMMUNE CELL	Cellular Therapy	CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.	mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.	NKG2D on mRNA-CIK cells recognizes ULBP3 on target cells, triggering 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