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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
ULBP4 NCT05858814 ULBP4 receptor ligand recognition RC1012 C189910 CULTURED CELLS Cellular Therapy Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse. Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse. RC1012 DNT cells express NKG2D and recognize ULBP4 (an NKG2D ligand) on target cells, triggering MHC-independent killing via perforin/granzyme-mediated cytolysis and IFN-γ release. Acute Myeloid Leukemia CANCER Myeloid Acute Myeloid Leukemia Acute Myeloid Leukemia ai
ULBP5 NCT05858814 ULBP5 receptor ligand recognition RC1012 C189910 CULTURED CELLS Cellular Therapy Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse. Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse. DNTs express NKG2D, which binds ULBP5 on target cells, activating cytotoxic granule release (perforin/granzymes) and inflammatory cytokines to lyse the target cell. Acute Myeloid Leukemia CANCER Myeloid Acute Myeloid Leukemia Acute Myeloid Leukemia ai
ULBP6 NCT05858814 ULBP6 receptor ligand recognition RC1012 C189910 CULTURED CELLS Cellular Therapy Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse. Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse. RC1012 DNT cells express NKG2D, which binds ULBP6 on target cells, triggering MHC-independent cytotoxicity via perforin/granzyme release (with IFN-γ) to lyse the target cells. Acute Myeloid Leukemia CANCER Myeloid Acute Myeloid Leukemia Acute Myeloid Leukemia ai
PVR NCT05858814 CD155 (PVR) receptor ligand recognition RC1012 C189910 CULTURED CELLS Cellular Therapy Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse. Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse. Allogeneic double‑negative T cells express DNAM‑1 (CD226) that binds CD155 (PVR) on target cells, triggering MHC‑independent cytotoxic degranulation (perforin/granzyme) and IFN‑γ release to kill the cells. Acute Myeloid Leukemia CANCER Myeloid Acute Myeloid Leukemia Acute Myeloid Leukemia ai
NECTIN2 NCT05858814 CD112 (NECTIN2) receptor ligand recognition RC1012 C189910 CULTURED CELLS Cellular Therapy Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse. Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse. Allogeneic double‑negative T cells express DNAM‑1 (CD226) and bind CD112 (NECTIN2) on target cells, triggering MHC‑independent cytotoxic degranulation (perforin/granzymes) and IFN‑γ release, leading to target cell lysis/apoptosis. Acute Myeloid Leukemia CANCER Myeloid Acute Myeloid Leukemia Acute Myeloid Leukemia ai
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