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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
MICA NCT05858814 MICA 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 NKG2D; engagement with MICA on target cells triggers MHC-independent cytotoxic degranulation (perforin/granzyme) and IFN-gamma release, leading to tumor cell lysis. Acute Myeloid Leukemia CANCER Myeloid Acute Myeloid Leukemia Acute Myeloid Leukemia ai
MICB NCT05858814 MICB 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 NKG2D, which binds MICB (an NKG2D ligand) on target cells, triggering MHC-independent cytotoxicity via perforin/granzyme-mediated lysis and IFN-gamma release. Acute Myeloid Leukemia CANCER Myeloid Acute Myeloid Leukemia Acute Myeloid Leukemia ai
ULBP1 NCT05858814 ULBP1 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 (the drug) express NKG2D; binding to ULBP1 (an NKG2D ligand) on target cells triggers MHC-independent cytotoxic degranulation (perforin/granzyme) and cytokine release, leading to target cell lysis/apoptosis. Acute Myeloid Leukemia CANCER Myeloid Acute Myeloid Leukemia Acute Myeloid Leukemia ai
ULBP2 NCT05858814 ULBP2 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 allogeneic double-negative T cells express NKG2D; binding to ULBP2 (an NKG2D ligand) on target cells triggers MHC-independent cytotoxicity via perforin/granzyme release and IFN-gamma, leading to tumor cell lysis. Acute Myeloid Leukemia CANCER Myeloid Acute Myeloid Leukemia Acute Myeloid Leukemia ai
ULBP3 NCT05858814 ULBP3 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. NKG2D on the infused double‑negative T cells binds ULBP3 on target cells, triggering MHC‑independent cytotoxicity via perforin/granzyme release (and IFN‑γ), leading to target cell apoptosis/lysis. Acute Myeloid Leukemia CANCER Myeloid Acute Myeloid Leukemia Acute Myeloid Leukemia ai
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