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|Molecular Profile||Indication/Tumor Type||Response Type||Relevant Treatment Approaches||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|NRAS G12D||Advanced Solid Tumor||no benefit||NS1||Preclinical - Cell culture||Actionable||In a preclinical study, transformed cells expressing NRAS G12D did not respond to treatment with NS1 in culture, resulting in sustained downstream signaling and cell transformation (PMID: 27820802).||27820802|
|NRAS G12D||acute myeloid leukemia||sensitive||MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor||Binimetinib||Preclinical||Actionable||In a preclinical study, Binimetinib (MEK162) inhibited growth of acute myeloid leukemia cells that have been demonstrated to harbor NRAS G12D in culture and decreased disease burden in xenograft models with NRAS G12D (PMID: 24569456, PMID: 11238126).||24569456 11238126|
|NRAS G12D||acute myeloid leukemia||sensitive||MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PIK3CA inhibitor||Alpelisib + Binimetinib||Preclinical - Cell line xenograft||Actionable||In a preclinical study, the combination of Binimetinib (MEK162) and Alpelisib (BYL719) inhibited proliferation in a human acute myeloid leukemia (AML) cell line harboring NRAS G12D in culture, and decreased disease burden in xenograft models (PMID: 24569456).||24569456|
|NRAS G12D||ovarian cancer||predicted - resistant||BI-3406||Preclinical - Cell culture||Actionable||In a preclinical study, BI-3406 treatment failed to inhibit growth of ovarian cancer cells harboring NRAS G12D in culture (PMID: 32816843).||32816843|
|NRAS G12D||B-lymphoblastic leukemia/lymphoma with BCR-ABL1||predicted - sensitive||Anti-CD19 CAR T cells||Case Reports/Case Series||Actionable||In a clinical case study, an investigational CD19-directed CAR T cells therapy resulted in rapid elimination of leukemic cells, including a subclone harboring NRAS G12D, in a patient with relapsed Philadelphia chromosome (Ph)-like acute lymphoblastic leukemia, the NRAS G12D subclone remained undetectable at disease progression 6 weeks after treatment (PMID: 31905241).||31905241|
|NRAS G12D||colorectal cancer||predicted - sensitive||RAS Inhibitor (Pan)||GI-4000||Phase I||Actionable||In a Phase I trial, GI-4000 was well tolerated, induced immune response in 61.3% (19/31) of evaluable subjects, and resulted in stable disease as best response in 18% (6/33) of patients with advanced pancreatic or colorectal cancer harboring KRAS mutations, including KRAS G12C (n=3), KRAS G12D (n=6), KRAS G12V (n=8), KRAS Q61L (n=1), and NRAS G12D (n=1) in patients with colorectal cancer (PMID: 29528991).||29528991|
|NRAS G12D||Advanced Solid Tumor||sensitive||N-Arachidonoyl Dopamine||Preclinical - Cell culture||Actionable||In a preclinical study, N-Arachidonoyl Dopamine (NADA) disrupted NRAS protein membrane localization and decreased NRAS downstream signaling, and inhibited proliferation and induced cell death in transformed cells expressing NRAS G12D in culture (PMID: 27760835).||27760835|
|Clinical Trial||Phase||Therapies||Title||Recruitment Status||Covered Countries||Other Countries|
|NCT04853017||Phase Ib/II||ELI-002||A Study of ELI-002 in Subjects With KRAS Mutated Pancreatic Ductal Adenocarcinoma (PDAC) and Other Solid Tumor (AMPLIFY-201)||Recruiting|
|NCT03745326||Phase Ib/II||Aldesleukin + anti-KRAS G12D mTCR cells + Cyclophosphamide + Fludarabine||Administering Peripheral Blood Lymphocytes Transduced With a Murine T-Cell Receptor Recognizing the G12D Variant of Mutated RAS in HLA-A*11:01 Patients||Suspended|