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    DRUG:

    E6201

    i
    Other names: E6201, E 6201
    Company:
    Eisai, JS InnoPharm, Strategia Therap
    Drug class:
    FLT3 inhibitor, MEK1 inhibitor, MEK2 inhibitor, ACVR1 inhibitor, MAP3K1 inhibitor
    Related drugs:
    3ms
    E6201 and Dabrafenib for the Treatment of Central Nervous System Metastases From BRAF V600 Mutated Metastatic Melanoma (clinicaltrials.gov)
    P1, N=25, Recruiting, Mayo Clinic | N=18 --> 25 | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2024 --> Dec 2025
    Enrollment change • Trial completion date • Trial primary completion date • Metastases
    |
    BRAF mutation • BRAF V600
    |
    Tafinlar (dabrafenib) • E6201
    2years
    A Phase 1, Multicenter, Open-Label, Dose-Escalation, Safety, Pharmacokinetic, and Pharmacodynamic Study of E6201 in Subjects With Advanced Solid Tumors (clinicaltrials.gov)
    P1, N=55, Completed, Eisai Inc. | Unknown status --> Completed
    Trial completion • Metastases
    |
    BRAF (B-raf proto-oncogene)
    |
    E6201
    over4years
    Mutant ACVR1 Arrests Glial Cell Differentiation to Drive Tumorigenesis in Pediatric Gliomas. (PubMed, Cancer Cell)
    Furthermore, we characterize E6201 as a dual inhibitor of ACVR1 and MEK1/2, and demonstrate its efficacy toward tumor cells in vivo. Collectively, our results describe an oncogenic mechanism of action for ACVR1 mutations, and suggest therapeutic strategies for DIPGs.
    Clinical • Journal
    |
    PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
    |
    PIK3CA mutation
    |
    E6201
    almost5years
    E6201, an intravenous MEK1 inhibitor, achieves an exceptional response in BRAF V600E-mutated metastatic malignant melanoma with brain metastases. (PubMed, Invest New Drugs)
    Correlative preclinical studies demonstrated broad activity for E6201 across BRAF V600E mutant melanoma cell lines and effective BBB penetration in vivo. Together, these results suggest that E6201 may represent a potential new treatment option for BRAF-mutant MM patients with BM.
    Journal • Tumor Mutational Burden
    |
    BRAF (B-raf proto-oncogene) • TMB (Tumor Mutational Burden)
    |
    BRAF V600
    |
    E6201
    almost5years
    The quiescent fraction of chronic myeloid leukemic stem cells depends on BMPR1B, Stat3 and BMP4-niche signals to persist in patients in remission. (PubMed, Haematologica)
    Moreover, while Jak2-inhibitors alone increased BMP4 production by mesenchymal cells, the addition of the newly described BMPR1B inhibitor (E6201) impaired BMP4-mediated production by stromal cells. Altogether, our data demonstrate that targeting both BMPR1B and Jak2/Stat3 efficiently impacts persisting and dormant leukemic stem cells hidden in their bone marrow microenvironment.
    Clinical • Journal
    |
    CD38 (CD38 Molecule) • CD34 (CD34 molecule)
    |
    E6201