beta-Catenin inhibitor BC2059 is efficacious as monotherapy or in combination withproteasome inhibitor bortezomib in multiple myeloma.
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β-Catenin (Armadillo in Drosophila) is a multitasking and evolutionary conserved molecule that in metazoans exerts a crucial role in a multitude of developmental and homeostatic processes. More specifically, β-catenin is an integral structural component of cadherin-based adherens junctions, and the key nuclear effector of canonical Wnt signalling in the nucleus[3]. BC2059 is a potent inhibitor of β-Catenin. BC2059 attenuates β-catenin levels, in both the cytoplasm and the nucleus, reducing the transcriptional activity of the TCF4/LEF complex and the expression of its target gene axin 2. Treatment of HMCL (human myeloma cell lines) with BC2059 inhibits proliferation and induces apoptosis in a dose-dependent manner. This is also observed in HMCL-stromal cell cocultures, mitigating the protective effect afforded by the stroma. Similarly, BC2059 induces apoptosis in primary multiple myeloma samples in vitro, causing minimal apoptosis on healthy peripheral blood mononuclear cells[4]. BC2059 treatment disrupted the binding of β-catenin with the scaffold protein transducin β-like 1 and proteasomal degradation and decline in the nuclear levels of β-catenin. BC2059 treatment dose-dependently induced apoptosis of cultured and primary AML BPCs (acute myeloid leukemia blast progenitor cells). Treatment with BC2059 also significantly improved the median survival of immune-depleted mice engrafted with either cultured or primary AML BPCs, exhibiting nuclear expression of β-catenin[5]. In xenograft models of human myelomatosis, BC2059 delayed tumor growth and prolonged survival with minor on-target side effects. These findings support further clinical evaluation of BC2059 for the treatment of multiple myeloma[4].
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