SML3279
BC-2059
≥98% (HPLC)
Sinónimos:
BC 2059, BC2059, Tegatrabetan, Tegavivint, rel-2,7-Bis[[(3R,5S)-3,5-dimethyl-1-piperidinyl]sulfonyl]-9,10-anthracenedione 9,10-dioxime
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About This Item
Fórmula empírica (notación de Hill):
C28H36N4O6S2
Número de CAS:
Peso molecular:
588.74
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77
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Quality Level
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
−20°C
Biochem/physiol Actions
BC-2059 is a cell penetrant, potent and selective inhibitor of the Wnt-signaling pathway that potently inhibits growth of cancer cell lines in vitro. BC-2059 inhibits β-catenin/transducin β-like 1 (TBL1) complex by direct binding to TBL1 complexed with β-catenin. BC-2059 does not inhibit interaction of TBL1 with either NCoR/SMRT or NFkB. It is a potential therapeutic for tumors with deregulated Wnt signaling pathway.
Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Dyana T Saenz et al.
Blood, 135(15), 1255-1269 (2020-02-19)
The promising activity of BET protein inhibitors (BETi's) is compromised by adaptive or innate resistance in acute myeloid leukemia (AML). Here, modeling of BETi-persister/resistance (BETi-P/R) in human postmyeloproliferative neoplasm (post-MPN) secondary AML (sAML) cells demonstrated accessible and active chromatin in
Raffaella Soldi et al.
The Journal of pharmacology and experimental therapeutics, 378(2), 77-86 (2021-05-20)
The central role of β-catenin in the Wnt pathway makes it an attractive therapeutic target for cancers driven by aberrant Wnt signaling. We recently developed a small-molecule inhibitor, BC-2059, that promotes apoptosis by disrupting the β-catenin/transducin β-like 1 (TBL1) complex
Dyana T Saenz et al.
Leukemia, 33(6), 1373-1386 (2018-12-24)
Transformation of post-myeloproliferative neoplasms into secondary (s) AML exhibit poor clinical outcome. In addition to increased JAK-STAT and PI3K-AKT signaling, post-MPN sAML blast progenitor cells (BPCs) demonstrate increased nuclear β-catenin levels and TCF7L2 (TCF4) transcriptional activity. Knockdown of β-catenin or
Dyana T Saenz et al.
Leukemia, 33(6), 1373-1386 (2018-12-24)
Transformation of post-myeloproliferative neoplasms into secondary (s) AML exhibit poor clinical outcome. In addition to increased JAK-STAT and PI3K-AKT signaling, post-MPN sAML blast progenitor cells (BPCs) demonstrate increased nuclear β-catenin levels and TCF7L2 (TCF4) transcriptional activity. Knockdown of β-catenin or
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