BRD0705 是一种有效的，具有旁系选择性和口服活性的 GSK3α 抑制剂，IC₅₀ 为 66 nM，K_d 为 4.8 μM。 BRD0705 与 GSK3β (IC₅₀ 为 515 nM) 相比，对 GSK3α 的选择性更高 (8 倍)。BRD0705 可用于急性髓细胞性白血病的研究。

BRD0705 is a potent, paralog selective and orally active GSK3α inhibitor with an IC 50 of 66 nM and a K d of 4.8 μM. BRD0705 displays increased selectivity for GSK3α (8-fold) versus GSK3β (IC 50 of 515 nM). BRD0705 can be used for acute myeloid leukemia (AML) research.

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GSK3α 66 nM (IC50) GSK3α 4.8 μM (Kd)

BRD0705 displays excellent selectivity in a penal of 311 kinases, the CDK family of kinases (CDK2, 3 and 5) are next most potently inhibits at values of 6.87 μM, 9.74 μM and 9.20 μM (87-fold, 123-fold and 116-fold selectivity relative to GSK3α).
BRD0705 (10-40 μM; 2-24 hours; U937 cells) treatment impairs GSK3α Tyr279 phosphorylation in a time-and concentration-dependent manner without affecting GSK3β Tyr216 phosphorylation.
Using a β-catenin dependent TCF/LEF luciferase reporter assay, the absence of β-catenin induced target activation after treatment with BRD0705 in AML cell lines.
BRD0705 impairs AML colony formation in all six tested cell lines, MOLM13, TF-1, U937, MV4-11, HL-60 and NB4, in a concentration-dependent manner, as opposed to BRD3731 which impairs colony formation in TF-1 while increasing colony forming ability in the MV4-11 cell line.

BRD0705 (30 mg/kg; oral gavage; twice daily; NSG mice) treatment impairs leukemia initiation and prolongs survival in AML mouse models. has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model:

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. Wagner FF, et al. Exploiting an Asp-Glu "switch" in glycogen synthase kinase 3 to design paralog-selective inhibitors for use in acute myeloid leukemia. Sci Transl Med. 2018 Mar 7;10(431). pii: eaam8460.

In Vitro: DMSO : 300 mg/mL (933.36 mM; Need ultrasonic)配制储备液