CC260 是一种选择性 PI5P4Kα 和 PI5P4Kβ 抑制剂，其 K_i 分别为 40 nM 和 30 nM。CC260 不抑制或弱抑制其他蛋白激酶，如 Plk1 和 RSK2。CC260 可用于细胞能量代谢、糖尿病和癌症研究。

CC260 is a selective PI5P4Kα and PI5P4Kβ inhibitor with K i s of 40 nM and 30 nM, respectively. CC260 does not inhibit or weakly inhibits other protein kinases, such as Plk1 and RSK2. CC260 can be used for cell energy metabolism, diabetes and cancer research.

Solid

Ki: 40 nM (PI5P4Kα) and 30 nM (PI5P4Kβ)

In cultured C2C12 myotubes, CC260 (20 μM) enhances Insulin-induced Akt phosphorylation at both Thr-308 and Ser-473 but suppresses S6K phosphorylation (Thr-389) by mTORC1.
CC260 (2.5 μM, 5 μM, 10 μM, 20 μM) significantly increases phosphorylation of acetyl-CoA carboxylase (ACC) in a dose-dependent manner.
CC260 treatment reduces the ability of BT474 cells to survive serum starvation, which could be rescued by expressing the PI5P4Kβ refractory mutant.
In BT474 cells, CC260 treatment causes an increase in glycolytic ATP production. has not independently confirmed the accuracy of these methods. They are for reference only.

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. Song Chen, et al. Pharmacological inhibition of PI5P4Kα/β disrupts cell energy metabolism and selectively kills p53-null tumor cells. Proc Natl Acad Sci U S A. 2021 May 25;118(21):e2002486118.

In Vitro: DMSO : 160 mg/mL (326.24 mM; Need ultrasonic)配制储备液