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FPA 124
本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。
FPA 124图片
CAS NO:902779-59-3
包装与价格：
包装价格(元)
1mg电议
5mg电议
10mg电议
25mg电议

产品介绍
FPA 124 是一种可渗透细胞的铜络合物，是一种选择性 Akt 抑制剂，IC50 为 0.1 μM。 FPA 124 与 pleckstrin 同源性 (PH) 和 Akt 的激酶结构域相互作用。 FPA 124 诱导细胞凋亡。
Cas No.902779-59-3
别名AKT抗化剂,Akt Inhibitor XI
化学名copper(II) (Z)-2-((4-oxo-4H-chromen-3-yl)methylene)hydrazinecarbimidothioate chloride hydrochloride
Canonical SMILESN=C([S-])N/N=C([H])\C1=COC2=CC=CC=C2C1=O.[Cl-].Cl.[Cu+2]
分子式C11H9Cl2CuN3O2S
分子量381.73
溶解度DMSO: 0.1 mg/ml
储存条件Store at -20℃
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

The kinase Akt (also known as protein kinase B or PKB) modulates cell proliferation, metabolism, and survival, as well as angiogenesis.[1],[2] Akt inhibitor XI is a cell-permeable, copper-containing 3-formylchromone derivative that inhibits Akt in an array of cancer cells (IC50s = 10-34 μM).[3] It also causes NF-κB inactivation in an orthotopic pancreatic tumor model using COLO 357 cells.3 Molecular modeling indicates that this inhibitor interacts with the pleckstrin homology and kinase domains of Akt. Akt inhibitor XI is commonly used in the range of 1-20 μM to assess the role of Akt in cellular responses.[4],[5],[6]

Reference:
[1]. Manning, B.D., and Cantley, L.C. AKT/PKB signaling: Navigating downstream. Cell 129(7), 1261-1274 (2007).
[2]. Yuan, T.L., and Cantley, L.C. PI3K pathway alterations in cancer: Variations on a theme. Oncogene 27(41), 5497-5510 (2008).
[3]. Barve, V., Ahmed, F., Adsule, S., et al. Synthesis, molecular characterization, and biological activity of novel synthetic derivatives of chromen-4-one in human cancer cells. Journal of Medicinal Chemistry 49(13), 3800-3808 (2006).
[4]. Frampton, G., Invernizzi, P., Bernuzzi, F., et al. Interleukin-6-driven progranulin expression increases cholangiocarcinoma growth by an Akt-dependent mechanism. Gut 61(2), 268-277 (2012).
[5]. Rybchyn, M.S., Slater, M., Conlgrave, A.D., et al. An Akt-dependent increase in canonical Wnt signaling and a decrease in sclerostin protein levels are involved in strontium ranelate-induced osteogenic effects in human osteoblasts. The Journal of Biological Chemisty 286(27), 23771-23779 (2011).
[6]. Zareen, N., Biswas, S.C., and Greene, L.A. A feed-forward loop involving Trib3, Akt and FoxO mediates death of NGF-deprived neurons. Cell Death and Differentiation 20(12), 1719-1730 (2013).