124008
Akt Inhibitor II
The Akt Inhibitor II controls the biological activity of Akt. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.
别名:
Akt Inhibitor II, SH-5
产品名称
Akt Inhibitor II, The Akt Inhibitor II controls the biological activity of Akt. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.
assay
≥98% (NMR)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
color
white
solubility
DMSO: 10 mg/mL
shipped in
ambient
storage temp.
−20°C
Quality Level
Biochem/physiol Actions
Cell permeable: yes
Primary Target
Akt
Akt
Product does not compete with ATP.
Reversible: yes
Disclaimer
Toxicity: Standard Handling (A)
General description
A cell permeable, reversible, and substrate competitive phosphatidylinositol analog that inhibits the activation of Akt and selected downstream substrates without affecting the phosphorylation of PDK-1 and other downstream kinases. Decreases phosphorylation of Akt without affecting the total Akt level. Reported to be a potent inducer of apoptosis and to selectively kill a variety of cancer cell lines expressing high levels of active Akt. When used at a concentration of 10 µM, it is reported to activate p38α/SAPK2α MAP kinase. At 10 µM it will also inhibit ~50% of PKA activity.
Other Notes
Gills, J.J., et al. 2007. J. Biol. Chem.in press.
Kozikowski, A.P., et al. 2003. J. Am. Chem. Soc.125, 1144.
Kozikowski, A.P., et al. 2003. J. Am. Chem. Soc.125, 1144.
Packaging
Packaged under inert gas
Preparation Note
Following reconstitution aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
存储类别
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Rakan Radi et al.
Antioxidants (Basel, Switzerland), 11(5) (2022-05-29)
The development of targeted therapies (BRAF/MEK inhibitors) and immunotherapy have had a major impact on the treatment of melanoma. However, the majority of patients with advanced melanomas succumb to their disease. The mechanisms of resistance to both targeted therapies and
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