Akt Inhibitor X

A cell-permeable, reversible, and selective inhibitor of the phosphorylation of Akt and its in vitro kinase activity (complete inhibition <5 M) with minimal effect on PI 3-K, PDK1, or SGK1. Shown to suppress growth of Rh (rhabdomyosarcoma) cell lines (IC₅₀ = 2-5 M), inhibit IGF-I-stimulated nuclear translocation of Akt, and prevent phosphorylation of the downstream targets, mTOR, p70S6 kinase, and S6 ribosomal protein. Unlike Akti1/2 (Cat. No. 124018), the mode of inhibition is not PH domain-dependent. Also shown to induce neuronal autophagy in an Akt- and mTOR-independent manner and enhances the clearance of misfolded protein. Also available as a 20 mM solution in H₂O(Cat. No. 124039).

A cell-permeable, reversible, and selective inhibitor of the phosphorylation of Akt and its in vitro kinase activity (complete inhibition <5 µM) with minimal effect on PI 3-K, PDK1, or SGK1. Shown to suppress growth of Rh (rhabdomyosarcoma) cell lines (IC₅₀ = 2-5 μM), inhibit IGF-I-stimulated nuclear translocation of Akt, and prevent phosphorylation of the downstream targets, mTOR, p70S6 kinase, and S6 ribosomal protein. Unlike Akti1/2 (Cat. No. 124018), the mode of inhibition is not PH domain-dependent. Also shown to induce neuronal autophagy in an Akt- and mTOR-independent manner and enhances the clearance of misfolded protein.

Cell permeable: yes

Primary Target
Akt

Product does not compete with ATP.

Reversible: yes

Secondary Target
Rn cell lines (IC₅₀ = 2-5 µM)

Target IC₅₀: <5 µM against Akt ; 2-5 µM against growth of Rh (rhabdomyosarcoma) cell lines

Packaged under inert gas

Toxicity: Irritant (B)

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Tsvetkov, A.S., et al. 2010. Proc. Natl. Acad. Sci. USAin press.
Thimmaiah, K.N., et al. 2005. J. Biol. Chem.280, 31924.

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