Skip to Content
MilliporeSigma
All Photos(1)

Documents

124020

Sigma-Aldrich

Akt Inhibitor X

The Akt Inhibitor X, also referenced under CAS 925681-41-0, controls the biological activity of Akt. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

Synonym(s):

Akt Inhibitor X, 10-(4ʹ-(N-diethylamino)butyl)-2-chlorophenoxazine, HCl, 10-NCP

Sign Into View Organizational & Contract Pricing


About This Item

Empirical Formula (Hill Notation):
C20H25ClN2O · xHCl
CAS Number:
Molecular Weight:
344.88 (free base basis)
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

Assay

≥95% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
desiccated (hygroscopic)
protect from light

color

white

solubility

water: 1 mg/mL

shipped in

ambient

storage temp.

2-8°C

InChI

1S/C20H25ClN2O.ClH/c1-3-22(4-2)13-7-8-14-23-17-9-5-6-10-19(17)24-20-12-11-16(21)15-18(20)23;/h5-6,9-12,15H,3-4,7-8,13-14H2,1-2H3;1H

InChI key

SVKSJUIYYCQZEC-UHFFFAOYSA-N

General description

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.

Biochem/physiol Actions

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

Packaging

Packaged under inert gas

Warning

Toxicity: Irritant (B)

Reconstitution

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

Other Notes

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

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

11 - Combustible Solids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

Already Own This Product?

Find documentation for the products that you have recently purchased in the Document Library.

Visit the Document Library

Miji Jeon et al.
The Journal of biological chemistry, 298(3), 101675-101675 (2022-02-06)
A multienzyme metabolic assembly for human glucose metabolism, namely the glucosome, has been previously demonstrated to partition glucose flux between glycolysis and building block biosynthesis in an assembly size-dependent manner. Among three different sizes of glucosome assemblies, we have shown

Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.

Contact Technical Service