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124011

Sigma-Aldrich

Akt Inhibitor IV

The Akt Inhibitor IV, also referenced under CAS 681281-88-9, controls the biological activity of Akt. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

Synonym(s):

Akt Inhibitor IV

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About This Item

Empirical Formula (Hill Notation):
C31H27IN4S
CAS Number:
681281-88-9
Molecular Weight:
614.54
MDL number:
MFCD00570739
UNSPSC Code:
12352200

Quality Level

100

Assay

≥98% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
desiccated (hygroscopic)
protect from light

color

yellow

solubility

DMSO: 5 mg/mL

shipped in

ambient

storage temp.

2-8°C

InChI

1S/C31H27N4S.HI/c1-3-34-28-22-23(31-32-26-16-10-11-17-29(26)36-31)18-19-27(28)35(25-14-8-5-9-15-25)30(34)20-21-33(2)24-12-6-4-7-13-24;/h4-22H,3H2,1-2H3;1H/q+1;/p-1

InChI key

NAYRELMNTQSBIN-UHFFFAOYSA-M

General description

A cell permeable and reversible benzimidazole compound that inhibits Akt phosphorylation/activation by targeting the ATP binding site of a kinase upstream of Akt, but downstream of PI 3-K. Shown to block Akt-mediated FOXO1a nuclear export (IC50 = 625 nM) and cell proliferation (IC50<1.25 M) in 786-O cells. Unlike phosphatidylinositol analog-based Akt inhibitors (Cat. Nos. 124005, 124008, 124009), this inhibitor does not affect PI3K. A 10 mM (1 mg/163 l) solution of Akt Inhibitor IV in DMSO is also available.
A cell-permeable and reversible benzimidazole compound that inhibits Akt phosphorylation/activation presumably by targeting the ATP binding site of a kinase upstream of Akt, but downstream of PI3-K. Shown to block Akt-mediated FOXO1a nuclear export (IC50 = 625 nM) and cell proliferation (IC50<1.25 µM) in 786-O cells. Unlike phosphatidylinositol analog-based Akt inhibitors (Cat. Nos. 124005, 124008, 124009), this inhibitor does not affect PI3-K.

Biochem/physiol Actions

Cell permeable: yes
Primary Target
Akt
Product does not compete with ATP.
Reversible: yes
Target IC50: 625 nM in blocking Akt-mediated FOXO1a nuclear export; <1.25 µM in blocking Akt-mediated cell proliferation in 786-O cells

Packaging

Packaged under inert gas

Warning

Toxicity: Standard Handling (A)

Reconstitution

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.

Other Notes

Kau, T.R., et al. 2003. Cancer Cell4, 463.



Selected Citations
Lee, J., et al. 2009. Cell Stem Cell5, 76.


Legal Information

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

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

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’.

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Bing Xu et al.
Frontiers in neuroscience, 14, 766-766 (2020-08-28)
Poor postoperative pain (POP) control increases perioperative morbidity, prolongs hospitalization days, and causes chronic pain. However, the specific mechanism(s) underlying POP is unclear and the identification of optimal perioperative treatment remains elusive. Akt and mammalian target of rapamycin (mTOR) are
Roshini Fernando et al.
Journal of immunology (Baltimore, Md. : 1950), 204(7), 1724-1735 (2020-02-23)
IL-23 and IL-12, two structurally related heterodimeric cytokines sharing a common subunit, divergently promote Th cell development and expansion. Both cytokines have been implicated in the pathogenesis of thyroid-associated ophthalmopathy (TAO), an autoimmune component of Graves disease. In TAO, CD34+
Yu-Ying Chao et al.
Journal of cellular physiology (2022-10-18)
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers because of its late diagnosis and chemoresistance. Primary cilia, the cellular antennae, are observed in most human cells to maintain development and differentiation. Primary cilia are gradually lost during
Bin Li et al.
The Journal of clinical endocrinology and metabolism, 99(9), 3363-3372 (2014-05-21)
TSH provokes expression of inflammatory genes in CD34(+) fibrocytes. These cells appear to infiltrate the orbit in Graves' disease (GD), where they putatively become the CD34(+) orbital fibroblast subset (GD-OF). This may have importance in solving the pathogenesis of thyroid-associated

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