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SML0382

Sigma-Aldrich

KU 0063794

≥98% (HPLC)

Synonym(s):

rel-5-[2-[(2R,6S)-2,6-Dimethyl-4-morpholinyl]-4-(4-morp holinyl)pyrido[2,3-d]pyrimidin-7-yl]-2-methoxybenzenemethanol

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About This Item

Empirical Formula (Hill Notation):
C25H31N5O4
CAS Number:
938440-64-3
Molecular Weight:
465.54
MDL number:
MFCD11977741
UNSPSC Code:
12352200
PubChem Substance ID:
329825382
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: >2 mg/mL (warmed)

storage temp.

2-8°C

SMILES string

COc1ccc(cc1CO)-c2ccc3c(nc(nc3n2)N4C[C@H](C)O[C@H](C)C4)N5CCOCC5

InChI

1S/C25H31N5O4/c1-16-13-30(14-17(2)34-16)25-27-23-20(24(28-25)29-8-10-33-11-9-29)5-6-21(26-23)18-4-7-22(32-3)19(12-18)15-31/h4-7,12,16-17,31H,8-11,13-15H2,1-3H3/t16-,17+

InChI key

RFSMUFRPPYDYRD-CALCHBBNSA-N

Application

KU 0063794 has been used:
  • as a mammalian target of rapamycin (mTOR) inhibitor to study the effects of follicular stimulating hormone (FSH) in mTOR phosphorylation and vascular cell adhesion molecule-1 (VCAM-1) expression in human umbilical vascular endothelial cells (HUVECs)
  • as a mTOR inhibitor to treat effector memory (EM) CD8+ T cells for metabolic flux analysis
  • as an autophagy inducer to demonstrate the utility of p62 and LC3B-II quantification in HEK293T cells and primary cultures of rat neurons and astrocytes using time-resolved fluorescence resonance energy transfer (TR-FRET)

Biochem/physiol Actions

KU 0063794 induces autophagy. It is cell-permeant and suppresses activation and hydrophobic motif phosphorylation of protein kinase B (Akt), p70 ribosomal S6 kinase (S6K) and serum and glucocorticoid protein kinase (SGK).
KU 0063794 is a potent and selective inhibitor of mammalian target of rapamycin (mTOR) (IC50 ~10 nM for both mTORC1 and mTORC2) that inhibits both mTORC1 and mTORC2 in vitro and in vivo (IC50 ~10 nM for both mTORC1 and mTORC2). KU 0063794 does not significantly inhibit 76 other protein kinases tested as well as seven lipid kinases including PI3K and AKT.

Features and Benefits

This compound is featured on the PKB/Akt page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

Storage Class

11 - Combustible Solids

wgk_germany

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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Ku-0063794 is a specific inhibitor of the mammalian target of rapamycin (mTOR)
Garcaa-Martanez JM, et al.
The Biochemical Journal, 421(1), 29-42 (2009)
Follicular stimulating hormone accelerates atherogenesis by increasing endothelial VCAM-1 expression
Li X, et al.
Theranostics, 7(19), 4671-4671 (2017)
Fang Hao et al.
Molecular cancer research : MCR, 15(7), 929-941 (2017-04-01)
We examined the impact of crosstalk between the insulin receptor and G protein-coupled receptor (GPCR) signaling pathways on the regulation of Yes-associated protein (YAP) localization, phosphorylation, and transcriptional activity in the context of human pancreatic ductal adenocarcinoma (PDAC). Stimulation of
Eyal Amiel et al.
Journal of immunology (Baltimore, Md. : 1950), 193(6), 2821-2830 (2014-08-12)
TLR-mediated activation of dendritic cells (DCs) is associated with a metabolic transition in which mitochondrial oxidative phosphorylation is inhibited by endogenously synthesized NO and the cells become committed to glucose and aerobic glycolysis for survival. We show that inhibition of
Xiaosa Li et al.
Theranostics, 7(19), 4671-4688 (2017-12-01)
Rationale: Postmenopausal atherosclerosis (AS) has for decades been attributed to estrogen deficiency. Although the follicular stimulating hormone (FSH) levels rise sharply in parallel, the direct effect of FSH on AS has never been investigated. In this study, we explored the
View All Related Papers

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