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Documenti fondamentali

SML0382

Sigma-Aldrich

KU 0063794

≥98% (HPLC)

Sinonimo/i:

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

Formula empirica (notazione di Hill):
C25H31N5O4
Numero CAS:
Peso molecolare:
465.54
Numero MDL:
Codice UNSPSC:
12352200
ID PubChem:
NACRES:
NA.77

Livello qualitativo

Saggio

≥98% (HPLC)

Forma fisica

powder

Colore

white to beige

Solubilità

DMSO: >2 mg/mL (warmed)

Temperatura di conservazione

2-8°C

Stringa SMILE

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+
RFSMUFRPPYDYRD-CALCHBBNSA-N

Applicazioni

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)

Azioni biochim/fisiol

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.

Caratteristiche e vantaggi

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.

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


Certificati d'analisi (COA)

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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

Protocolli

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