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Merck
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Dokumente

C0993

Sigma-Aldrich

CGP 57380

≥98% (HPLC)

Synonym(e):

CGP57380, N3-(4-fluorophenyl)-1h-pyrazolo[3,4-d]pyrimidine-3,4-diamine

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About This Item

Empirische Formel (Hill-System):
C11H9FN6
CAS-Nummer:
522629-08-9
Molekulargewicht:
244.23
MDL-Nummer:
MFCD03861062
UNSPSC-Code:
12352200
PubChem Substanz-ID:
24724432
NACRES:
NA.77

Qualitätsniveau

100

Assay

≥98% (HPLC)

Form

powder

Farbe

white to beige

Löslichkeit

DMSO: 10 mg/mL, clear
H2O: <2 mg/mL

Lagertemp.

2-8°C

SMILES String

Nc1ncnc2[nH]nc(Nc3ccc(F)cc3)c12

InChI

1S/C11H9FN6/c12-6-1-3-7(4-2-6)16-11-8-9(13)14-5-15-10(8)17-18-11/h1-5H,(H4,13,14,15,16,17,18)

InChIKey

UQPMANVRZYYQMD-UHFFFAOYSA-N

Anwendung

CGP 57380 has been used:
  • as a mitogen-activated protein kinase-interacting kinase 1 (MNK1) inhibitor to investigate the role of Mnk1 on eukaryotic translation initiation factor 4F (eIF4F) assembly and Newcastle disease virus (NDV) replication in HeLa cells
  • as an MNK1 inhibitor to block eIF4 complex to evaluate the contribution of interferon (IFN-γ) translation during m157- transgenic (Tg) stimulation
  • as a β-catenin nuclear translocation inhibitor to analyze its effects on cytoplasmic and nuclear fractions of cells

Biochem./physiol. Wirkung

CGP 57380 is a β-catenin nuclear translocation inhibitor, which prevents the proliferation of several cancers. It enhances radiation-induced apoptosis in nasopharyngeal carcinoma (NPC). CGP 57380 upregulates β-catenin in the cytoplasm and inhibits epithelial-mesenchymal transition (EMT).
CGP 57380 is a cell-permeable selective inhibitor of mitogen-activated protein kinase-interacting kinase 1 (MNK1).

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Persönliche Schutzausrüstung

Eyeshields, Gloves, type N95 (US)

Analysenzertifikate (COA)

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Die Dokumentenbibliothek aufrufen

Michael Schümann et al.
Cancer research, 66(3), 1282-1288 (2006-02-03)
The Raf/mitogen-activated protein/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK signaling cascade enhances tumor cell proliferation in many cases. Here, we show that adenovirus type 5, a small DNA tumor virus used in experimental cancer therapy, strongly induces ERK phosphorylation during the
David Müller et al.
Translation (Austin, Tex.), 1(2), e25819-e25819 (2013-01-01)
In eukaryotes, mRNA translation is dependent on the cap-binding protein eIF4E. Through its simultaneous interaction with the mRNA cap structure and with the ribosome-associated eIF4G adaptor protein, eIF4E physically posits the ribosome at the 5' extremity of capped mRNA. eIF4E
W-C Huangfu et al.
Oncogene, 31(2), 161-172 (2011-06-15)
Interferon alpha (IFNα) is widely used for treatment of melanoma and certain other malignancies. This cytokine as well as the related IFNβ exerts potent anti-tumorigenic effects; however, their efficacy in patients is often suboptimal. Here, we report that inflammatory signaling
Jonathan B Bell et al.
Molecular cancer research : MCR, 16(1), 32-46 (2017-10-19)
Mesenchymal (MES) and proneural (PN) are two distinct glioma stem cell (GSC) populations that drive therapeutic resistance in glioblastoma (GBM). We screened a panel of 650 small molecules against patient-derived GBM cells to discover compounds targeting specific GBM subtypes. Arsenic
Weiyuan Wang et al.
Theranostics, 7(7), 2134-2149 (2017-06-29)
Nuclear localization of β-catenin is essential for the progression of various human cancers via transcriptional upregulation of downstream genes. The MAP kinase interacting serine/threonine kinase (MNK)-eukaryotic translation initiation factor 4E (eIF4E) axis has been reported to activate Wnt/β-catenin signaling, and
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