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G1171

Sigma-Aldrich

Gö 6976

≥98% (HPLC), powder

Sinônimo(s):

12-(2-Cyanoethyl)-6,7,12,13-tetrahydro-13-methyl-5-oxo-5H-indolo[2,3-a]pyrrolo[3,4-c]carbazole, Go 6976

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About This Item

Fórmula empírica (Notação de Hill):
C24H18N4O
Número CAS:
136194-77-9
Peso molecular:
378.43
Número MDL:
MFCD00236434
Código UNSPSC:
12352200
ID de substância PubChem:
329799832

Ensaio

≥98% (HPLC)

Formulário

powder

cor

white

solubilidade

DMSO: >5 mg/mL

temperatura de armazenamento

−20°C

cadeia de caracteres SMILES

Cn1c2ccccc2c3c4C(=O)NCc4c5c6ccccc6n(CCC#N)c5c13

InChI

1S/C24H18N4O/c1-27-17-9-4-2-7-14(17)20-21-16(13-26-24(21)29)19-15-8-3-5-10-18(15)28(12-6-11-25)23(19)22(20)27/h2-5,7-10H,6,12-13H2,1H3,(H,26,29)

chave InChI

VWVYILCFSYNJHF-UHFFFAOYSA-N

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Aplicação

Gö 6976 has been used:
  • as an inhibitor of protein kinase C (PKC) in mammalian cell lines
  • as a PKCμ inhibitor in oocytes
  • as a PKC-α to test its effect on phosphorylation of protein kinase-B (Akt) and extracellular-signal-regulated kinase (ERK) levels

Ações bioquímicas/fisiológicas

Go¨6976 also acts as an effective inhibitor of protein kinase C isoform (PKCμ) and abolishes phorbol ester mediated potentiation in oocytes. It inhibits PKC α and β selectively. Go-6976 may also inhibit S6-kinase 1.
Gö 6976 is an inhibitor of protein kinase C (PKC) specific for α (IC50=2.3 nM) and β1 (IC50=6.2 nM) isozymes.

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Equipamento de proteção individual

Eyeshields, Gloves, type N95 (US)

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Certificados de análise (COA)

Lot/Batch Number
122M4710V
022M4702V
061M4721V
061M4702V
110M4710V

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Katherine A Robinson et al.
PloS one, 9(10), e108963-e108963 (2014-10-21)
Chronic hyperglycemia induces insulin resistance by mechanisms that are incompletely understood. One model of hyperglycemia-induced insulin resistance involves chronic preincubation of adipocytes in the presence of high glucose and low insulin concentrations. We have previously shown that the mTOR complex
Hairuo Wen et al.
Journal of neurochemistry, 108(2), 331-340 (2008-12-03)
The potentiation of P2X(1) receptor currents by phorbol ester (PMA) treatment and stimulation of mGluR1alpha receptors was sensitive to inhibition of novel forms of protein kinase C. Potentiation was also reduced by co-expression of an amino terminal P2X(1) receptor minigene.
Shaon Naskar et al.
PloS one, 9(8), e104711-e104711 (2014-08-15)
A cardiac hypertrophy is defined as an increase in heart mass which may either be beneficial (physiological hypertrophy) or detrimental (pathological hypertrophy). This study was undertaken to establish the role of different protein kinase-C (PKC) isoforms in the regulation of
Ho-June Lee et al.
Cancer discovery, 3(2), 168-181 (2012-12-12)
Approximately half of EGFR-mutant non-small cell lung cancer (NSCLC) patients treated with small-molecule EGFR kinase inhibitors develop drug resistance associated with the EGF receptor (EGFR) T790M "gatekeeper" substitution, prompting efforts to develop covalent EGFR inhibitors, which can effectively suppress EGFR
Jian Hong et al.
The Journal of clinical investigation, 122(6), 2165-2175 (2012-05-16)
Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies resistant to current chemotherapies or radiotherapies, which makes it urgent to identify new therapeutic targets for HCC. In this study, we found that checkpoint kinase 1 (CHK1) was frequently overexpressed
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