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527450

Sigma-Aldrich

Imidazolo-oxindole PKR inhibitor C16

≥90% (HPLC), solid, PKR inhibitor, Calbiochem®

Synonyme(s) :

PKR Inhibitor, Double-stranded RNA-dependent Protein Kinase Inhibitor, C16, Double-stranded RNA-activated Protein Kinase Inhibitor I, EIF2AK2 Inhibitor I

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About This Item

Formule empirique (notation de Hill):
C13H8N4OS
Numéro CAS:
608512-97-6
Poids moléculaire :
268.29
Numéro MDL:
MFCD06735404
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77

product name

PKR Inhibitor, The PKR Inhibitor, also referenced under CAS 608512-97-6, controls the biological activity of PKR. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

Niveau de qualité

100

Pureté

≥90% (HPLC)

Forme

solid

Fabricant/nom de marque

Calbiochem®

Conditions de stockage

OK to freeze
protect from light

Couleur

orange to orange-brown

Solubilité

DMSO: 5 mg/mL

Conditions d'expédition

ambient

Température de stockage

2-8°C

InChI

1S/C13H8N4OS/c18-13-8(3-7-4-14-5-15-7)11-9(17-13)1-2-10-12(11)19-6-16-10/h1-6H,(H,14,15)(H,17,18)/b8-3-

Clé InChI

VFBGXTUGODTSPK-BAQGIRSFSA-N

Description générale

An imidazolo-oxindole compound that acts as a potent, ATP-binding site directed inhibitor of PKR. Shown to effectively inhibit RNA-induced PKR autophosphorylation (IC50 = 210 nM) and rescue PKR-dependent translation block (IC50 = 100 nM). Inactive control is also available (Cat. No. 527455). Shown to increase the late phase of long-lasting synaptic potentiation, and enhance long-term memory in mice. Also available as a 50 mM solution in DMSO (Cat. No. 527451).
An imidazolo-oxindole compound that acts as a potent, ATP-binding site directed inhibitor of PKR. Shown to effectively inhibit RNA-induced PKR autophosphorylation (IC50 = 210 nM) and rescue PKR-dependent translation block (IC50 = 100 nM). Shown to increase the late phase of long-lasting synaptic potentiation, and enhance long-term memory in mice. Inactive control is also available (Cat. No. 527455).

Actions biochimiques/physiologiques

Cell permeable: no
Primary Target
PKR
Product does not compete with ATP.
Reversible: no
Target IC50: 210 nM inhibiting RNA-induced PKR autophosphorylation and 100 nM in rescuing PKR-dependent translation block

Conditionnement

Packaged under inert gas

Avertissement

Toxicity: Carcinogenic / Teratogenic (D)

Reconstitution

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Autres remarques

Zhu, P.J., et al. 2011. Cell147, 1384.
Jammi, N.V., et al. 2003. Biochem. Biophys. Res. Commun.308, 50.

Informations légales

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

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Lasse Reimer et al.
Brain pathology (Zurich, Switzerland), 31(1), 103-119 (2020-07-28)
Deposition of extensively hyperphosphorylated tau in specific brain cells is a clear pathological hallmark in Alzheimer's disease and a number of other neurodegenerative disorders, collectively termed the tauopathies. Furthermore, hyperphosphorylation of tau prevents it from fulfilling its physiological role as
Kenneth T Farabaugh et al.
eLife, 9 (2020-03-17)
The inability of cells to adapt to increased environmental tonicity can lead to inflammatory gene expression and pathogenesis. The Rel family of transcription factors TonEBP and NF-κB p65 play critical roles in the switch from osmoadaptive homeostasis to inflammation, respectively.
Sanket S Ponia et al.
Cell reports, 37(4), 109888-109888 (2021-10-28)
Dysregulated inflammation dominated by chemokine expression is a key feature of disease following infection with the globally important human pathogens Zika virus (ZIKV) and dengue virus, but a mechanistic understanding of how pro-inflammatory responses are initiated is lacking. Mitophagy is
Upayan Patra et al.
Oxidative medicine and cellular longevity, 2020, 7289120-7289120 (2020-04-24)
Eukaryotic cells adopt highly tuned stress response physiology under threats of exogenous stressors including viruses to maintain cellular homeostasis. Not surprisingly, avoidance of cellular stress response pathways is an essential facet of virus-induced obligatory host reprogramming to invoke a cellular

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