420104
JAK3 Inhibitor II
The JAK3 Inhibitor II, also referenced under CAS 211555-04-3, controls the biological activity of JAK3. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.
Synonyme(s) :
JAK3 Inhibitor II, 4-[(3ʹ-Bromo-4ʹ-hydroxyphenyl)amino]-6,7-dimethoxyquinazoline, WHI-P154
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About This Item
Formule empirique (notation de Hill):
C16H14BrN3O3
Numéro CAS:
Poids moléculaire :
376.20
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77
Produits recommandés
Niveau de qualité
Pureté
≥97% (HPLC)
Forme
solid
Fabricant/nom de marque
Calbiochem®
Conditions de stockage
OK to freeze
protect from light
Couleur
pale yellow
Solubilité
DMSO: 100 mg/mL
Conditions d'expédition
ambient
Température de stockage
−20°C
InChI
1S/C16H14BrN3O3/c1-22-14-6-10-12(7-15(14)23-2)18-8-19-16(10)20-9-3-4-13(21)11(17)5-9/h3-8,21H,1-2H3,(H,18,19,20)
Clé InChI
CBIAKDAYHRWZCU-UHFFFAOYSA-N
Description générale
A potent, cell-permeable, reversible, ATP-competitive, and specific inhibitor of JAK3 (IC50 = 5.6 µM). Has no effect on either JAK1 or JAK2. Has also been shown to prevent the ionizing radiation-induced activation of c-Jun in DT-40 cells. Also acts as a potent inhibitor of glioblastoma cell adhesion and migration.
A potent, cell-permeable, reversible, ATP-competitive, and specific inhibitor of JAK3. Has no effect on either JAK1 or JAK2. Has also been shown to prevent the ionizing radiation-induced activation of c-jun in DT-40 cells.
Actions biochimiques/physiologiques
Cell permeable: yes
Primary Target
JAK-3
JAK-3
Product competes with ATP.
Reversible: yes
Target IC50: 5.6 µM against JAK3
Conditionnement
Packaged under inert gas
Avertissement
Toxicity: Standard Handling (A)
Reconstitution
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Autres remarques
Ghosh, S., et al. 2001. Acta Crystallogr. C.57, 76.
Sudbeck, E.A., et al. 1999. Clin. Cancer Res. 5, 1569.
Goodman, P.A., et al. 1998. J. Biol. Chem. 273, 17742.
Narla, R.K., et al. 1998. Clin Cancer Res.4, 2463.
Sudbeck, E.A., et al. 1999. Clin. Cancer Res. 5, 1569.
Goodman, P.A., et al. 1998. J. Biol. Chem. 273, 17742.
Narla, R.K., et al. 1998. Clin Cancer Res.4, 2463.
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
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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.
R K Narla et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 4(10), 2463-2471 (1998-10-31)
Glioblastoma multiforme is a highly invasive primary brain tumor with a disappointingly high local recurrence rate and mortality despite intensive multimodality treatment programs. Therefore, new agents that are capable of inhibiting the infiltration of normal brain parenchyma by glioblastoma cells
S Ghosh et al.
Acta crystallographica. Section C, Crystal structure communications, 57(Pt 1), 76-78 (2001-02-15)
The title compounds, C16H15BrN3(O3)(+).Cl(-).CH4O (WHI-P154) and C16H16N3(O3)(+).Cl(-) (WHI-P180), are potent inhibitors [WHI-P154 with IC50 = 5.6 microM and WHI-P180 with IC50 = 4.0 microM for epidermal growth factor receptor (EGFR) kinase inhibition] of the EGFR tyrosine kinase as well as
E A Sudbeck et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 5(6), 1569-1582 (1999-07-02)
A novel homology model of the kinase domain of Janus kinase (JAK) 3 was used for the structure-based design of dimethoxyquinazoline compounds with potent and specific inhibitory activity against JAK3. The active site of JAK3 in this homology model measures
P A Goodman et al.
The Journal of biological chemistry, 273(28), 17742-17748 (1998-07-04)
Exposure of B-lineage lymphoid cells to ionizing radiation induces an elevation of c-jun proto-oncogene mRNA levels. This signal is abrogated by protein-tyrosine kinase (PTK) inhibitors, indicating that activation of an as yet unidentified PTK is mandatory for radiation-induced c-jun expression.
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