AG 1478 hydrochloride - CAS 170449-18-0
Catalog number: B0084-425374
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C16H14ClN3O2.HCl
Molecular Weight:
352.22
COA:
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Targets:
EGFR
Description:
The hydrochloride salt form of AG 1478, which has been found to be an epidermal growth factor receptor tyrosine kinase inhibitor.
Purity:
≥98% by HPLC
Appearance:
Cream Solid
Synonyms:
N-(3-Chlorophenyl)-6,7-dimethoxy-4-quinazolinanine hydrochloride
MSDS:
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InChIKey:
WDJDYIUSDDVWKB-UHFFFAOYSA-N
InChI:
InChI=1S/C16H14ClN3O2.ClH/c1-21-14-7-12-13(8-15(14)22-2)18-9-19-16(12)20-11-5-3-4-10(17)6-11;/h3-9H,1-2H3,(H,18,19,20);1H
Canonical SMILES:
COC1=C(C=C2C(=C1)C(=NC=N2)NC3=CC(=CC=C3)Cl)OC.Cl
1.Interleukin-1beta-induced mucin production in human airway epithelium is mediated by cyclooxygenase-2, prostaglandin E2 receptors, and cyclic AMP-protein kinase A signaling.
Gray T;Nettesheim P;Loftin C;Koo JS;Bonner J;Peddada S;Langenbach R Mol Pharmacol. 2004 Aug;66(2):337-46.
We reported recently that interleukin (IL)-1beta exposure resulted in a prolonged increase in MUC5AC mucin production in normal, well differentiated, human tracheobronchial epithelial (NHTBE) cell cultures, without significantly increasing MUC5AC mRNA (Am J Physiol 286:L320-L330, 2004). The goal of the present study was to elucidate the signaling pathways involved in IL-1beta-induced MUC5AC production. We found that IL-1beta increased cyclooxygenase-2 (COX-2) mRNA expression and prostaglandin (PG) E(2) production and that the COX-2 inhibitor celecoxib suppressed IL-1beta-induced MUC5AC production. Addition of exogenous PGE(2) to NHTBE cultures also increased MUC5AC production and IL-1beta-induced Muc5ac hypersecretion in tracheas from wild-type but not from COX-2-/- mice. NHTBE cells expressed all four E-prostanoid (EP) receptor subtypes and misoprostol, an EP2 and EP4 agonist, increased MUC5AC production, whereas sulprostone, an EP1 and EP3 agonist, did not. Furthermore, specific protein kinase A (PKA) inhibitors blocked IL-1beta and PGE(2)-induced MUC5AC production. However, neither inhibition of epidermal growth factor receptor (EGFR) activation with the tyrosine kinase inhibitor 4-(3-chloroanilino)-6,7-dimethoxyquinazoline HCl (AG-1478) or EGFR blocking antibody nor inhibition of extracellular signal-regulated kinase/P-38 mitogen activated protein kinases with specific inhibitors blocked IL-1beta stimulation of MUC5AC mucin production.
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CAS 170449-18-0 AG 1478 hydrochloride

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