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AG-1478 (Tyrphostin AG-1478)

  Cat. No.:  DC1078   Featured
Chemical Structure
153436-53-4
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More than 5000 active chemicals with high quality for research!
Field of application
AG-1478 (Tyrphostin AG-1478) is a selective EGFR inhibitor with IC50 of 3 nM.
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 153436-53-4
Chemical Name: N-(3-Chlorophenyl)-6,7-dimethoxyquinazolin-4-amine
Synonyms: 4-Quinazolinamine,N-(3-chlorophenyl)-6,7-dimethoxy-;Tyrphostin AG 1478;AG 1478 HYDROCHLORIDE;AG1478;AG-1478;AG-1478 (Tyrphostin AG-1478);N-(3-chlorophenyl)-6,7-dimethoxy-4-Quinazolinamine;N-(3-chlorophenyl)-6,7-dimethoxyquinazolin-4-amine;Tyrphostin AG 1478 (AG 1478,NSC-693255);AG-1478 hydrochloride;NSC693255;Tyrphostin;Tyrphostin AG-1478;(3-Chlorophenyl)(6,7-dimethoxyquinazolin-4-yl)amine;AG1478HCl;AG-1478 (NSC-693255);4-(3-CHLOROANILINO)-6,7-DIMETHOXYQUINAZOLINE HCL;NSC 693255;Tyrphostin AG 1478, free base >99%;AG-1478, 97.5%, a selective EGFR inhibitor;4-(3-Chloroanilino)-6,7-dimethoxyquinazoline;AG 1478;4-Quinazolinamine, N-(3-chlorophenyl)-6,7-dimethoxy-;SUH0SEZ9HY;N-(3-chlorophenyl)-6,7-dimethoxy-quinazolin-4-amine;BRD6408;4-(3-Chloroanilino)-6,7-Dimethoxyquinazoline Hydrochloride
SMILES: ClC1=C([H])C([H])=C([H])C(=C1[H])N([H])C1C2=C([H])C(=C(C([H])=C2N=C([H])N=1)OC([H])([H])[H])OC([H])([H])[H]
Formula: C16H14ClN3O2
M.Wt: 315.7543
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: AG-1478 is a selective EGFR tyrosine kinase inhibitor with IC50 of 3 nM.
In Vivo: AG-1478 (AG1478) is irreversible for growth regulation of human lung (A549) and prostate (DU145) cancer cell lines, cultured in chemically defined DMEM/F12 medium. AG-1478 seems to be more effective at lower concentrations, but is unable to completely inhibit growth of A549 cells[1]. Inhibition of EGFR by specific tyrosine kinase inhibitor AG-1478 (AG1478) significantly decreases the angiotensin II-mediated synthesis of TGF-β and fibronectin by cardiac fibroblasts. EGFR is pharmacologically inhibited by small-molecule inhibitor AG-1478 with IC50 of 4 nM[2]. Both Polyfect (PF) and Superfect (SF) treatment lead to increased apoptosis in HEK 293 cells to a similar extent as assessed by flow cytometry. The antioxidant, tempol, significantly reduced dendrimer-mediated apoptosis for both PF and SF. AG-1478 (AG1478), at a 10-fold higher dose (100 μM) than used in signaling studies, is used as a positive control and significantly induced apoptosis in HEK 293 cells[3].
In Vitro: AG-1478 (AG1478) is irreversible for growth regulation of human lung (A549) and prostate (DU145) cancer cell lines, cultured in chemically defined DMEM/F12 medium. AG-1478 seems to be more effective at lower concentrations, but is unable to completely inhibit growth of A549 cells[1]. Inhibition of EGFR by specific tyrosine kinase inhibitor AG-1478 (AG1478) significantly decreases the angiotensin II-mediated synthesis of TGF-β and fibronectin by cardiac fibroblasts. EGFR is pharmacologically inhibited by small-molecule inhibitor AG-1478 with IC50 of 4 nM[2]. Both Polyfect (PF) and Superfect (SF) treatment lead to increased apoptosis in HEK 293 cells to a similar extent as assessed by flow cytometry. The antioxidant, tempol, significantly reduced dendrimer-mediated apoptosis for both PF and SF. AG-1478 (AG1478), at a 10-fold higher dose (100 μM) than used in signaling studies, is used as a positive control and significantly induced apoptosis in HEK 293 cells[3].
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
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