For research use only. Not for therapeutic Use.
EHT-5372（Cat No.:I006632）is a potent and selective small-molecule inhibitor of fibroblast growth factor receptor 4 (FGFR4). This compound plays a key role in modulating FGFR4 activity, making it valuable for cancer research, particularly in studies focusing on liver cancer and other FGFR4-driven tumors. Its specificity allows for the investigation of FGFR4’s function without significantly affecting other fibroblast growth factor receptors. EHT-5372’s potential in targeted cancer therapy research highlights its importance in advancing personalized medicine and understanding FGFR4-related signaling pathways.
| Catalog Number | I006632 |
| CAS Number | 1425945-63-6 |
| Synonyms | EHT-5372; EHT 5372; EHT5372.;methyl 9-((2,4-dichlorophenyl)amino)thiazolo[5,4-f]quinazoline-2-carbimidate |
| Molecular Formula | C17H11Cl2N5OS |
| Purity | ≥95% |
| Target | Cell Cycle/DNA Damage |
| Solubility | Soluble in DMSO |
| Storage | 0 - 4°C for short term or -20 °C for long term |
| IUPAC Name | methyl 9-(2,4-dichloroanilino)-[1,3]thiazolo[5,4-f]quinazoline-2-carboximidate |
| InChI | InChI=1S/C17H11Cl2N5OS/c1-25-15(20)17-24-12-5-4-11-13(14(12)26-17)16(22-7-21-11)23-10-3-2-8(18)6-9(10)19/h2-7,20H,1H3,(H,21,22,23) |
| InChIKey | QSGKPYRFWJINEH-UHFFFAOYSA-N |
| SMILES | COC(=N)C1=NC2=C(S1)C3=C(C=C2)N=CN=C3NC4=C(C=C(C=C4)Cl)Cl |
| Reference | 1:J Med Chem. 2016 Nov 23;59(22):10315-10321. Epub 2016 Nov 2. An Unusual Binding Model of the Methyl 9-Anilinothiazolo[5,4-f] quinazoline-2-carbimidates (EHT 1610 and EHT 5372) Confers High Selectivity for Dual-Specificity Tyrosine Phosphorylation-Regulated Kinases.Chaikuad A,Diharce J,Schröder M,Foucourt A,Leblond B,Casagrande AS,Désiré L,Bonnet P,Knapp S,Besson T, PMID: 27766861 DOI: 10.1021/acs.jmedchem.6b01083 </br><span>Abstract:</span> Methyl 9-anilinothiazolo[5,4-f]quinazoline-2-carbimidates 1 (EHT 5372) and 2 (EHT 1610) are strong inhibitors of DYRK/’s family kinases. The crystal structures of the complex revealed a noncanonical binding mode of compounds 1 and 2 in DYRK2, explaining the remarkable selectivity and potency of these inhibitors. The structural data and comparison presented here provide therefore a template for further improvement of this inhibitor class and for the development of novel inhibitors selectively targeting DYRK kinases. |
