For research use only. Not for therapeutic Use.
CE3F4 is a selective antagonist of exchange protein directly activated by cAMP (Epac1), with IC50s of 10.7 μM and 66 μM for Epac1 and Epac2(B), respectively.
CE3F4 is a selective antagonist of Epac1, with IC50s of 10.7 μM and 66 μM for Epac1 and Epac2(B), respectively. CE3F4 is more active on Epac1 than (S)-stereoisomer ((S)-CE3F4, IC50, 56 μM), but less active than (R)-CE3F4 (IC50, 5.8 μM). CE3F4 (50 μM) shows more inhibitory activities against GEF activity of Epac1, than that of Epac2(AB) or Epac2(B)[1]. CE3F4 reduces the exchange activity of Epac1 induced by 007, with IC50 of 23 ± 3 μM. CE3F4 (40 μM) specifically inhibits Epac1 guanine nucleotide exchange activity without interference with Rap1 activity or Epac1-Rap1 interaction. CE3F4 has no influence on PKA activity. CE3F4 (20 μM) inhibits Epac-induced Rap1 activation in living cultured HEK293 cells[2]. CE3F4 (20 μM) significantly inhibits the late phase of ERK activation stimulated by glucose in INS-1 cells[3].
CE3F4 (1-3 mg/kg; through a catheter in the internal jugular vein) inhibits atrial fibrillation (AF) and CE3F4 (3 mg/kg; i.v.) inhibits ventricular arrhythmias[4].
CE3F4 (10 mg/kg; i.v.) improves cardiac function after myocardial infarction in mice[5].
| Catalog Number | I011031 |
| CAS Number | 143703-25-7 |
| Synonyms | 5,7-dibromo-6-fluoro-2-methyl-3,4-dihydro-2H-quinoline-1-carbaldehyde |
| Molecular Formula | C11H10Br2FNO |
| Purity | ≥95% |
| InChI | InChI=1S/C11H10Br2FNO/c1-6-2-3-7-9(15(6)5-16)4-8(12)11(14)10(7)13/h4-6H,2-3H2,1H3 |
| InChIKey | ZZLQPWXVZCPUGC-UHFFFAOYSA-N |
| SMILES | CC1CCC2=C(C(=C(C=C2N1C=O)Br)F)Br |
| Reference | [1]. Courilleau D, et al. The (R)-enantiomer of CE3F4 is a preferential inhibitor of human exchange protein directly activated by cyclic AMP isoform 1 (Epac1). Biochem Biophys Res Commun. 2013 Oct 25;440(3):443-8. [2]. Courilleau D, et al. Identification of a tetrahydroquinoline analog as a pharmacological inhibitor of the cAMP-binding protein Epac. J Biol Chem. 2012 Dec 28;287(53):44192-202. [3]. Pratt EP, et al. Ca2+ influx through L-type Ca2+ channels and Ca2+-induced Ca2+ release regulate cAMP accumulation and Epac1-dependent ERK 1/2 activation in INS-1 cells. Mol Cell Endocrinol. 2016 Jan 5;419:60-71. [4]. Prajapati R, et al. Usefulness of Exchanged Protein Directly Activated by cAMP (Epac)1-Inhibiting Therapy for Prevention of Atrial and Ventricular Arrhythmias in Mice. Circ J. 2019;83(2):295-303. [5]. Abstract 17548: Inhibition of Exchange Protein 1 Directly Activated by cAMP (Epac1) is Cardioprotective Against Ischemia-reperfusion Injury |
