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Submit ReviewCE3F4
Description: Noncompetitive Epac1 inhibitor
Chemical Name: 5,7-Dibromo-6-fluoro-3,4-dihydro-2-methyl-1(2H)-quinolinecarboxaldehyde
Purity: ≥98% (HPLC)
Biological Activity for CE3F4
CE3F4 is a noncompetitive Epac1 inhibitor. Blocks Epac-induced Rap activation and prevents isoprenaline-induced autophagy flux in cardiomyocytes. Has no effect on PKA activity in the presence of cAMP.
Compound Libraries for CE3F4
CE3F4 is also offered as part of the Tocriscreen 2.0 Max. Find out more about compound libraries available from Tocris.
Technical Data for CE3F4
| M. Wt | 351.01 |
| Formula | C11H10Br2FNO |
| Storage | Store at -20°C |
| Purity | ≥98% (HPLC) |
| CAS Number | 143703-25-7 |
| PubChem ID | 21781066 |
| InChI Key | ZZLQPWXVZCPUGC-UHFFFAOYSA-N |
| Smiles | BrC1=C(F)C(Br)=C(CCC(C)N2C=O)C2=C1 |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Product Datasheets for CE3F4
References for CE3F4
References are publications that support the biological activity of the product.
Laurent et al (2015) Exchange protein directly activated by cAMP 1 promotes autophagy during cardiomyocyte hypertrophy. Cardiovasc.Res. 105 55 PMID: 25411381
Courilleau et al (2012) Identification of a tetrahydroquinoline analog as a pharmacological inhibitor of the cAMP-binding protein Epac. J.Biol.Chem. 287 44192 PMID: 23139415
Chen et al (2022) The peripheral Epac1/p-Cav-1 pathway underlies the disruption of the vascular endothelial barrier following skin/muscle incision and retraction-induced chronic postsurgical pain. Ann.Transl.Med. 10 1377
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Keywords: CE3F4, CE3F4 supplier, noncompetitive, Epac1, inhibitors, inhibits, autophagy, Exchange, proteins, Rap, guanine, nucleotide, exchange, factor, 3, RAPGEF3, cAMP, GEFI, EPAC, 4793, Tocris Bioscience
4 Citations for CE3F4
Citations are publications that use Tocris products. Selected citations for CE3F4 include:
Chen et al (2022) The peripheral Epac1/p-Cav-1 pathway underlies the disruption of the vascular endothelial barrier following skin/muscle incision and retraction-induced chronic postsurgical pain. Ann.Trans.Med. 10 1377
Paul A et al (2020) Inhibition of IRF4 in dendritic cells by PRR-independent and -dependent signals inhibit Th2 and promote Th17 responses. Elife 9 PMID: 32014112
Jakobsen et al (2019) Soluble adenylyl cyclase-mediated cAMP signaling and the putative role of PKA and EPAC in cerebral mitochondrial function. J Neurosci Res 97 1018 PMID: 31172581
Derek C et al (2021) Regulation of Mitochondrial Function by Epac2 Contributes to Acute Inflammatory Hyperalgesia. J Neurosci 41 2883-2898 PMID: 33593853
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