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About This Item
Empirical Formula (Hill Notation):
C27H22BrNO4S
CAS Number:
Molecular Weight:
536.44
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352204
MDL number:
Product Name
L-798106, ≥98% (HPLC)
InChI key
ODTKFNUPVBULRJ-NTCAYCPXSA-N
SMILES string
COc1ccc(Br)cc1S(=O)(=O)NC(=O)\C=C\c2ccccc2Cc3ccc4ccccc4c3
InChI
1S/C27H22BrNO4S/c1-33-25-14-13-24(28)18-26(25)34(31,32)29-27(30)15-12-21-7-3-5-9-23(21)17-19-10-11-20-6-2-4-8-22(20)16-19/h2-16,18H,17H2,1H3,(H,29,30)/b15-12+
assay
≥98% (HPLC)
form
powder
solubility
DMSO: >20 mg/mL
originator
Merck & Co., Inc., Kenilworth, NJ, U.S.
storage temp.
2-8°C
Quality Level
Application
L-798106, a selective prostanoid receptor EP3 antagonist, is used in prostanoid receptor signaling studies that regulate COX-2 levels and the central excitatory effects of PGE(2) on PVN neurons.
Biochem/physiol Actions
L-798106 is a potent, selective prostanoid receptor EP3-selective antagonists.
L-798106 was among the first prostanoid receptor EP3-selective antagonists. It has been used in multiple studies to tease out EP3 agonist activity, both in vitro and in vivo. It successfully blocks the actions of sulprostone, an EP3-selective agonist, and it helped show that the vascular contraction effect of PGE2 is due to its prostanoid EP3 agonist activity.
Features and Benefits
This compound was developed by Merck & Co., Inc., Kenilworth, NJ, U.S.. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.
hcodes
pcodes
Hazard Classifications
Aquatic Chronic 4
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Lixing Zhao et al.
Journal of periodontology, 84(12), 1847-1857 (2013-03-30)
During periodontitis and orthodontic tooth movement, periodontal vasculature is severely impaired, leading to a hypoxic microenvironment of periodontal cells. However, the impact of hypoxia on periodontal cells is poorly defined. The present study investigates responses of cocultured endothelial cells (ECs)
Alexis A Gonzalez et al.
American journal of physiology. Renal physiology, 313(4), F1038-F1049 (2017-07-14)
During the early phase of ANG II-dependent hypertension, tubular PGE
Shoujin Hao et al.
American journal of physiology. Renal physiology, 311(4), F822-F829 (2016-07-29)
The mechanisms by which prostanoids contribute to the maintenance of whole body water homeostasis are complex and not fully understood. The present study demonstrates that an EP3-dependent feedback mechanism contributes to the regulation of water homeostasis under high-salt conditions. Rats
Carlos P Vio et al.
American journal of physiology. Renal physiology, 303(3), F449-F457 (2012-05-25)
Cyclooxygenase-2 (COX-2) is constitutively expressed and highly regulated in the thick ascending limb (TAL). As COX-2 inhibitors (Coxibs) increase COX-2 expression, we tested the hypothesis that a negative feedback mechanism involving PGE(2) EP3 receptors regulates COX-2 expression in the TAL.
Samar Rezq et al.
The Journal of pharmacology and experimental therapeutics, 359(2), 290-299 (2016-08-31)
Whereas few studies have dealt with the central sympathoexcitatory action of the inflammatory prostanoid prostaglandin E2 (PGE2), there is no information on the expression and cardiovascular function of different PGE2 (EP) receptors in one of the major cardiovascular-regulating nuclei, the
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