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Merck
CN

L4545

L-798106

≥98% (HPLC)

Synonym(s):

(2E)-N-[(5-bromo-2-methoxyphenyl)sulfonyl]-3-[2-(2-naphthalenylmethyl)phenyl]-2-propenamide

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About This Item

Empirical Formula (Hill Notation):
C27H22BrNO4S
CAS Number:
244101-02-8
Molecular Weight:
536.44
MDL number:
MFCD08272644
UNSPSC Code:
12352204
PubChem Substance ID:
329817411
NACRES:
NA.77

Key Documents

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Quality Level

100

Assay

≥98% (HPLC)

form

powder

solubility

DMSO: >20 mg/mL

originator

Merck & Co., Inc., Kenilworth, NJ, U.S.

storage temp.

2-8°C

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+

InChI key

ODTKFNUPVBULRJ-NTCAYCPXSA-N

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.

Hazard Statements

H413

Precautionary Statements

P273 - P501

Hazard Classifications

Aquatic Chronic 4

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

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Certificates of Analysis (COA)

Lot/Batch Number
0000211937
0000211937
0000163793
0000163794
0000163793

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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
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.
Gen-Lin He et al.
Journal of neuroinflammation, 13(1), 296-296 (2016-11-23)
Prostaglandin E2 (PGE2)-involved neuroinflammatory processes are prevalent in several neurological conditions and diseases. Amyloid burden is correlated with the activation of E-prostanoid (EP) 2 receptors by PGE2 in Alzheimer's disease. We previously demonstrated that electromagnetic field (EMF) exposure can induce
Huifeng Hao et al.
Arteriosclerosis, thrombosis, and vascular biology, 38(5), 1115-1124 (2018-03-31)
Deletion of mPGES-1 (microsomal prostaglandin E synthase-1)-an anti-inflammatory target alternative to COX (cyclooxygenase)-2-attenuates injury-induced neointima formation in mice. This is attributable to the augmented levels of PGI2 (prostacyclin)-a known restraint of the vascular response to injury, acting via IP (I
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