L-798,106 - CAS 244101-02-8
Category: Inhibitor
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Prostanoid Receptor
L-798,106 is a potent and highly selective prostanoid receptor EP3 antagonist wth Ki value of 0.3 nM. It is used in prostanoid receptor signaling studies that regulates the central excitatory effects of PGE(2) and COX-2 levels on PVN neurons. It has been used to tease out EP3 agonist activity both in vitro and in vivo. It successfully blocks the EP3 agonist activity of sulprostone on guinea pig vas deferens and trachea at 0.2 µM. It attenuates sulprostone-induced inhibition of EFS-evoked twitch and contractile responses in vivo.
≥99% by HPLC
L-798,106; L 798,106; L798,106. N-[(5-Bromo-2-methoxyphenyl)sulfonyl]-3-[2-(2-naphthalenylmethyl)phenyl]-2-propenamide; L-798106; (2E)-N-[(5-Bromo-2-methoxyphenyl)sulfonyl]-3-[2-(2-naphthalenylmethyl)phenyl]-2-propenamide; CM 9; GW 671021; (E)-N-(5-bromo-2-methoxyphenyl)sulfonyl-3-[2-(naphthalen-2-ylmethyl)phenyl]prop-2-enamide
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1.Cytosolic and Calcium-Independent Phospholipases A2 Activation and Prostaglandins E2 Are Associated with Escherichia coli-Induced Reduction of Insulin Secretion in INS-1E Cells.
Caporarello N;Salmeri M;Scalia M;Motta C;Parrino C;Frittitta L;Olivieri M;Cristaldi M;Avola R;Bramanti V;Toscano MA;Anfuso CD;Lupo G PLoS One. 2016 Sep 15;11(9):e0159874. doi: 10.1371/journal.pone.0159874. eCollection 2016.
It is suspected that microbial infections take part in the pathogenesis of diabetes mellitus type 1 (T1DM). Glucose-induced insulin secretion is accompanied by the release of free arachidonic acid (AA) mainly by cytosolic- and calcium independent phospholipases A2 (cPLA2 and iPLA2). Insulinoma cell line (INS-1E) was infected with E. coli isolated from the blood culture of a patient with sepsis. Invasion assay, Scanning Electron Microscopy and Transmission Electron Microscopy demonstrated the capacity of E. coli to enter cells, which was reduced by PLA2 inhibitors. Glucose-induced insulin secretion was significantly increased after acute infection (8h) but significantly decreased after chronic infection (72h). PLA2 activities, cPLA2, iPLA2, phospho-cPLA2, and COX-2 expressions were increased after acute and, even more, after chronic E. coli infection. The silencing of the two isoforms of PLA2s, with specific cPLA2- or iPLA2-siRNAs, reduced insulin secretion after acute infection and determined a rise in insulin release after chronic infection. Prostaglandins E2 (PGE2) production was significantly elevated in INS-1E after long-term E. coli infection and the restored insulin secretion in presence of L798106, a specific EP3 antagonist, and NS-398, a COX-2 inhibitor, and the reduction of insulin secretion in presence of sulprostone, a specific EP3 agonist, revealed their involvement in the effects triggered by bacterial infection.
2.Importance of adipocyte cyclooxygenase-2 and prostaglandin E2-prostaglandin E receptor 3 signaling in the development of obesity-induced adipose tissue inflammation and insulin resistance.
Chan PC;Hsiao FC;Chang HM;Wabitsch M;Hsieh PS FASEB J. 2016 Jun;30(6):2282-97. doi: 10.1096/fj.201500127. Epub 2016 Mar 1.
We examined the involvement of adipocyte cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2)-prostaglandin E receptor (EP)3-mediated signaling during hypertrophy and hypoxia in the development of obesity-associated adipose tissue (AT) inflammation and insulin resistance. The experiments were conducted with high-fat diet (HFD)-induced obese rats, db/db mice, human subjects, and 3T3-L1 and the human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes; the groups were treated with selective inhibitors of COX-2 [celecoxib 30 mg/kg, half maximal inhibitory concentration (IC50) ≈ 0.04 µM] and EP3 (L-798106 100 µg/kg, IC50 ≈ 0.5 µM) or a short interfering RNA. There were strong, positive correlations between adipocyte COX-2 and EP3 gene expressions and the AT TNF-α and monocyte chemotactic protein-1 contents and the homeostatic model assessment for insulin resistance in HFD-induced obese rats, as well as body mass index in human subjects. Treatment with COX-2 and EP3 inhibitors significantly reversed AT inflammatory gene and protein expressions (-50%) and impaired glucose and insulin tolerance in db/db mice. COX-2 inhibition diminished the chemotaxis of adipocytes isolated from HFD rats to macrophages and T cells.
3.The roles of prostaglandin EP 1 and 3 receptors in the control of human myometrial contractility.
Arulkumaran S;Kandola MK;Hoffman B;Hanyaloglu AC;Johnson MR;Bennett PR J Clin Endocrinol Metab. 2012 Feb;97(2):489-98. doi: 10.1210/jc.2011-1991. Epub 2011 Dec 7.
CONTEXT: ;Prostaglandins are central to the processes of human labor. Prostaglandin E(2) (PGE(2)) synthesized within the uterus mediates cervical ripening and uterine contractions. PGE receptors, EP1 and EP3, may each mediate contractions, and represent potential therapeutic targets in the management of preterm labor. Studies of the expression and function of EP1 and EP3 in pregnant myometrium are inconsistent.;OBJECTIVE: ;The objective of the study was to determine the relative importance of EP1 and EP3 in human myometrial contractility.;DESIGN: ;We studied the expression of EP1 and EP3 in upper- and lower-segment myometrium at term in vivo and the effects of specific inhibitors on contractions in vitro.;PATIENTS: ;Myometrial biopsies for both in vivo and in vitro studies were taken at cesarean section at term before or in labor in uncomplicated pregnancies.;RESULTS: ;We found no differences in the expression of EP1 or EP3 at mRNA or protein level between the upper and lower segment myometrium and no overall changes associated with the onset of labor. Upon labor, EP1, but not EP3, was found to relocalize to the nucleus. In studies of contractility, we found no differences in spontaneous or PGE(2)-induced contractility between the upper- and lower-segment samples.
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CAS 244101-02-8 L-798,106

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