N-palmitoylglycine
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N-palmitoylglycine

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N-palmitoylglycine contains a 16-carbon saturated fatty acid that is amide-linked to glycine and is structurally similar to the phospholipid-derived N-acyl ethanolamines. It inhibits heat-evoked firing of wide dynamic range (WDR) neurons, activates calcium influx in DRG cells and stimulates NO production.

Category
Other Unnatural Amino Acids
Catalog number
BAT-004274
CAS number
2441-41-0
Molecular Formula
C18H35NO3
Molecular Weight
313.50
N-palmitoylglycine
IUPAC Name
2-(hexadecanoylamino)acetic acid
Synonyms
palmitoyl glycine; PalGly; N-(1-Oxohexadecyl)Glycine; N-Ethanoyl-Hexadecanamide
Appearance
White to off-white powder
Purity
≥ 98% (HPLC)
Density
0.96 g/cm3
Melting Point
113-119 °C
Boiling Point
491.8°C
Storage
Store at -20°C
Solubility
Soluble in DMSO
InChI
InChI=1S/C18H35NO3/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-17(20)19-16-18(21)22/h2-16H2,1H3,(H,19,20)(H,21,22)
InChI Key
KVTFEOAKFFQCCX-UHFFFAOYSA-N
Canonical SMILES
CCCCCCCCCCCCCCCC(=O)NCC(=O)O
1. N-Palmitoylglycine and other N-acylamides activate the lipid receptor G2A/GPR132
Andrew J Brown,Mao Xiang Chen,Andrew J Irving,James R Foster,Simon J Dowell,Shohta Ueno,Jenni Harvey Pharmacol Res Perspect . 2019 Nov 21;7(6):e00542. doi: 10.1002/prp2.542.
The G-protein-coupled receptor GPR132, also known as G2A, is activated by 9-hydroxyoctadecadienoic acid (9-HODE) and other oxidized fatty acids. Other suggested GPR132 agonists including lysophosphatidylcholine (LPC) have not been readily reproduced. Here, we identifyN-acylamides in particularN-acylglycines, as lipid activators of GPR132 with comparable activity to 9-HODE. The order-of-potency isN-palmitoylglycine > 9-HODE ≈N-linoleoylglycine > linoleamide > N-oleoylglycine ≈N-stereoylglycine >N-arachidonoylglycine >N-docosehexanoylglycine. Physiological concentrations ofN-acylglycines in tissue are sufficient to activate GPR132.N-linoleoylglycine and 9-HODE also activate rat and mouse GPR132, despite limited sequence conservation to human. We describe pharmacological tools for GPR132, identified through drug screening. SKF-95667 is a novel GPR132 agonist. SB-583831 and SB-583355 are peptidomimetic molecules containing core amino acids (glycine and phenylalanine, respectively), and structurally related to previously described ligands. A telmisartan analog, GSK1820795A, antagonizes the actions ofN-acylamides at GPR132. The synthetic cannabinoid CP-55 940 also activates GPR132. Molecular docking to a homology model suggested a site for lipid binding, predicting the acyl side-chain to extend into the membrane bilayer between TM4 and TM5 of GPR132. Small-molecule ligands are envisaged to occupy a "classical" site encapsulated in the 7TM bundle. Structure-directed mutagenesis indicates a critical role for arginine at position 203 in transmembrane domain 5 to mediate GPR132 activation byN-acylamides. Our data suggest distinct modes of binding for small-molecule and lipid agonists to the GPR132 receptor. Antagonists, such as those described here, will be vital to understand the physiological role of this long-studied target.
2. Global metabolite profiling analysis of lipotoxicity in HER2/neu-positive breast cancer cells
Jason Wong,Douglas S Conklin,Jan Baumann,Yan Sun,Rakshika Balasubramaniyam,Mostafa Kokabee Oncotarget . 2018 Jun 5;9(43):27133-27150. doi: 10.18632/oncotarget.25500.
Recent work has shown that HER2/neu-positive breast cancer cells rely on a unique Warburg-like metabolism for survival and aggressive behavior. These cells are dependent on fatty acid (FA) synthesis, show markedly increased levels of stored fats and disruption of the synthetic process results in apoptosis. In this study, we used global metabolite profiling and a multi-omics network analysis approach to model the metabolic changes in this physiology under palmitate-supplemented growth conditions to gain insights into the molecular mechanism and its relevance to disease prevention and treatment. Computational analyses were used to define pathway enrichment based on the dataset of significantly altered metabolites and to integrate metabolomics and transcriptomics data in a multi-omics network analysis. Network-predicted changes and functional relationships were tested with cell assaysin vitro. Palmitate-supplemented growth conditions induce distinct metabolic alterations. Growth of HER2-normal MCF7 cells is unaffected under these conditions whereas HER2/neu-positive cells display unchanged neutral lipid content, AMPK activation, inhibition of fatty acid synthesis and significantly altered glutamine, glucose and serine/glycine metabolism. The predominant upregulated lipid species is the novel bioactive lipid N-palmitoylglycine, which is non-toxic to these cells. Limiting the availability of glutamine significantly ameliorates the lipotoxic effects of palmitate, reduces CHOP and XBP1(s) induction and restores the expression levels of HER2 and HER3. The study shows that HER2/neu-positive breast cancer cells change their metabolic phenotype in the presence of palmitate. Palmitate induces AMPK activation and inhibition of fatty acid synthesis that feeds back into glycolysis as well as anaplerotic glutamine metabolism.
3. [Pharmacologic profile of n-palmitoylglycine. Its effect on reserpine and haloperidol catalepsy]
A Vamvakidès Boll Chim Farm . 1995 May;134(5):258-62.
N-palmitoyl glycine (PG), synthesized by the mixed anhydrides method, displayed nootropic effects (in the "step-down" test) as well as an anti-immobility action in the forced swimming test, in mice. However no anticonvulsant effects were obtained, even at high dose (300 mg/Kg, po), in the maximal electroshock or against the convulsions induced by pentetrazol. In the study reported in this paper PG potentiated the reserpine or the haloperidol catalepsy in rats. The potentiation of the haloperidol catalepsy was antagonized by imipramine which displayed antiglutamatergic and antimuscarinic properties. On the other hand at 150 mg/Kg (ip), a dose which potentiated the haloperidol catalepsy, PG stimulated the dopaminergic function in the striatum. These results could therefore constitute a first clue suggesting a stimulation, by PG, of the cholinergic and GABAergic interneurons, by glycinergic potentiation of the NMDA receptors in the striatum.
4. Pre-Diagnostic Circulating Metabolites and Colorectal Cancer Risk in the Cancer Prevention Study-II Nutrition Cohort
Ying Wang,Peter T Campbell,Rebecca A Hodge,Marjorie L McCullough,Victoria L Stevens Metabolites . 2021 Mar 9;11(3):156. doi: 10.3390/metabo11030156.
Untargeted metabolomic studies have identified potential biomarkers of colorectal cancer risk, but evidence is still limited and broadly inconsistent. Among 39,239 Cancer Prevention Study II Nutrition cohort participants who provided a blood sample between 1998-2001, 517 newly diagnosed colorectal cancers were identified through 30 June 2015. In this nested case-control study, controls were matched 1:1 to cases on age, sex, race and date of blood draw. Mass spectroscopy-based metabolomic analyses of pre-diagnostic plasma identified 886 named metabolites, after quality control exclusions. Conditional logistic regression models estimated multivariable-adjusted odds ratios (OR) and 95% confidence intervals (CI) for 1 standard deviation (SD) increase in each metabolite with risk of colorectal cancer. Six metabolites were associated with colorectal cancer risk at a false discovery rate < 0.20. These metabolites were of several classes, including cofactors and vitamins, nucleotides, xenobiotics, lipids and amino acids. Five metabolites (guanidinoacetate, 2'-O-methylcytidine, vanillylmandelate, bilirubin (E,E) andN-palmitoylglycine) were positively associated (OR per 1 SD = 1.29 to 1.32), and one (3-methylxanthine) was inversely associated with CRC risk (OR = 0.79, 95% CI, 0.69-0.89). We did not replicate findings from two earlier prospective studies of 250 cases each after adjusting for multiple comparisons. Large pooled prospective analyses are warranted to confirm or refute these findings and to discover and replicate metabolites associated with colorectal cancer risk.
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