544-31-0 Usage
Description
Palmitoylethanolamide (PEA) is a fatty acid amide produced in the body that binds to and activates the peroxisome proliferator-activated receptor alpha (PPAR-α). It was initially described as an agonist to the type 2 cannabinoid receptor (CB2), though it is now recognized that PEA does not bind to cannabinoid receptors. PEA is known to have anti-inflammatory, analgesic, and neuroprotective properties. PEA supplements have been used by people with chronic pain as well as those with neuropathic pain.
Chemical Properties
Palmitoylethanolamide is a natural occurring lipid belonging to the class of autacoids. It is a fine white to yellow powder. PEA consists of palmitic acid and ethanolamine. It is the hydrolyzed form of N-(2-hydroxyethyl)-palmitamide, a crystalline structure isolated in soy lecithin. It is this hydrolyzed substance that accounts for the anti-inflammatory properties that were first noted by scientists in 1957. PEA's effects on the immune system have been studied since 1939.
Uses
Palmitoylethanolamide is a natural substance produced by the body and it is very effective and safe to use as a supplement for pain and reduce inflammation.PEA can be synthesized within the human body from the abundant fatty acid palmitic acid, but it is not dependent or influenced by dietary consumption of fatty acids. Palmitic acid in the diet is derived from dairy products such as cheese and butter, palm tree oil, and animal meat products. However, increasing palmitic acid in the hope of increasing endogenous PEA synthesis will not be effective.The anti-inflammatory properties of PEA are due to its ability to inhibit inflammation-causing proteins called cytokines. Cytokines are released during periods of inflammation. PEA can suppress the secretion of tumor necrosis factor alpha (TNF alpha), a cytokine, while also inhibiting the release of interleukins. Interleukins are a specific class of cytokines which belong in the immunological system and are activated during the process of inflammation.Chronic Pain and the Use of Palmitoylethanolamide: An Update
Definition
ChEBI: Palmitoylethanolamide is an N-(long-chain-acyl)ethanolamine that is the ethanolamide of palmitic (hexadecanoic) acid. It has a role as an anti-inflammatory drug, an antihypertensive agent, a neuroprotective agent and an anticonvulsant. It is a N-(long-chain-acyl)ethanolamine, an endocannabinoid and a N-(saturated fatty acyl)ethanolamine. It is functionally related to a hexadecanoic acid.
Biological Functions
Palmitoylethanolamide (PEA) is a fatty acid amide molecule involved in a variety of cellular functions in chronic pain and inflammation. It has been shown to have neuroprotective, anti-inflammatory, anti-nociceptive (antipain) and anti-convulsant properties. Often in people with chronic disorders, the body does not produce enough PEA, which causes problems.Taking PEA to supplement the body’s shortage is may be beneficial if you have chronic and neuropathic pain and inflammation, as has been demonstrated in clinical trials. These include peripheral neuropathies such as diabetic neuropathy, chemotherapy-induced peripheral neuropathy, carpal tunnel syndrome, sciatic pain, osteoarthritis, low-back pain, failed back surgery syndrome, dental pains, neuropathic pain in stroke and multiple sclerosis, chronic regional pain syndrome, chronic pelvic pain, postherpetic neuralgia, and vaginal pains.
Flammability and Explosibility
Notclassified
Biological Activity
Palmitoylethanolamide (PEA) is a natural fatty acid amide of ethanolamine and palmitic acid. It is found in soybeans, egg yolk, and many other food sources. PEA is an endogenous cannabinoid receptor agonist. It is a peroxisome proliferator-activated receptor α (PPAR-α) ligand. PEA possesses anti-inflammatory, anti-allergic, neuroprotective, and analgesic activities. It belongs to the class of lipid mediators and the N-acylethanolamine family. PEA blocks the release of pro-inflammatory mediators from activated mast cells and prevents the recruitment of activated mast cells at the site of nerve injury.
Side effects
Different sources of media describe the Side effects of 544-31-0 differently. You can refer to the following data:
1. There are no known problematic side-effects. PEA can be taken together with any other substance. It enhances the pain-relieving effect of classic analgesics and anti-inflammatories. Palmitoylethanolamide can be used in combination with other substances without any side effects.ARE THERE ANY SIDE EFFECTS
2. There are no known problematic side-effects. PEA can be taken together with any other substance. It enhances the pain-relieving effect of classic analgesics and anti-inflammatories. Palmitoylethanolamide can be used in combination with other substances without any side effects.
Check Digit Verification of cas no
The CAS Registry Mumber 544-31-0 includes 6 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 3 digits, 5,4 and 4 respectively; the second part has 2 digits, 3 and 1 respectively.
Calculate Digit Verification of CAS Registry Number 544-31:
(5*5)+(4*4)+(3*4)+(2*3)+(1*1)=60
60 % 10 = 0
So 544-31-0 is a valid CAS Registry Number.
InChI:InChI=1/C18H37NO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-18(21)19-16-17-20/h20H,2-17H2,1H3,(H,19,21)
544-31-0Relevant articles and documents
Anandamide inhibits nuclear factor-κB activation through a cannabinoid receptor-independent pathway
Sancho, Rocio,Calzado, Marco A.,Di Marzo, Vincenzo,Appendino, Giovanni,Munoz, Eduardo
, p. 429 - 438 (2003)
Anandamide (arachidonoylethanolamine, AEA), an endogenous agonist for both the cannabinoid CB, receptor and the vanilloid VR1 receptor, elicits neurobehavioral, anti-inflammatory, immunomodulatory, and proapoptotic effects. Because of the central role of nuclear factor-κB (NF-κB) in the inflammatory process and the immune response, we postulated that AEA might owe some of its effects to the suppression of NF-κB. This study shows that AEA inhibits tumor necrosis factor-α (TNFα)-induced NF-κB activation by direct inhibition of the IκB kinase (IKK)β and, to a lesser extent, the IKKα subunits of κB inhibitor (IκB) kinase complex, and that IKKs inhibition by AEA correlates with inhibition of IκBα degradation, NF-κB binding to DNA, and NF-κB-dependent transcription in TNFα-stimulated cells. AEA also prevents NF-κB-dependent reporter gene expression induced by mitogen-activated protein kinase kinase kinase and NF-κB-inducing kinase. The NF-κB inhibitory activity of AEA was independent of CB1 and CB2 activation in TNFα-stimulated 5.1 and A549 cell lines, which do not express vanilloid receptor 1, and was not mediated by hydrolytic products formed through the activity of the enzyme fatty acid amide hydrolase. Chemical modification markedly affected AEA inhibitory activity on NF-κB, suggesting rather narrow structure-activity relationships and the specific interaction with a molecular target. Substitution of the alkyl moiety with less saturated fatty acids generally reduced or abolished activity. However, replacement of the ethanolamine "head" with a vanillyl group led to potent inhibition of TNFα-induced NF-κB-dependent transcription. These findings provide new mechanistic insights into the anti-inflammatory and proapoptotic activities of AEA, and should foster the synthesis of improved analogs amenable to pharmaceutical development as anti-inflammatory agents.
Different roles for the acyl chain and the amine leaving group in the substrate selectivity of N-Acylethanolamine acid amidase
Ghidini, Andrea,Scalvini, Laura,Palese, Francesca,Lodola, Alessio,Mor, Marco,Piomelli, Daniele
, p. 1411 - 1423 (2021/07/17)
N-acylethanolamine acid amidase (NAAA) is an N-terminal nucleophile (Ntn) hydrolase that catalyses the intracellular deactivation of the endogenous analgesic and anti-inflammatory agent palmitoylethanolamide (PEA). NAAA inhibitors counteract this process and exert marked therapeutic effects in animal models of pain, inflammation and neurodegeneration. While it is known that NAAA preferentially hydrolyses saturated fatty acid ethanolamides (FAEs), a detailed profile of the relationship between catalytic efficiency and fatty acid-chain length is still lacking. In this report, we combined enzymatic and molecular modelling approaches to determine the effects of acyl chain and polar head modifications on substrate recognition and hydrolysis by NAAA. The results show that, in both saturated and monounsaturated FAEs, the catalytic efficiency is strictly dependent upon fatty acyl chain length, whereas there is a wider tolerance for modifications of the polar heads. This relationship reflects the relative stability of enzyme-substrate complexes in molecular dynamics simulations.
A catalyst-free, waste-less ethanol-based solvothermal synthesis of amides
Dalu, Francesca,Scorciapino, Mariano A.,Cara, Claudio,Luridiana, Alberto,Musinu, Anna,Casu, Mariano,Secci, Francesco,Cannas, Carla
supporting information, p. 375 - 381 (2018/02/07)
A green, one-pot approach based on the solvothermal amidation of carboxylic acids with amines has been developed for the synthesis of diverse aliphatic and aromatic amides. It does not require the use of catalysts or coupling reagents and it occurs in the presence of ethanol that has been proved to have a key role in the process. The proposed strategy is also extendable to biologically active amides and could represent a low-cost and waste-less alternative to the common synthetic pathways.
