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NIKKOL PMEA (PALMITAMIDE MEA)

NIKKOL PMEA (PALMITAMIDE MEA) is a fatty acid amide produced in the body that binds to and activates the peroxisome proliferator-activated receptor alpha (PPAR-α). 
NIKKOL PMEA (PALMITAMIDE MEA) 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. 
NIKKOL PMEA (PALMITAMIDE MEA) is known to have anti-inflammatory, analgesic, and neuroprotective properties. 

CAS:    544-31-0
MF:    C18H37NO2
MW:    299.49
EINECS:    208-867-9

Synonyms
N-(2-HYDROXYETHYL)HEXADECANAMIDE;N-HEXADECANOYLETHANOLAMINE;PEA PALMIDROL;PALMITYLETHANOLAMIDE;PALMITOYLETHANOLAMIDE;PALMITOYLETHANOLAMIDE N-(2-HYDROXYETHYL)HEXADECANAMIDE;n-(2-hydroxyethyl)-hexadecanamid;Palmidrol

NIKKOL PMEA (PALMITAMIDE MEA) supplements have been used by people with chronic pain as well as those with neuropathic pain.
NIKKOL PMEA (PALMITAMIDE MEA) is an N-(long-chain-acyl)ethanolamine that is the ethanolamide of palmitic (hexadecanoic) acid. 
NIKKOL PMEA (PALMITAMIDE MEA) has a role as an anti-inflammatory drug, an antihypertensive agent, a neuroprotective agent and an anticonvulsant. 
NIKKOL PMEA (PALMITAMIDE MEA) is a N-(long-chain-acyl)ethanolamine, an endocannabinoid and a N-(saturated fatty acyl)ethanolamine. 
NIKKOL PMEA (PALMITAMIDE MEA) is functionally related to a hexadecanoic acid.

NIKKOL PMEA (PALMITAMIDE MEA) is a fatty acid amide molecule involved in a variety of cellular functions in chronic pain and inflammation. 
NIKKOL PMEA (PALMITAMIDE MEA) 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 NIKKOL PMEA (PALMITAMIDE MEA) 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.

NIKKOL PMEA (PALMITAMIDE MEA) is a naturally occurring fatty acid amide, specifically an N-acyl ethanolamine, that is derived from palmitic acid. 
NIKKOL PMEA (PALMITAMIDE MEA) is characterized by its role as an endogenous lipid mediator, primarily involved in modulating pain and inflammation. 
NIKKOL PMEA (PALMITAMIDE MEA) exhibits anti-inflammatory, analgesic, and neuroprotective properties, making it a subject of interest in various therapeutic applications. 
NIKKOL PMEA (PALMITAMIDE MEA) is soluble in lipids and has low solubility in water, which influences its bioavailability and pharmacokinetics. 
NIKKOL PMEA (PALMITAMIDE MEA) interacts with the endocannabinoid system, particularly by influencing the activity of cannabinoid receptors and other receptors such as TRPV1, contributing to its effects on pain perception and inflammation. 
Additionally, NIKKOL PMEA (PALMITAMIDE MEA) is considered safe for use, with a favorable side effect profile, and is often explored in dietary supplements and alternative medicine for conditions like chronic pain and neuropathic disorders. 
NIKKOL PMEA (PALMITAMIDE MEA)'s CAS number, 544-31-0, is used for identification in chemical databases and regulatory contexts.
A main target of NIKKOL PMEA (PALMITAMIDE MEA) is proposed to be the peroxisome proliferator-activated receptor alpha (PPAR-α).
NIKKOL PMEA (PALMITAMIDE MEA) also has affinity to cannabinoid-like G-coupled receptors GPR55 and GPR119.
NIKKOL PMEA (PALMITAMIDE MEA) cannot strictly be considered a classic endocannabinoid because it lacks affinity for the cannabinoid receptors CB1 and CB2.

NIKKOL PMEA (PALMITAMIDE MEA) Chemical Properties
Melting point: 97-98℃
Boiling point: 461.5±28.0 °C(Predicted)
density: 0.910±0.06 g/cm3(Predicted)
vapor pressure: 0.45Pa at 20℃
RTECS: ML8950000
storage temp.: -20°C
solubility: Soluble in DMSO (up to 25 mg/ml) or in Ethanol (up to 25 mg/ml).
form: White solid
pka: 14.49±0.10(Predicted)
color: White
Water Solubility: 4.01mg/L at 20℃
Stability: Stable for 2 years from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20° for up to 3 months.
Cosmetics Ingredients Functions    SURFACTANT - FOAM BOOSTING
ANTISTATIC
VISCOSITY CONTROLLING
Cosmetic Ingredient Review (CIR): Palmitoylethanolamide (544-31-0)
InChI: 1S/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)
InChIKey: HXYVTAGFYLMHSO-UHFFFAOYSA-N
LogP: 3.989 at 20℃
CAS DataBase Reference: 544-31-0
EPA Substance Registry System: NIKKOL PMEA (PALMITAMIDE MEA) (544-31-0)

NIKKOL PMEA (PALMITAMIDE MEA) is a natural occurring lipid belonging to the class of autacoids. 
NIKKOL PMEA (PALMITAMIDE MEA) is a fine white to yellow powder. 
NIKKOL PMEA (PALMITAMIDE MEA) consists of palmitic acid and ethanolamine. 
NIKKOL PMEA (PALMITAMIDE MEA) is the hydrolyzed form of N-(2-hydroxyethyl)-palmitamide, a crystalline structure isolated in soy lecithin. 
NIKKOL PMEA (PALMITAMIDE MEA) is this hydrolyzed substance that accounts for the anti-inflammatory properties that were first noted by scientists in 1957. 
NIKKOL PMEA (PALMITAMIDE MEA)'s effects on the immune system have been studied since 1939.

Uses    
NIKKOL PMEA (PALMITAMIDE MEA) 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.
NIKKOL PMEA (PALMITAMIDE MEA) 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. 
NIKKOL PMEA (PALMITAMIDE MEA) 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 NIKKOL PMEA (PALMITAMIDE MEA)PEA are due to its ability to inhibit inflammation-causing proteins called cytokines. 
Cytokines are released during periods of inflammation. 
NIKKOL PMEA (PALMITAMIDE MEA) 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.

Biological Activity    
NIKKOL PMEA (PALMITAMIDE MEA) is a natural fatty acid amide of ethanolamine and palmitic acid. 
NIKKOL PMEA (PALMITAMIDE MEA) is found in soybeans, egg yolk, and many other food sources. 
NIKKOL PMEA (PALMITAMIDE MEA)PEA is an endogenous cannabinoid receptor agonist. 
NIKKOL PMEA (PALMITAMIDE MEA) is a peroxisome proliferator-activated receptor α (PPAR-α) ligand. PEA possesses anti-inflammatory, anti-allergic, neuroprotective, and analgesic activities. 
NIKKOL PMEA (PALMITAMIDE MEA) belongs to the class of lipid mediators and the N-acylethanolamine family. 
NIKKOL PMEA (PALMITAMIDE MEA) 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 
There are no known problematic side-effects. 
NIKKOL PMEA (PALMITAMIDE MEA) can be taken together with any other substance. 
NIKKOL PMEA (PALMITAMIDE MEA) enhances the pain-relieving effect of classic analgesics and anti-inflammatories. 
NIKKOL PMEA (PALMITAMIDE MEA) can be used in combination with other substances without any side effects.

Synthesis
1) Under nitrogen protection, triethylamine (2 mL) was slowly added dropwise to a reaction vessel containing mercaptomethyl resin (2 g, MATRIX-INN), N-hydroxymaleimide (1.1 g, 9.7 mmol) and DMF (40 mL). 
After stirring at room temperature for 24 hours, the temperature was raised to 55°C and stirring was continued for 4 hours. 
The reaction mixture was cooled to room temperature and filtered, and the resulting NHS resin was washed twice each with DMF, distilled water and isopropanol sequentially, and dried under vacuum. 2) Palmitic acid (1.465 g, 5.72 mmol), NHS resin (1.50 g) prepared above, DIC (diisopropylcarbodiimide, 0.72 g, 5.72 mmol) and triethylamine (2 mL) were suspended in dichloromethane (15 mL). 

After stirring for 4 h at room temperature, the filtrate was filtered and retained for subsequent reactions (the amount of palmitic acid, DIC and solvent in the filtrate was detected by HPLC). 
The resin was washed twice each with DMF, water, isopropanol and dichloromethane sequentially, and dried under vacuum to obtain 1.70 g of dried resin with a loading of 1.0 mmol/g of immobilized palmitic acid active ester. 3) Ethanolamine (93.2 mg, 1.58 mmol) was added to a flask containing the activated ester (1.75 g) and 50 mL of ethanol, and suspended and stirred for 0.5 hr. 
The solid resin was removed by centrifugation and the resin was washed twice with ethanol (the resin was vacuum dried after washing). 
The liquid phases were combined and concentrated under reduced pressure to give 453 mg of palmitic acid monoethanolamide in 96.6% yield and >99.5% purity (HPLC detection).

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