CAS number 544-31-0 YesY
PubChem 4671
Jmol-3D images Image 1
Molecular formula C18H37NO2
Molar mass 299.49
Appearance White solid
Density 0.91g/cm3
Melting point

59-60 °C

Boiling point

461.5°C @ 760mmHg

Solubility in other solvents soluble in ethanol,chloroform,THF and DMSO
Flash point 323.9°C
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Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references

Palmitoylethanolamide (PEA) is an endogenous fatty acid amide, belonging to the class of endocannabinoids. PEA has been demonstrated to bind to a receptor in the cell-nucleus (a nuclear receptor) and exerts a great variety of biological functions related to chronic pain and inflammation. The main target is thought to be the peroxisome proliferator-activated receptor alpha (PPAR-α)[1][2]. PEA also has affinity to cannabinoid-like G-coupled receptors GPR55 and GPR119.[3] However, its affinity for the classical cannabis receptors CB1and CB2 is absent. Therefore, PEA (and its structural analogue oleoylethanolamide, OEA) can not strictly be considered classic endocannabinoids. [4]

PEA has been shown to have anti-inflammatory[2], anti-nociceptive [5], neuroprotective[6], and anticonvulsant properties [7]

Palmitoylethanolamide is available for clinical use and is marketed by the Italian company Epitech under the trade name Normast.[8] Two different formulations have been developed, a ultra-micronized formulation of palmitoylethanolamide for sublingual use, containing 600 mg, and palmitoylethanolamide in a tablet, in 300 and 600 mg.


Early studies

In 1968 the first paper on PEA was indexed in Pubmed and since then more than 200 entries can be found using the keyword 'palmitoylethanolamide'. [9] In the 1990s the relation between anandamide and PEA was described, and the expression of receptors sensitive for those two molecules on mast cells was first demonstrated. [10] In this period more insight into the function of the endogenous fatty acid derivatives emerged, and compounds such as oleamide, palmitoylethanolamide, 2-lineoylglycerol, 2-palmitoylglycerol were explored for their capacity to modulate pain sensitivity and inflammation via endocannabinoid signalling. [11][12] One group demonstrated that PEA could alleviate, in a dose-dependent manner, pain behaviors elicited in mice-pain models and could downregulate hyperactive mast cells. [13][14] PEA and related compounds such as anandamide also seem to have synergistic effects in models of pain and analgesia. [15]

Animal models

In a variety of animal models PEA seems promising, and researchers could demonstrate relevant clinical activity in a variety of disorders, from multiple sclerosis to neuropathic pain. [16] [17]

In the so called mice forced swimming test palmitoylethanolamide was comparable in anti-depressant effects to fluoxetine. [18] Palmitoylethanolamide could reduced the raised intraocular pressure in glaucoma. [19] The compound could also reduce neurological deficit in a spinal trauma model, through the reduction of mast cell infiltration and activation. Palmitoylethanolamide in this model also reduced the activation of microglia and astrocytes. [20] Its activity as an inhibitor of inflammation could counteracts reactive astrogliosis induced by beta-amyloid peptide, in a model relevant for neurodegeneration, most probably via the PPAR-α mechanism of action. [21] In models of stroke and other traumata of the central nervous system, palmitoylethanolamide exerted neuroprotective properties. [22] [6] [23] [24] [25]

Animal models of chronic pain and inflammation

Chronic pain and neuropathic pain are indications for which there is high unmet need in the clinic. PEA has been tested In a variety of animal models for chronic and neuropathic pain. As Cannabinoids such as THC have been proven to be effective in neuropathic pain states, it makes sense to further explore the analgesic efficacy of endocannabinoids. [26] The analgesic and antihyperalgesic effects of PEA in two models of acute and persistent pain seemed to be explained at least partly via the de novo neurosteroid synthesis. [27] [28] In chronic granulomatous pain and inflammation model PEA could prevent nerve formation and sprouting, mechanical allodynia, and PEA inhibited dorsal root ganglia activation, which is a hallmark for winding up in neuropathic pain. [29] The mechanism of action of PEA as an analgesic and anti-inflammatory drug is probably based on different aspects. PEA inhibits the release of both preformed and newly synthesised mast cell mediators, such as histamine and TNF-alpha. [30]PEA, as well as its analogue adelmidrol (di-amide derivative of azelaic acid) both can down-regulate mast cells. [31] PEA reduces the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) and prevents IkB-alpha degradation and p65 NF-kappaB nuclear translocation, the latter related to PEA as a endogenous PPAR-alpha agonist. [32]

In a model of visceral pain (inflammation of the urinary bladder) PEA was able to attenuate the viscero-visceral hyper-reflexia induced by inflammation of the urinary bladder, one of the reasons why PEA is currently explored in the painful bladdersyndrome. [33] In a different model for bladder pain, the turpentine-induced urinary bladder inflammation in the rat, PEA also attenuated a referred hyperalgesia in a dose-dependent way. [34] Chronic pelvic pain in patients indeed seems to respond favourably to a treatment with PEA. [35] [36] PEA seems to be produced in human as well as in animals as a biological response and a repair mechanism in chronic inflammation and chronic pain. [37]

ALIAmide and glia-modulator

PEA is has physico-chemical properties comparable to anandamide and is mostly referred to as belonging to the class of endogenous cannabinoids. Lipid molecules like PEA often act as signaling molecules, activating intracellular and membrane-associated receptors to regulate a variety of physiological functions. The signaling lipid PEA is known to activate intracellular, nuclear and membrane-associated receptors and regulate many physiological functions related to the inflammatory cascade and chronic pain states. Endocannabinoid lipids like PEA are widely distributed in nature, in a variety of plant, invertebrate, and mammalian tissues.[38]

PEA's mechanism of action sometimes is described using the acronym ALIA. [10] ALIA stands for Autacoid Local Injury (or inflammation) Antagonism, and PEA under this nomenclature is an ALIAmide. It was the group of the Nobel price laureate Rita Levi-Montalcini who in 1993 first presented evidence supporting that lipid amides of the N-acylethanolamine type (such as PEA) are potential prototypes of naturally occurring molecules capable of modulating mast cell activation and her group coined in that paper the acronym ALIA. [39] An autocoid is a regulating molecule, locally produced. Prostaglandins are classical examples of autocoids. An ALIAmide is an autocoid synthesized in response to injury or inflammation, and acting locally to counteract such pathology. PEA is a classical example of an ALIAmide. The mast cell soon after the breakthrough paper of Levi-Montalcini indeed appeared to be an important target for the anti-inflammatory activity of PEA, and in the period 1993-2011 at least 25 papers were published on the various effects of PEA on the mast cell. Since 2005 we understand that much of the biological effects on cells as the mast cell, most probably can be understood via its affinity of the PPARα receptor. Even rapid analgesic activity is partly described via the PPARα interaction. [40] Mast cells are often found in proximity to sensory nerve endings and their degradation can enhance the nociceptive signal, the reason why peripheral mast cells are considered to be pro-inflammatory and pro-nociceptive. [41] Mast cells also can be found in the spinal dura, the thalamus and the dura mater. Meanwhile, due to PEA's affinity to the PPARα receptor and due to the wide presence of those receptors in the central nervous system, especially also in glia and astrocytes [42][28], PEA's activity is currently seen as an important new inroad in the treatment of neuropathic pain. Glia and astrocytes play a key role in the winding up phenomena and central sensitization. [43] [44]

Clinical relevance

PEA has been explored in man in various clinical trials in a variety of pain states, as well as in pet animals, for inflammatory and painsyndromes. [45] [46] [47] [48] [49] [50] Its positive influence in atopic eczema for instance seems to originate from PPAR alpha activation. [51] [45] PEA is available for human use as food for medical purposes in Italy and Spain and as a diet supplement in the Netherlands. A parent moleule, adelmidrol, is available as a topical preparation for dermatological indications. [52]

From a clinical perspective the most important and promising indications for palmitoylethanolamide are linked to neuropathic and chronic pain states, such as diabetic neuropathic pain, sciatic pain, pelvic pain and entrapment neuropathic painstates. [46] [47] [53] [54] [37] [55] In a blind pilot trial in 25 patients affected by temporomandibular joint's (TMJ) osteoarthritis or synovitis pain, patients were randomly to PEA or ibuprofen 600 mg 3 times a day for 2 weeks. Pain decrease after two weeks of treatment was significantly higher PEA treated patients than in patients receiving the NSAID) (p=0.0001). Masticatory function also improves more on PEA compared to the NSAID (p=0.0001).

One of the targets of PEA is the glia. [56] Modern neurobiological research increasingly points out the relevance of the glia and asterocytes in the pathogenesis of neuropathic pain. One even coined the term gliopathic pain as an alternative for neuropathic pain. [57] Glia and asterocytes therefore are an important new target for the development of new analgesic compounds in the treatment of neuropathic pain. [58]

Treating neuropathic pain prescribing the current anti-neuropathic pain drugs, belonging to the classes of antidepressants and anticonvulsants, is often not satisfactory. [59] New drugs aiming for different non-neuronal targets, in this case the glia, such as palmitoylethanolamide, are needed. [60]


PEA is metabolized by cellular enzymes, fatty acid amide hydrolase (FAAH) and N-acylethanolamine-hydrolyzing acid amidase (NAAA), the latter of which has more specificity toward PEA over other fatty acid amides.[61] Due to this cellular metabolism, it seems that dose adjustment for renal insufficiency will be unnecessary, although formal human studies are not yet available. To date, no drug interactions have been reported in literature, neither any clinical relevant or dose-limiting side effect.

See also


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