
Endogenous fatty acid amide for neuroinflammatory balance and comfort support
Palmitoylethanolamide (PEA) is an endogenous fatty acid amide, belonging to the N-acylethanolamine (NAE) family. Naturally present in mammalian tissues, PEA is also found in foods such as egg yolks and soy lecithin. It plays a regulatory role in neuroinflammation, mast cell activity, and cellular homeostasis.
As a PPAR-α agonist, PEA has been extensively studied for its effects in the following areas:
With the continuously rising global demand for scientifically-backed nutraceutical ingredients, micronized PEA powder has emerged as a crucial raw material for dietary supplements and medical nutrition products in Europe and North America.

| Test Items | Specifications |
|---|---|
| Assay | 98.0% Min |
| Identification | Positive |
| Loss on drying | 1.0% Max |
| Residue on ignition | 1.0% Max |
| Bulk density | 0.3g/ml Min |
| Mesh | 40 mesh |
| As | 1ppm Max |
| Pb | 0.5ppm Max |
| Cd | 0.5ppm Max |
| Hg | 0.1ppm Max |
| Fe | 10ppm Max |
| Total Plate Count | 1000Cfu/g Max |
| Yeast&Mold | 100Cfu/g Max |
*Regular PEA data
AIDU Biotech employs physical modification technology to offer the following three core specifications:
Regular PEA: 100% passes through a 40-mesh sieve, suitable for basic formulations and cost-sensitive bulk applications.
Micronized PEA: The particle size is precisely controlled at D(0.80∼1.00) 10 μm. With an ultra-large specific surface area, it accelerates dissolution and absorption in the gastrointestinal tract, significantly enhancing bioavailability.
Liposomal PEA: Available with core content levels of 50% and 70%, it leverages lipid encapsulation technology to mimic biological membrane structures, achieving optimal transmembrane transport efficiency.
Palmitoylethanolamide (PEA) is recognized as an endogenous ligand of Peroxisome Proliferator-Activated Receptor-α (PPAR-α). PPAR-α belongs to the nuclear receptor superfamily and is involved in the transcriptional regulation of inflammatory signals as well as the maintenance of lipid metabolic balance.
Upon binding to the receptor, the activation of PPAR-α can regulate the transcriptional activities of genes related to cytokine expression and oxidative stress balance, thereby modulating the dynamic changes of inflammatory signaling pathways.
Literature References:Verme et al., 2005 – Demonstrated that the biological activity of PEA relies on the PPAR-α pathway,Molecular Pharmacology,DOI: 10.1124/mol.104.010439;D’Agostino et al., 2007 – Reported that PEA participates in the regulation of inflammatory signals via PPAR-α,European Journal of Pharmacology*,DOI: 10.1016/j.ejphar.2007.07.024
PEA possesses the classic Autacoid Local Injury Antagonism (ALIA) effect, the core of which lies in the precise regulation of mast cell reactivity.
Mast cells play a key role in tissue inflammation and the crosstalk between neuro-immune signals. Studies have confirmed that PEA can effectively intervene in the activation and degranulation processes of mast cells, thus providing solid support for maintaining local tissue homeostasis under physiological stress conditions.
Literature References:Aloe et al., 1993 – First proposed the regulatory effect of PEA on mast cells,Agents and Actions,DOI: 10.1007/BF01972767;Levi-Montalcini et al., 1996 – Explained the theoretical basis of ALIA,NeuroReport*,DOI: 10.1097/00001756-199610020-00027
PEA participates in the regulation of cellular lipid signaling networks, and its roles in the following aspects have been reported in studies:
In addition, PEA is believed to indirectly act on the endocannabinoid system by regulating the levels of endogenous lipid mediators. This synergistic mechanism is referred to as the "Entourage Effect".
Literature References:Petrosino & Di Marzo, 2017 – Reviewed the relationship between PEA and the endocannabinoid system,British Journal of Pharmacology,DOI: 10.1111/bph.13627;Skaper et al., 2015 – Reviewed the molecular mechanism of PEA in the regulation of neuroinflammation,CNS & Neurological Disorders – Drug Targets,DOI: 10.2174/1871527314666150821102842
*The listed references are for scientific and mechanistic discussion purposes only. This ingredient is not intended to diagnose, treat, cure, or prevent any disease.
Given that PEA is highly lipophilic and insoluble in water, its absorption efficiency is largely determined by formulation techniques.
PEA regulates the inflammatory microenvironment, while Pterostilbene activates the SIRT1 protein to modulate cellular longevity pathways. Together, they act synergistically on mitochondria, forming a cutting-edge combination in the field of Healthy Aging.
For chronic neurological discomfort, PEA is responsible for Supporting comfort, while B-complex vitamins are tasked with repairing the nerve sheath.
Packaging Specifications: 1kg/aluminum foil bag; 25kg/fiber drum (customizable specifications available).
Storage Conditions: Store sealed in a cool, dry, and light-protected environment.
Shelf Life: 36 months.
Three grades: Regular PEA (100% pass 40 mesh), Micronized PEA with particle size controlled at D(0.80~1.00) 10 μm, and Liposomal PEA at 50% and 70% core content. The published specification table reflects Regular PEA.
PEA is CAS 544-31-0 (C₁₈H₃₇NO₂, MW 299.49), supplied at 98.0% minimum assay as a white to off-white powder.
Absorption is largely determined by formulation. We recommend liposomal softgels using MCT oil or lecithin matrices, or micronized material (D50 <10 μm) for capsules and tablets where a large specific surface area speeds dissolution in the intestinal lipid environment.
36-month shelf life; 1 kg aluminum foil bags and 25 kg fiber drums, customizable. For MOQ, pricing and delivery from our Los Angeles, CA warehouse, contact idusc@aidubio.com.
Tell us the ingredient and volume you need. Our team will respond with pricing, lead time and documentation.