Classification Term: 4088
N-acylethanolamines (ontology term: CHEMONTID:0001145)
Compounds containing an N-acyethanolamine moiety, which is characterized by an acyl group is linked to the nitrogen atom of ethanolamine." []
found 26 associated metabolites at no_class-level_7 metabolite taxonomy ontology rank level.
Ancestor: 1,2-aminoalcohols
Child Taxonomies: There is no child term of current ontology term.
Anandamide
Anandamide, also known as arachidonoylethanolamide (AEA), is a highly potent endogenous agonist of the cannabinoid CB1 and CB2 receptors. CB1 receptors are predominantly found in the central nervous system (CNS) where they mainly mediate the psychotropic effects of tetrahydrocannabinol (THC) and endocannabinoids, whereas the expression of the CB2 receptor is thought to be restricted to cells of the immune system. It was suggested that AEA might inhibit tumour cell proliferation or induce apoptosis independently of CB1 and CB2 receptors, via interaction with the type 1 vanilloid receptor (VR1). VR1 is an ion channel expressed almost exclusively by sensory neurons, activated by pH, noxious heat (> 48-degree centigrade), and plant toxins and is thought to play an important role in nociception. Cervical cancer cells are sensitive to AEA-induced apoptosis via VR1 that is aberrantly expressed in vitro and in vivo while CB1 and CB2 receptors play a protective role. (PMID: 15047233). Novel prostaglandins (prostaglandin glycerol esters and prostaglandin ethanolamides) are COX-2 oxidative metabolites of endogenous cannabinoids (such as anandamide). Recent evidence suggests that these new types of prostaglandins are likely novel signalling mediators involved in synaptic transmission and plasticity (PMID: 16957004). Anandamide is a highly potent endogenous agonist of the cannabinoid CB1 and CB2 receptors. CB1 receptors are predominantly found in the central nervous system (CNS) where they mainly mediate the psychotropic effects of Tetrahydrocannabinol (THC) and endocannabinoids, whereas the expression of the CB2 receptor is thought to be restricted to cells of the immune system. It was suggested that AEA might inhibit tumor cell proliferation or induce apoptosis independently of CB1 and CB2 receptors, via interaction with the type 1 vanilloid receptor (VR1). VR1 is an ion channel expressed almost exclusively by sensory neurons, activated by pH, noxious heat (>48 degree centigrade) and plant toxins and is thought to play an important role in nociception. Cervical cancer cells are sensitive to AEA-induced apoptosis via VR1 that is aberrantly expressed in vitro and in vivo while CB1 and CB2 receptors play a protective role. (PMID 15047233) D006730 - Hormones, Hormone Substitutes, and Hormone Antagonists > D006728 - Hormones > D063385 - Cannabinoid Receptor Modulators D018377 - Neurotransmitter Agents > D063385 - Cannabinoid Receptor Modulators > D063386 - Cannabinoid Receptor Agonists D002317 - Cardiovascular Agents > D002121 - Calcium Channel Blockers D000077264 - Calcium-Regulating Hormones and Agents CONFIDENCE standard compound; INTERNAL_ID 41 D049990 - Membrane Transport Modulators
Adrenoyl ethanolamide
Adrenoyl ethanolamide is a N-acylethanolamine. N-acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation has been attributed a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. N-oleoylethanolamine is an inhibitor of the sphingolipid signaling pathway, via specific ceramidase inhibition (ceramidase converts ceramide to sphingosine). N-oleoylethanolamine blocks the effects of TNF- and arachidonic acid on intracellular Ca concentration. (PMID: 12692337, 12056855, 12560208, 11997249) [HMDB] Adrenoyl ethanolamide is a N-acylethanolamine. N-acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation has been attributed a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. N-oleoylethanolamine is an inhibitor of the sphingolipid signaling pathway, via specific ceramidase inhibition (ceramidase converts ceramide to sphingosine). N-oleoylethanolamine blocks the effects of TNF- and arachidonic acid on intracellular Ca concentration. (PMID: 12692337, 12056855, 12560208, 11997249).
(±)11(12)-EET Ethanolamide
(±)11(12)-EET ethanolamide is a potential cytochrome P450 (CYP450) metabolite of arachidonoyl ethanolamide (AEA; anandamide), although specific stereochemistry rather than a racemic mixture would likely ensue from enzymatic metabolism. AEA is an endogenous lipid neurotransmitter with cannibingeric activity, binding to both the central cannabinoid (CB1) and peripheral cannabinoid CB2 receptors (PMID: 8395053, 16078824). Fatty acid amide hydrolase (FAAH) is the enzyme responsible for the hydrolysis and inactivation of AEA (PMID: 12052036). Metabolism of AEA by cyclooxygenase-2, leading to formation of prostaglandin ethanolamides, and by lipoxygenases has also been documented (PMID: 12052037). CYP450 metabolism of AEA may be particularly relevant under conditions of FAAH inhibition. Evidence for the formation of 11(12)-EET ethanolamide in vivo has not been documented. Arachidonoyl ethanolamide (AEA; anandamide) is an endogenous lipid neurotransmitter with cannibingeric activity, binding to both the central cannabinoid (CB1) and peripheral cannabinoid CB2 receptors.1,2 Fatty acid amide hydrolase (FAAH) is the enzyme responsible for the hydrolysis and inactivation of AEA.3 Metabolism of AEA by cyclooxygenase-2, leading to formation of prostaglandin ethanolamides, and by lipoxygenases has also been documented.4 (?)11(12)-EET ethanolamide is a potential cytochrome P450 (CYP450) metabolite of AEA, although specific stereochemistry rather than a racemic mixture would likely ensue from enzymatic metabolism. CYP450 metabolism of AEA may be particularly relevant under conditions of FAAH inhibition. Evidence for the formation of 11(12)-EET ethanolamide in vivo has not been documented. [HMDB]
(±)8(9)-EET Ethanolamide
(±)8(9)-EET ethanolamide is a cytochrome P450 (CYP450) metabolite of arachidonoyl ethanolamide (AEA), although specific stereochemistry rather than a racemic mixture would likely ensue from enzymatic metabolism (PMID: 17272674). AEA is an endogenous lipid neurotransmitter with cannabingeric activity, binding to both the central cannabinoid (CB1) and peripheral cannabinoid (CB2) receptors (PMID: 8395053, 16078824). Fatty acid amide hydrolase (FAAH) is the enzyme responsible for the hydrolysis and inactivation of AEA (PMID: 12052036). Metabolism of AEA by COX-2, lipoxygenases, and CYP450 enzymes has also been documented (PMID: 12052037, 17272674). Human liver microsomes metabolize AEA to 5,6-, 8,9-, 11,12-, and 14,15-EET ethanolamides in a time and protein concentration dependent manner (PMID: 17272674). (±)8(9)-EET reduces glomerular filtration rate through cyclooxygenase dependent preglomerular vasoconstriction (PMID: 1928373). The physiological actions of (±)8(9)-EET ethanolamide have not been examined. Arachidonoyl ethanolamide (AEA) is an endogenous lipid neurotransmitter with cannabingeric activity, binding to both the central cannabinoid (CB1) and peripheral cannabinoid (CB2) receptors.1,2 Fatty acid amide hydrolase (FAAH) is the enzyme responsible for the hydrolysis and inactivation of AEA.3 Metabolism of AEA by COX-2, lipoxygenases, and CYP450 enzymes has also been documented.4,5 (?)8(9)-EET ethanolamide is a cytochrome P450 (CYP450) metabolite of AEA, although specific stereochemistry rather than a racemic mixture would likely ensue from enzymatic metabolism.5 Human liver microsomes metabolize AEA to 5,6-, 8,9-, 11,12-, and 14,15-EET ethanolamides in a time and protein concentration dependent manner.5 (?)8(9)-EET reduces glomerular filtration rate through cyclooxygenase dependent preglomerular vasoconstriction.6 The physiological actions of (?)8(9)-EET ethanolamide have not been examined. [HMDB]
Alpha-Linolenoyl ethanolamide
alpha-Linolenoyl ethanolamide is a N-acylethanolamine. N-acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation has been attributed a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. N-oleoylethanolamine is an inhibitor of the sphingolipid signaling pathway, via specific ceramidase inhibition (ceramidase converts ceramide to sphingosine). N-oleoylethanolamine blocks the effects of TNF- and arachidonic acid on intracellular Ca concentration. (PMID: 12692337, 12056855, 12560208, 11997249) [HMDB] alpha-Linolenoyl ethanolamide is a N-acylethanolamine. N-acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation has been attributed a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. N-oleoylethanolamine is an inhibitor of the sphingolipid signaling pathway, via specific ceramidase inhibition (ceramidase converts ceramide to sphingosine). N-oleoylethanolamine blocks the effects of TNF- and arachidonic acid on intracellular Ca concentration. (PMID: 12692337, 12056855, 12560208, 11997249).
Oleoylethanolamide
N-Oleoylethanolamine (NOE or OEA) is a N-acylethanolamine. N-acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation has been attributed a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. N-oleoylethanolamine is an inhibitor of the sphingolipid signaling pathway, via specific ceramidase inhibition (ceramidase converts ceramide to sphingosine). N-oleoylethanolamine blocks the effects of TNF- and arachidonic acid on intracellular Ca concentration. (PMID: 12692337, 12056855, 12560208, 11997249). N-oleoyl ethanolamine is related to the endocannabinoid anandamide. Endocannabinoids signal through cannabinoid receptors (also stimulated by the active ingredient of cannabis) but although related in structure, synthesis and degradation to anandamide, NOE cannot be considered an endocannabinoid as it does not activate the cannabinoid receptors. Most of the reported responses to NOE can be attributed to activation of peroxisome proliferator-activated receptor-alpha (PPAR-alpha). Administration of NOE inhibits body weight gain in rats. In adipocytes and hepatocytes, NOE inhibits mitogenic and metabolic signaling by the insulin receptor and produces glucose intolerance. It also inhibits gastric emptying, which might act together with the sensory neuronal signals to achieve satiety. NOE is permanently elevated in diabetic obese patients. NOE also reduces visceral and inflammatory responses through a PPAR-alpha-activation independent mechanism (PMID: 17449181). NOE has been shown to be an antagonist of TRVP1 (the transient receptor potential vanilloid type 1 receptor). Overall, NOE has beneficial effects on health by inducing food intake control, lipid beta-oxidation, body weight loss and analgesic effects (PMID: 18704536). [HMDB] Oleoylethanolamide (OEA or NOE) is an N-acylethanolamine. N-Acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation have been attributed to a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. Oleoylethanolamide is an inhibitor of the sphingolipid signalling pathway, via specific ceramidase inhibition (ceramidase converts ceramide to sphingosine). Oleoylethanolamide blocks the effects of TNF and arachidonic acid on intracellular Ca concentration (PMID: 12692337, 12056855, 12560208, 11997249). Oleoylethanolamide is related to the endocannabinoid anandamide. Endocannabinoids signal through cannabinoid receptors (also stimulated by the active ingredient of cannabis) but although related in structure, synthesis, and degradation to anandamide, OEA cannot be considered an endocannabinoid as it does not activate the cannabinoid receptors. Most of the reported responses to OEA can be attributed to the activation of peroxisome proliferator-activated receptor-alpha (PPAR-alpha). Administration of OEA inhibits body weight gain in rats. In adipocytes and hepatocytes, OEA inhibits mitogenic and metabolic signalling by the insulin receptor and produces glucose intolerance. It also inhibits gastric emptying, which might act together with the sensory neuronal signals to achieve satiety. OEA is permanently elevated in diabetic obese patients. OEA also reduces visceral and inflammatory responses through a PPAR-alpha-activation independent mechanism (PMID: 17449181). OEA is an antagonist of TRVP1 (the transient receptor potential vanilloid type 1 receptor). Overall, OEA has beneficial effects on health by inducing food intake control, lipid beta-oxidation, body weight loss and analgesic effects (PMID: 18704536). D006730 - Hormones, Hormone Substitutes, and Hormone Antagonists > D006728 - Hormones > D063385 - Cannabinoid Receptor Modulators D018377 - Neurotransmitter Agents > D063385 - Cannabinoid Receptor Modulators > D063386 - Cannabinoid Receptor Agonists COVID info from DrugBank Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS Oleoylethanolamide is a high affinity endogenous PPAR-α agonist, which plays an important role in the treatment of obesity and arteriosclerosis. Oleoylethanolamide is a high affinity endogenous PPAR-α agonist, which plays an important role in the treatment of obesity and arteriosclerosis.
Docosahexaenoyl Ethanolamide
Docosahexaenoic Acid (DHA) is an essential fatty acid and the most abundant ω-3 fatty acid in neural tissues, especially in the retina and brain. Docosahexaenoyl ethanolamide (DHEA) is the ethanolamine amide of DHA that has been detected in both brain and retina at concentrations similar to those for arachidonoyl ethanolamide (AEA).1,2 A 9.5 fold increase of DHEA was observed in brain lipid extracts from piglets fed a diet supplemented with DHA compared to a control diet without DHA.3 DHEA binds to the rat brain CB1 receptor with a Ki of 324 nM, which is approximately 10-fold higher than the Ki for AEA.4 DHEA inhibits shaker-related voltage-gated potassium channels in brain slightly better than AEA, with an IC50 of 1.5 ?M [HMDB] Docosahexaenoic Acid (DHA) is an essential fatty acid and the most abundant ω-3 fatty acid in neural tissues, especially in the retina and brain. Docosahexaenoyl ethanolamide (DHEA) is the ethanolamine amide of DHA that has been detected in both brain and retina at concentrations similar to those for arachidonoyl ethanolamide (AEA).1,2 A 9.5 fold increase of DHEA was observed in brain lipid extracts from piglets fed a diet supplemented with DHA compared to a control diet without DHA.3 DHEA binds to the rat brain CB1 receptor with a Ki of 324 nM, which is approximately 10-fold higher than the Ki for AEA.4 DHEA inhibits shaker-related voltage-gated potassium channels in brain slightly better than AEA, with an IC50 of 1.5 ¬µM.
Palmitoleoylethanolamde
Palmitoleoylethanolamde (POEA), belongs to the class of organic compounds known as N-acylethanolamines. N-Acylethanolamines are compounds containing an N-acyethanolamine moiety, which is characterized by an acyl group is linked to the nitrogen atom of ethanolamine. Thus, palmitoleoylethanolamde is considered to be a fatty amide lipid molecule. Palmitoleoylethanolamde is a very hydrophobic molecule, practically insoluble (in water), and relatively neutral. During abstinence, young adults with a history of alcohol binge drinking had elevated plasma levels of monounsaturated and polyunsaturatedacylethanolamides, specifically oleoylethanolamide (OEA), palmitoleoylethanolamide (POEA), arachidonoylethanolamide (AEA), and dihomo-gamma-linolenoylethanolamide (DGLEA). Changes in these lipids positively correlated with mRNA upregulation of inflammatory markers in peripheral blood mononuclear cells (PBMCs), such as toll-like receptors (TLR4), pro-inflammatory cytokines/chemokines, and cyclooxygenase-2 (PMID: 29178411). Palmitoylethanolamide (PEA) is an endogenous fatty acid amide. PEA has been shown to have anti-inflammatory[2] and anti-nociceptive properties. D013501 - Surface-Active Agents > D011092 - Polyethylene Glycols D001697 - Biomedical and Dental Materials
Dihomo-gamma-linolenoylethanolamide
Dihomo-gamma-linolenoylethanolamide (DGLEA) is an N-acylethanolamine. N-acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation have been attributed to a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. During abstinence, young adults with a history of alcohol binge drinking had elevated plasma levels of monounsaturated and polyunsaturatedacylethanolamides, specifically oleoylethanolamide (OEA), palmitoleoylethanolamide (POEA), arachidonoylethanolamide (AEA), and dihomo-gamma-linolenoylethanolamide (DGLEA). Changes in these lipids positively correlated with mRNA upregulation of inflammatory markers in peripheral blood mononuclear cells (PBMCs), such as toll-like receptors (TLR4), pro-inflammatory cytokines/chemokines, and cyclooxygenase-2 (PMID: 29178411). Dihomo-gamma-Linolenoyl ethanolamide is a N-acylethanolamine. N-acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation has been attributed a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. N-oleoylethanolamine is an inhibitor of the sphingolipid signaling pathway, via specific ceramidase inhibition (ceramidase converts ceramide to sphingosine). N-oleoylethanolamine blocks the effects of TNF- and arachidonic acid on intracellular Ca concentration. (PMID: 12692337, 12056855, 12560208, 11997249) [HMDB]
Linoleoyl ethanolamide
Linoleoyl ethanolamide inhibits arachidonoylethanolamide amidohydrolase. [HMDB] Linoleoyl ethanolamide inhibits arachidonoylethanolamide amidohydrolase.
Stearoylethanolamide
Stearoylethanolamide is a N-acylethanolamine. N-acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation has been attributed a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. N-oleoylethanolamine is an inhibitor of the sphingolipid signaling pathway, via specific ceramidase inhibition (ceramidase converts ceramide to sphingosine). N-oleoylethanolamine blocks the effects of TNF- and arachidonic acid on intracellular Ca concentration. (PMID: 12692337, 12056855, 12560208, 11997249) [HMDB] Stearoylethanolamide is an N-acylethanolamine. N-acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation has been attributed a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. N-oleoylethanolamine is an inhibitor of the sphingolipid signaling pathway, via specific ceramidase inhibition (ceramidase converts ceramide to sphingosine). N-oleoylethanolamine blocks the effects of TNF- and arachidonic acid on intracellular Ca concentration. (PMID: 12692337, 12056855, 12560208, 11997249). Stearoylethanolamide is an endocannabinoid-like compound with pro-apoptotic activity.
20-HETE ethanolamide
20-HETE ethanolamide is a N-acylethanolamine. N-acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation has been attributed a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. N-oleoylethanolamine is an inhibitor of the sphingolipid signaling pathway, via specific ceramidase inhibition (ceramidase converts ceramide to sphingosine). N-oleoylethanolamine blocks the effects of TNF- and arachidonic acid on intracellular Ca concentration. (PMID: 12692337, 12056855, 12560208, 11997249) [HMDB] 20-HETE ethanolamide is an N-acylethanolamine. N-Acylethanolamines (NAEs) constitute a class of lipid compounds naturally present in both animal and plant membranes as constituents of the membrane-bound phospholipid, N-acylphosphatidylethanolamine (NAPE). NAPE is composed of a third fatty acid moiety linked to the amino head group of the commonly occurring membrane phospholipid, phosphatidylethanolamine. NAEs are released from NAPE by phospholipase D-type hydrolases in response to a variety of stimuli. Transient NAE release and accumulation has been attributed a variety of biological activities, including neurotransmission, membrane protection, and immunomodulation in animals. N-Oleoylethanolamine is an inhibitor of the sphingolipid signalling pathway via specific ceramidase inhibition (ceramidase converts ceramide to sphingosine). N-Oleoylethanolamine blocks the effects of TNF- and arachidonic acid on intracellular Ca concentration (PMID: 12692337, 12056855, 12560208, 11997249).
Eicosapentaenoyl Ethanolamide
Eicosapentaenoyl Ethanolamide (EPEA) is an endogenous fatty acid amide. EPEA is metabolized by 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. DHEA and eicosapentaenoyl ethanolamide (EPEA) bind to the CB1 receptor in rat brains.23 DHA levels in the mouse brain have been shown to inversely affect the levels of 2AG. Eicosapentaenoyl Ethanolamide (EPEA) is an endogenous fatty acid amide.
Leukotriene B4 ethanolamide
Leukotriene B4 ethanolamide is a synthetic agonist of leukotriene B4 (LTB4), that interacts with both leukotriene B4 receptors and Vanilloid TRPV1 receptors. Leukotriene B4 is the major metabolite in neutrophil polymorphonuclear leukocytes. Leukotrienes are metabolites of arachidonic acid derived from the action of 5-LO (5-lipoxygenase). The immediate product of 5-LO is LTA4 (leukotriene A4), which is enzymatically converted into either LTB4 (leukotriene B4) by LTA4 hydrolase or LTC4 (leukotriene C4) by LTC4 synthase. The regulation of leukotriene production occurs at various levels, including expression of 5-LO, translocation of 5-LO to the perinuclear region and phosphorylation to either enhance or inhibit the activity of 5-LO. Biologically active LTB4 is metabolized by w-oxidation carried out by specific cytochrome P450s (CYP4F) followed by beta-oxidation from the w-carboxy position and after CoA ester formation. Other specific pathways of leukotriene metabolism include the 12-hydroxydehydrogenase/ 15-oxo-prostaglandin-13-reductase that form a series of conjugated diene metabolites that have been observed to be excreted into human urine. Metabolism of LTC4 occurs by sequential peptide cleavage reactions involving a gamma-glutamyl transpeptidase that forms LTD4 (leukotriene D4) and a membrane-bound dipeptidase that converts LTD4 into LTE4 (leukotriene E4) before w-oxidation. These metabolic transformations of the primary leukotrienes are critical for termination of their biological activity, and defects in expression of participating enzymes may be involved in specific genetic disease. (PMID 17623009, 16207832)Leukotrienes are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways. Leukotriene B4 ethanolamide is a synthetic agonist of leukotriene B4 (LTB4), that interacts with both leukotriene B4 receptors and Vanilloid TRPV1 receptors. Leukotriene B4 is the major metabolite in neutrophil polymorphonuclear leukocytes. Leukotrienes are metabolites of arachidonic acid derived from the action of 5-LO (5-lipoxygenase). The immediate product of 5-LO is LTA4 (leukotriene A4), which is enzymatically converted into either LTB4 (leukotriene B4) by LTA4 hydrolase or LTC4 (leukotriene C4) by LTC4 synthase. The regulation of leukotriene production occurs at various levels, including expression of 5-LO, translocation of 5-LO to the perinuclear region and phosphorylation to either enhance or inhibit the activity of 5-LO. Biologically active LTB4 is metabolized by w-oxidation carried out by specific cytochrome P450s (CYP4F) followed by beta-oxidation from the w-carboxy position and after CoA ester formation. Other specific pathways of leukotriene metabolism include the 12-hydroxydehydrogenase/ 15-oxo-prostaglandin-13-reductase that form a series of conjugated diene metabolites that have been observed to be excreted into human urine. Metabolism of LTC4 occurs by sequential peptide cleavage reactions involving a gamma-glutamyl transpeptidase that forms LTD4 (leukotriene D4) and a membrane-bound dipeptidase that converts LTD4 into LTE4 (leukotriene E4) before w-oxidation. These metabolic transformations of the primary leukotrienes are critical for termination of their biological activity, and defects in expression of participating enzymes may be involved in specific genetic disease. (PMID 17623009, 16207832)
N-Gluconyl ethanolamine
N-Gluconyl ethanolamine is used as a food additive [EAFUS] ("EAFUS: Everything Added to Food in the United States. [http://www.eafus.com/]") It is used as a food additive .
N-Lactoyl ethanolamine
N-Lactoyl ethanolamine is used as a food additive [EAFUS] ("EAFUS: Everything Added to Food in the United States. [http://www.eafus.com/]")
Adelmidrol
C78273 - Agent Affecting Respiratory System > C29712 - Anti-asthmatic Agent > C29714 - Mast Cell Stabilizer Adelmidrol exerts important anti-inflammatory effects that are partly dependent on PPARγ. Adelmidrol reduces NF-κB translocation, and COX-2 expression.
Etanidazole
C274 - Antineoplastic Agent > C798 - Radiosensitizing Agent D011838 - Radiation-Sensitizing Agents D000970 - Antineoplastic Agents
