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D4 aea

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D4-AEA is a biotechnology product designed for research purposes. It is a chemical compound that serves as a tool for scientific investigations, but its specific core function and intended use should not be extrapolated beyond the factual information provided.

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Lab products found in correlation

Oea d2, by Cayman Chemical (4 mentions) 2 ag d5, by Cayman Chemical (4 mentions) Pea d4, by Cayman Chemical (4 mentions) Gw6471, by Merck Group (2 mentions) Fura 2 am, by Thermo Fisher Scientific (2 mentions) Amg9810, by Cayman Chemical (1 mentions) Capsazepine, by Cayman Chemical (1 mentions) Acetonitrile, by Thermo Fisher Scientific (1 mentions) Methanol, by Thermo Fisher Scientific (1 mentions) Chloroform, by Thermo Fisher Scientific (1 mentions) Am251, by Cayman Chemical (1 mentions) Urb937, by Cayman Chemical (1 mentions) Gw6471, by Cayman Chemical (1 mentions) Pf3845, by Cayman Chemical (1 mentions) Lei 401, by Cayman Chemical (1 mentions) Capsaicin, by Merck Group (1 mentions)

4 protocols using d4 aea

1

Endocannabinoid Quantification Protocol

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PEA, d4-PEA, OEA, d2-OEA, 2-AG, d5-2-AG, and AMG9810 were from Cayman Chemical (Ann Arbor, MI). AEA and d4-AEA were from R&D systems. [14C]AEA (arachidonoyl-[1-14C]ethanolamide) and rimonabant were provided by the Drug Supply Program at the National Institute on Drug Abuse. GW6471 was purchased from Sigma. All other chemicals were obtained from Fisher Scientific.
Peng X., Studholme K., Kanjiya M.P., Luk J., Bogdan D., Elmes M.W., Carbonetti G., Tong S., Gary Teng Y.H., Rizzo R.C., Li H., Deutsch D.G., Ojima I., Rebecchi M.J., Puopolo M, & Kaczocha M. (2017). Fatty-acid-binding protein inhibition produces analgesic effects through peripheral and central mechanisms. Molecular Pain, 13, 1744806917697007.
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2

Endocannabinoid Quantification Protocols

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PEA, d4-PEA, OEA, d2-OEA, 2-AG and d5-2-AG were from Cayman Chemical while AEA and d4-AEA were from R&D systems. [14C]AEA, rimonabant and SR144528 were obtained from the Drug Supply Program at the National Institute on Drug Abuse. GW6471 was purchased from Sigma while capsazepine was purchased from Cayman Chemical.
Kaczocha M., Glaser S.T., Maher T., Clavin B., Hamilton J., O’Rourke J., Rebecchi M., Puopolo M., Owada Y, & Thanos P.K. (2015). Fatty acid binding protein deletion suppresses inflammatory pain through endocannabinoid/N-acylethanolamine-dependent mechanisms. Molecular Pain, 11, 52.
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3

Radiolabeled Lipid Signaling Molecules

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12-NBD-stearate [12-N-methyl-(7-nitrobenz-2-oxa-1,3-diazo)aminostearicacid] was from Avanti Polar Lipids (Alabaster, AL). PEA, d4-PEA, OEA, d2-OEA, 2-AG and d5-2-AG were from Cayman Chemical (Ann Arbor, MI). AEA and d4-AEA were from R&D systems. [14C]AEA (arachidonoyl-[1-14C]ethanolamide, 60 mCi/mmol) was provided by the Drug Supply Program at the National Institute on Drug Abuse while [3H]2-oleoylglycerol ([3H]2-OG) was purchased from Perkin Elmer. Acetonitrile, chloroform, and methanol were of the highest possible purity and were obtained from Fisher Scientific.
Kaczocha M., Rebecchi M.J., Ralph B.P., Teng Y.H., Berger W.T., Galbavy W., Elmes M.W., Glaser S.T., Wang L., Rizzo R.C., Deutsch D.G, & Ojima I. (2014). Inhibition of Fatty Acid Binding Proteins Elevates Brain Anandamide Levels and Produces Analgesia. PLoS ONE, 9(4), e94200.
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4

Pharmacological Compounds for Endocannabinoid Research

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GW6471, AM251, URB937, PF3845, AMC-AEA, LEI-401, PEA, d4-PEA, OEA, d2-OEA, 2-AG, and d5-2-AG were purchased from Cayman Chemical (Ann Arbor, MA). NGF was from Gibco (Waltham. MA). AEA and d4-AEA were from R&D Systems (Minneapolis, MN). Capsaicin was from Sigma-Aldrich (St. Louis, MO), Fura-2AM and PED-A1 were from Thermo Fisher (Waltham, MA) and Cyclosporin A was from TCI (Portland, OR).
Bogdan D.M., Studholme K., DiBua A., Gordon C., Kanjiya M.P., Yu M., Puopolo M, & Kaczocha M. (2022). FABP5 deletion in nociceptors augments endocannabinoid signaling and suppresses TRPV1 sensitization and inflammatory pain. Scientific Reports, 12, 9241.
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