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Abnormal cannabidiol

From Wikipedia, the free encyclopedia
Synthetic, cannabinoid-like compound

Pharmaceutical compound
Abnormal cannabidiol
Identifiers
  • 4-[(1R,6R)-3-methyl-6-(prop-1-en-2-yl)cyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol
CAS Number
PubChemCID
ChemSpider
UNII
CompTox Dashboard(EPA)
Chemical and physical data
FormulaC21H30O2
Molar mass314.469 g·mol−1
3D model (JSmol)
  • CCCCCC1=CC(=CC(=C1[C@H]2C=C(CC[C@H]2C(=C)C)C)O)O
  • InChI=1S/C21H30O2/c1-5-6-7-8-16-12-17(22)13-20(23)21(16)19-11-15(4)9-10-18(19)14(2)3/h11-13,18-19,22-23H,2,5-10H2,1,3-4H3/t18-,19-/m0/s1 checkY
  • Key:YWEZXUNAYVCODW-OALUTQOASA-N checkY
 ☒NcheckY (what is this?)  (verify)

Abnormal cannabidiol (Abn-CBD) is a syntheticregioisomer ofcannabidiol, which unlike most other cannabinoids producesvasodilator effects, lowersblood pressure, and inducescell migration,cell proliferation andmitogen-activated protein kinase activation inmicroglia, but without producing anypsychoactive orsedative effects.[1][2] Abn-CBD can be found as an impurity in syntheticcannabidiol.[3]

Receptor activity

[edit]

It has been shown that the actions of abnormal cannabidiol are mediated through a site separate from theCB1 andCB2 receptors,[2][4] which responds to abnormal cannabidiol,O-1602, and theendogenous ligands:anandamide (AEA),N-arachidonoylglycine (NAGly) andN-arachidonoyl-L-serine.[2][5][6][7] Multiple lines of evidence support the proposed identification of this novel target inmicroglia as the previouslyorphan receptorGPR18.[2] Another possible target of abnormal cannabidiol isGPR55, which has also received much attention as a putative cannabinoid receptor,[8][9] although a growing body of evidence points tolysophosphatidylinositol (LPI) as theendogenous ligand for GPR55.[10][11] Further research suggests there are yet more additional cannabinoid receptors.[12][13][14][15]

Pharmacodynamics

[edit]

Research of the effects on abnormal cannabidiol in mice has indicated that atypical cannabinoids have therapeutic potential in a variety of inflammatory conditions, including those of the gastrointestinal tract. After inducingcolitis by means oftrinitrobenzene sulfonic acid, wound healing of bothhuman umbilical vein endothelial andepithelial cells was enhanced by the Abn-CBD.[16]

See also

[edit]

References

[edit]
  1. ^Adams MD, Earnhardt JT, Martin BR, Harris LS, Dewey WL, Razdan RK (September 1977). "A cannabinoid with cardiovascular activity but no overt behavioral effects".Experientia.33 (9):1204–1205.doi:10.1007/BF01922330.PMID 891878.S2CID 21488700.
  2. ^abcdMcHugh D, Hu SS, Rimmerman N, Juknat A, Vogel Z, Walker JM, et al. (March 2010)."N-arachidonoyl glycine, an abundant endogenous lipid, potently drives directed cellular migration through GPR18, the putative abnormal cannabidiol receptor".BMC Neuroscience.11: 44.doi:10.1186/1471-2202-11-44.PMC 2865488.PMID 20346144.
  3. ^Citti C, Russo F, Linciano P, Strallhofer SS, Tolomeo F, Forni F, et al. (2021)."Origin of Δ9-Tetrahydrocannabinol Impurity in Synthetic Cannabidiol".Cannabis and Cannabinoid Research.6 (1):28–39.doi:10.1089/can.2020.0021.PMC 7891213.PMID 33614950.
  4. ^Járai Z, Wagner JA, Varga K, Lake KD, Compton DR, Martin BR, et al. (November 1999)."Cannabinoid-induced mesenteric vasodilation through an endothelial site distinct from CB1 or CB2 receptors".Proceedings of the National Academy of Sciences of the United States of America.96 (24):14136–14141.Bibcode:1999PNAS...9614136J.doi:10.1073/pnas.96.24.14136.PMC 24203.PMID 10570211.
  5. ^Walter L, Franklin A, Witting A, Wade C, Xie Y, Kunos G, et al. (February 2003)."Nonpsychotropic cannabinoid receptors regulate microglial cell migration".The Journal of Neuroscience.23 (4):1398–1405.doi:10.1523/JNEUROSCI.23-04-01398.2003.PMC 6742252.PMID 12598628.
  6. ^Offertáler L, Mo FM, Bátkai S, Liu J, Begg M, Razdan RK, et al. (March 2003). "Selective ligands and cellular effectors of a G protein-coupled endothelial cannabinoid receptor".Molecular Pharmacology.63 (3):699–705.doi:10.1124/mol.63.3.699.PMID 12606780.
  7. ^Milman G, Maor Y, Abu-Lafi S, Horowitz M, Gallily R, Batkai S, et al. (February 2006)."N-arachidonoyl L-serine, an endocannabinoid-like brain constituent with vasodilatory properties".Proceedings of the National Academy of Sciences of the United States of America.103 (7):2428–2433.Bibcode:2006PNAS..103.2428M.doi:10.1073/pnas.0510676103.PMC 1413724.PMID 16467152.
  8. ^McCollum L, Howlett AC, Mukhopadhyay S (June 2007). "Anandamide-mediated CB1/CB2 cannabinoid receptor--independent nitric oxide production in rabbit aortic endothelial cells".The Journal of Pharmacology and Experimental Therapeutics.321 (3):930–937.doi:10.1124/jpet.106.117549.PMID 17379772.S2CID 24492397.
  9. ^Ryberg E, Larsson N, Sjögren S, Hjorth S, Hermansson NO, Leonova J, et al. (December 2007)."The orphan receptor GPR55 is a novel cannabinoid receptor".British Journal of Pharmacology.152 (7):1092–1101.doi:10.1038/sj.bjp.0707460.PMC 2095107.PMID 17876302.
  10. ^Kapur A, Zhao P, Sharir H, Bai Y, Caron MG, Barak LS, et al. (October 2009)."Atypical responsiveness of the orphan receptor GPR55 to cannabinoid ligands".The Journal of Biological Chemistry.284 (43):29817–29827.doi:10.1074/jbc.M109.050187.PMC 2785612.PMID 19723626.
  11. ^Henstridge CM, Balenga NA, Ford LA, Ross RA, Waldhoer M, Irving AJ (January 2009)."The GPR55 ligand L-alpha-lysophosphatidylinositol promotes RhoA-dependent Ca2+ signaling and NFAT activation".FASEB Journal.23 (1):183–193.doi:10.1096/fj.08-108670.PMID 18757503.S2CID 27142069.
  12. ^Brown AJ (November 2007)."Novel cannabinoid receptors".British Journal of Pharmacology.152 (5):567–575.doi:10.1038/sj.bjp.0707481.PMC 2190013.PMID 17906678.
  13. ^Johns DG, Behm DJ, Walker DJ, Ao Z, Shapland EM, Daniels DA, et al. (November 2007)."The novel endocannabinoid receptor GPR55 is activated by atypical cannabinoids but does not mediate their vasodilator effects".British Journal of Pharmacology.152 (5):825–831.doi:10.1038/sj.bjp.0707419.PMC 2190033.PMID 17704827.
  14. ^McHugh D, Tanner C, Mechoulam R, Pertwee RG, Ross RA (February 2008). "Inhibition of human neutrophil chemotaxis by endogenous cannabinoids and phytocannabinoids: evidence for a site distinct from CB1 and CB2".Molecular Pharmacology.73 (2):441–450.doi:10.1124/mol.107.041863.PMID 17965195.S2CID 15182303.
  15. ^Kreutz S, Koch M, Böttger C, Ghadban C, Korf HW, Dehghani F (February 2009). "2-Arachidonoylglycerol elicits neuroprotective effects on excitotoxically lesioned dentate gyrus granule cells via abnormal-cannabidiol-sensitive receptors on microglial cells".Glia.57 (3):286–294.doi:10.1002/glia.20756.PMID 18837048.S2CID 37531270.
  16. ^Krohn RM, Parsons SA, Fichna J, Patel KD, Yates RM, Sharkey KA, et al. (2016)."Abnormal cannabidiol attenuates experimental colitis in mice, promotes wound healing and inhibits neutrophil recruitment".Journal of Inflammation.13 (21): 21.doi:10.1186/s12950-016-0129-0.PMC 4944257.PMID 27418880.
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