Open Access Articles- Top Results for CP 55,940

CP 55,940

CP 55,940
Systematic (IUPAC) name
2-[(1R,2R,5R)-5-hydroxy-2-(3-hydroxypropyl) cyclohexyl]-5-(2-methyloctan-2-yl)phenol
Clinical data
PubChem CID 3086156
ChEMBL CHEMBL559612 7pxY
Chemical data
Formula C24H40O3
376.573 g/mol

CP 55,940 is a cannabinoid which mimics the effects of naturally occurring THC (one of the psychoactive compounds found in cannabis). CP 55,940 was created by Pfizer in 1974 but was never marketed. It is currently used to study the endocannabinoid system. Some effects that have been noted are a greatly decreased rates of lever pressing in exposed mice,[citation needed] and a greater reaction to opiates in exposed mice.[citation needed]

A study found that CP 55,940 can upregulate 5-HT2A receptors in mice.[1]

CP 55,940 is 45 times more potent than Δ9-THC, and fully antagonized by rimonabant (SR141716A).[2]

CP 55,940 is considered a full agonist at both CB1 and CB2 receptors and has Ki values of 0.58nM and 0.68nM respectively, but is an antagonist at GPR55, the putative "CB3" receptor.[3]

CP 55,940 showed protective effects on rat brain mitochondria upon paraquat exposure.[4]

It also showed neuroprotective effects by reducing intracellular calcium release and reducing hippocampal cell death in cultured neurons subjected to high levels of NMDA.[5]

CP 55,940 induced cell death in NG 108-15 Mouse neuroblastoma x Rat glioma hybrid brain cancer (genetically engineered mouse x rat brain cancer) cells.[6][7]

See also


  1. ^ Franklin, J. M.; Carrasco, G. A. (2013). "Cannabinoid receptor agonists upregulate and enhance serotonin 2A (5-HT2A) receptor activity via ERK1/2 signaling". Synapse 67 (3): 145–159. PMID 23151877. doi:10.1002/syn.21626. 
  2. ^ Rinaldi-Carmona, M.; Pialot, F.; Congy, C.; Redon, E.; Barth, F.; Bachy, A.; Brelière, J. C.; Soubrié, P.; le Fur, G. (1996). "Characterization and distribution of binding sites for [3H]-SR 141716A, a selective brain (CB1) cannabinoid receptor antagonist, in rodent brain". Life Sciences 58 (15): 1239–1247. PMID 8614277. doi:10.1016/0024-3205(96)00085-9. 
  3. ^ Kapur, A.; Zhao, P.; Sharir, H.; Bai, Y.; Caron, M. G.; Barak, L. S.; Abood, M. E. (2009). "Atypical responsiveness of the orphan receptor GPR55 to cannabinoid ligands". The Journal of Biological Chemistry 284 (43): 29817–29827. PMC 2785612. PMID 19723626. doi:10.1074/jbc.M109.050187. 
  4. ^ Velez-Pardo, C.; Jimenez-Del-Rio, M.; Lores-Arnaiz, S.; Bustamante, J. (2010). "Protective effects of the synthetic cannabinoids CP55,940 and JWH-015 on rat brain mitochondria upon paraquat exposure". Neurochemical Research 35 (9): 1323–1332. PMID 20514518. doi:10.1007/s11064-010-0188-1. 
  5. ^ Zhuang, S. Y.; Bridges, D.; Grigorenko, E.; McCloud, S.; Boon, A.; Hampson, R. E.; Deadwyler, S. A. (2005). "Cannabinoids produce neuroprotection by reducing intracellular calcium release from ryanodine-sensitive stores". Neuropharmacology 48 (8): 1086–1096. PMID 15910885. doi:10.1016/j.neuropharm.2005.01.005. 
  6. ^ Tomiyama, K.; Funada, M. (2011). "Cytotoxicity of synthetic cannabinoids found in 'Spice' products: The role of cannabinoid receptors and the caspase cascade in the NG 108-15 cell line". Toxicology Letters 207 (1): 12–17. PMID 21907772. doi:10.1016/j.toxlet.2011.08.021. 
  7. ^ "General Cell Collection: NG108-15". Public Health England Culture Collections. 

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