|CompTox Dashboard (EPA)|
|Chemical and physical data|
|Molar mass||312.497 g·mol−1|
|3D model (JSmol)|
|(what is this?)|
It's important to note that JWH-133 has been confused with other analogs of Delta-8-THC in professionally published peer-reviewed literature. Including being confused with Dimethylpentyl-Delta-8-THC as well as Dimethylbutyl-Delta-8-THC. Including confusing the chemical name with Dimethylbutyl-Delta-8-THC itself. Including confusing it with the Delta-9 isomer Including using the structural image of Dimethylbutyl-Delta-8-THC instead of Dimethylbutyl-deoxy-Delta-8-THC.
It's important to note that 3-(1',1'-Dimethylbutyl)-1-deoxy-delta-8-THC is a selective CB2 agonist, binding 677nM at Cb1 and 132 3.4nM at CB2 while 3-(1',1'-Dimethylbutyl)-delta-8-THC itself binds 65nM at CB1. Structurally the only difference between JWH-133 and dimethylbutyl-D8-THC is that JWH-133 lacks the hydroxy group seen on on dimethylbutyl-D8-THCs phenol structure (the C1 position of the A ring), turning this group into a phenyl (JWH-133) instead of phenol. It's generally accepted that removing the hydroxy group from the phenol structure of any classical cannabinoid benzoypran (such as THC) results in dramatically less CB1 activity and heightened CB2 activity.
JWH-133, alongside WIN 55,212-2 and HU-210, is responsible for preventing the inflammation caused by Amyloid beta proteins involved in Alzheimer's disease, in addition to preventing cognitive impairment and loss of neuronal markers. This anti-inflammatory action is induced through agonist action at the CB2 receptor, which prevents microglial activation that elicits the inflammation. Additionally, cannabinoids at this receptor completely abolish neurotoxicity related to microglia activation in rat models.
As the U.S. Drug Enforcement Administration criminalizes any extract "containing one or more cannabinoids," JWH-133 is a scheduled substance in the U.S. This is despite the low potential for abuse relative to its sister compounds such as JWH-018, as JWH-133 is selective for the non-psychoactive CB2 receptor and thus lacks significant psychoactive effects.
- Bow, Eric W.; Rimoldi, John M. (28 June 2016). "The Structure–Function Relationships of Classical Cannabinoids: CB1/CB2 Modulation". Perspectives in Medicinal Chemistry. 8: 17–39. doi:10.4137/PMC.S32171. PMC 4927043. PMID 27398024.
- Huffman, John W.; Liddle, John; Yu, Shu; Aung, Mie Mie; Abood, Mary E.; Wiley, Jenny L.; Martin, Billy R. (1 December 1999). "3-(1′,1′-Dimethylbutyl)-1-deoxy-Δ8-THC and related compounds: synthesis of selective ligands for the CB2 receptor". Bioorganic & Medicinal Chemistry. 7 (12): 2905–2914. doi:10.1016/S0968-0896(99)00219-9. PMID 10658595.
- Huffman, John W; Miller, John R.A; Liddle, John; Yu, Shu; Thomas, Brian F; Wiley, Jenny L; Martin, Billy R (April 2003). "Structure–activity relationships for 1′,1′-dimethylalkyl-Δ 8 -tetrahydrocannabinols". Bioorganic & Medicinal Chemistry. 11 (7): 1397–1410. doi:10.1016/s0968-0896(02)00649-1. PMID 12628666.
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- "PART 1308 - Section 1308.11 Schedule I". www.deadiversion.usdoj.gov. Retrieved 2020-01-08.
- Ramirez, B. G.; Blázquez, C; Gómez del Pulgar, T; Guzmán, M; de Ceballos, ML (23 February 2005). "Prevention of Alzheimer's Disease Pathology by Cannabinoids: Neuroprotection Mediated by Blockade of Microglial Activation". Journal of Neuroscience. 25 (8): 1904–1913. doi:10.1523/JNEUROSCI.4540-04.2005. PMC 6726060. PMID 15728830.