JWH-133
200px | |
Systematic (IUPAC) name | |
---|---|
(6aR,10aR)-3-(1,1-Dimethylbutyl)-6a,7,10,10a-tetrahydro -6,6,9-trimethyl-6H-dibenzo[b,d]pyran | |
Identifiers | |
CAS Number | 259869-55-1 |
PubChem | CID 6918505 |
IUPHAR/BPS | 747 |
Chemical data | |
Formula | C22H32O |
Molar mass | 312.489 g/mol[[Script error: No such module "String".]] |
JWH-133 is a potent selective CB2 receptor agonist, with a Ki of 3.4nM and selectivity of around 200x for CB2 over CB1 receptors. It was discovered by, and named after, John W. Huffman.
JWH-133, alongside WIN 55,212-2 and HU-210, is implicated in 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 antiinflamatory action is induced through agonist action at cannabinoid receptors, which prevents microglial activation that elicits the inflammation. Additionally, cannabinoids completely abolish neurotoxicity related to microglia activation in rat models.
It may be linked with anti-cancer properties, according to pre-trial data from a 2010 study in Madrid. [1]
Legal Status
The substance commonly referred to as "JWH-133" is not a scheduled substance in the U.S., although its young age prevents it from having received the level of government attention as with the older, more widely used and well known chemicals. Low abuse potential makes it less likely for regulation a priori relative to its sister drugs such as JWH-018, as JWH-133 (chemical name (6aR,10aR)-3-(1,1-Dimethylbutyl)-6a,7,10,10a-tetrahydro -6,6,9-trimethyl-6H-dibenzo[b,d]pyran) is selective for the non-psychoactive CB2 receptor and hence devoid of any psychoactive side effects or abuse potential.[2]
References
- ↑ http://www.enewspf.com/index.php/latest-news/health-and-fitness/18029-marijuana-compound-halts-breast-cancer-tumor-growth-
- ↑ http://www.usdoj.gov/dea/pubs/scheduling.html
External links
- JNeurosci.org Prevention of Alzheimer's Disease Pathology by Cannabinoids: Neuroprotection Mediated by Blockade of Microglial Activation
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