Monday, March 27, 2017
Breaking News

JWH-133

jwh133JWH-133 is Unscheduled in the United States.

Addictive Potential: Unknown

Emergency Room Visits Yearly: Unknown

Mandatory Minimum Sentence: Unknown

Mechanism of Action: Cannabinoid receptor agonist

Overview:

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. 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.

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 Side Effects and Adverse Reactions:

JWH-133 is a research chemical. Research chemicals are experimental chemicals that are not approved for human consumption. This is because not enough data exists currently about their side effects, adverse reactions, long term damage, addiction potential, etc. Although some people are willing to ingest research chemicals, it is not reasonable to assume that they are in any way safe to use recreationally.

JWH-133 and Drug Tests:

JWH-133 is a synthetic cannabinoid that currently cannot be detected with drug tests. This is because of how drug tests work. The basic concept is that your body attempts to break down any drugs you ingest. Metabolites are formed as part of this process; testing looks for the specific types of metabolites that could only occur as a result of drug taking. There is currently (as of Nov, 2009) no test that tests for the metabolites of synthetic cannabinoids. Rumor has it that scientists are developing a drug test that tests for them, although, the development and implementation process could take years.

Research:

Prevention of Alzheimer’s Disease Pathology by Cannabinoids: Neuroprotection Mediated by Blockade of Microglial Activation

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