Tylenol’s Analgesic Effect is Mediated By Cannabinoid Receptors

Written by  Thursday, 02 January 2014 15:58

Acetaminophen, also known as Tylenol, is one of the most commonly used non-steroidal anti-inflammatory drugs (NSAIDs) for pain relief. But did you know that its compound’s pain fighting activity arises partially through its activity on the endocannabinoid system?

The acidic cannabinoids (THCA and CBDA) along with non-acidic CBD exhibit anti-inflammatory properties by inhibiting enzymes called cyclooxygenases (COX’s). These enzymes are responsible for the production of pro-inflammatory factors called prostaglandins. This same inhibition occurs when an NSAID is taken.

Isn’t it ironic that cannabis, a compound that is significantly less toxic and harsh on the liver is illegal yet it acts on the same pathways as a commercial pain reliever? Here’s how it works:

The Prostaglandin Synthesis Pathway: 

Prostaglandins are synthesized from arachidonic acid. This compound is also the precursor for the synthesis of endogenous cannabinoids.

Acetaminophen Metabolism:

When acetaminophen is metabolized it results in a compound p-aminophenol that is conjugated to arachidonic acid to form N-Arachidonylphenolamine (also known as AM-404).


This compound is a CB1 receptor agonist and is partially responsible for the anti-inflammatory and analgesic effects of Tylenol.

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Read 7359 times Last modified on Sunday, 08 June 2014 08:21