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THCA and CBDA provide significant anti-nausea and anti-vomiting effects. In rats,THCA was more potent compound in this regard than THC both via serotonin-receptor activation.
Non-steroidal anti-inflammatory (NSAID) drugs such as acetylsalicylic acid (aspirin), ibuprofen, naproxen, indomethacin, and diclofenac all work via COX 1 and 2 inhibition, and, like CBDA and THCA, contain a carboxylic acid group in their structures that suggests this part of the molecule is integral to the way they work.
Conversion of THCA to THC in vivo appears to be very limited, giving it only very slight efficacy as a prodrug for THC.[1] It is generally thought to be pharmacologically inactive.[1] In receptor binding assays it is promiscuous;[4] there are papers showing it being an inhibitor of PC-PLC, COX-1, COX-2, TRPM8, TRPV1, FAAH, NAAA, MGL, and DGLα, and an inhibitor of anandamide transport, as well as an agonist of TRPA1 and TRPV2.