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For a long time no real natural CB1-cannabinoid-agonists were known except of the ones in Cannabis, then came exotic substances like 2-Sciadonoylglycerol from the seeds of Sciadopitys verticillata. This is a analog of the endogene 2-AG but has only a tenth to 1/20 of its action, so its not usable. The Echinacea- and Spilanthes- Alkylamides, noni-juice, pinen-derivatives, Tabernanthine and beta-Caryophyllene only act on the CB2-receptor in the immune system and not on the CB1. In a liverwort from New Zealand there was found Perrottetinene which has a very similar structure to THC, but it is thought to be an inhibitor of the receptor. Also Capsaicin, Falcarinol, Cinnamaldehyde, Voacamine and Voacangin-derivatives are inhibitors, and as such not usable for THC-like effects. Beta-Asarone is a allosteric modulator of the receptor, Thujone and Grenadamide are only very weak agonists. So it was a long way to find natural substances which act on the CB1-cannabinoid-receptor and now there came studies which described the occurence of them in well known plants. But: be aware of deducing psychoactive effects only from neurological findings of a plant with unknown psychological action. The neurological interrelationships are extremely complex and there are always new findings. They can only be used as a hint. In the following cases of plants, their actions are also well known, so there could be seen some coherences: First of all there is a study on Kanna (Sceletium tortuosum), which describes an action on CB1-cannabinoid-receptors of the alkaloid-extract. Its not the Mesembrine but other alkaloids responsible for this action and mainly from the nonfermented material. Additional to the SSRI-action, PDE4-inhibiting now there you can see a CB1-cannabinoid- activating and Acetylcholinesterase- inhibiting effect. It should be half as potent as THC. I wrote books about Kratom and Kanna, so this is of great interest to me. Also others and I could observe a potentiating effect on Cannabis from Kanna. They don't describe the Ki. The study: http://www.ifrj.upm.edu.my/17%20(02)%202010/IFRJ-2010-349-355_Alfi_Netherlands_(S).pdf (you may copy the complete link) Kava (Piper methysticum) was also tested positive for CB1-cannabinoid- action. Yangonin was the main active kavalactone with a K(i)= 0.72 μM on the CB1-receptor. THC is 15-times as strong but if one consumed a great dose of kava there must be some cannabinoid action additional to the others. The studies: http://sciencealerts...ml#.UEnAdbLN_k8 http://members.iif.h...resentation.pdf Then there is green tea (Camellia sinensis), which is also CB1-cannabinoid because of its catechins (3 of them). They found that EGCG (Epigallocatechin gallate) has a Ki of 33,6μM on the CB1-receptor, so it is much weaker than Yangonin, but it is also possible to drink a great amount of greentea... The study: http://www.missclass...a/cannaboid.pdf This one is for science: In a marine sponge Dasychalina fragilis from Papua New Guinea they found Haplosamate A, which was tested positive for cannabinoid action: http://www.ncbi.nlm....pubmed/19175306 The cannabinoid-like action of Lion's tail (Leonotis leonurus) isn't yet explained by action on CB1-receptors but Leonurine could be an Adenosine-reuptake-inhibitor (structurally very similar to Dilazep) or an action on the vanilloid-receptor (structurally similar to Capsaicin). Leonurine could in general produce cannabis-like effects (Auwarter, 2009).