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Hashish
Hashish, also known as 'hash', is a drug made by compressing and processing trichomes of the cannabis plant.[2][3] It is consumed by smoking, typically in a pipe, bong, vaporizer or joint, or sometimes via oral ingestion. Hash has a long history of usage in eastern countries such as Afghanistan, India, Iran, Morocco, and Pakistan.[4] Hash consumption is also popular in Europe, where it is the most common form of cannabis use. In the United States, dried flowers or concentrates are more popular, though hash has seen a rise in popularity following changes in law.[5][6] Like many recreational drugs, multiple synonyms and alternative names for hash exist, and vary greatly depending on the country and native language.[7] Hash is a cannabis concentrate product composed of compressed or purified preparations of stalked resin glands, called trichomes, from the plant
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2-Arachidonoylglycerol
2-Arachidonoylglycerol (2-AG) is an endocannabinoid, an endogenous agonist of the CB1 receptor and the primary endogenous ligand for the CB2 receptor.[1][2] It is an ester formed from the omega-6 fatty acid arachidonic acid and glycerol. It is present at relatively high levels in the central nervous system, with cannabinoid neuromodulatory effects. It has been found in maternal bovine and human milk.[3] The chemical was first described in 1994-1995, although it had been discovered some time before that
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2-Arachidonyl Glyceryl Ether
2-Arachidonyl glyceryl ether (2-AGE, Noladin ether) is a putative endocannabinoid discovered by Lumír Hanuš and colleagues at the Hebrew University of Jerusalem, Israel. It is an ether formed from the alcohol analog of arachidonic acid and glycerol. Its isolation from porcine brain and its structural elucidation and synthesis were described in 2001.[1] Lumír Hanuš, Saleh Abu-Lafi, Ester Fride, Aviva Breuer, Zvi Vogel, Deborah E. Shalev, Irina Kustanovich, and Raphael Mechoulam found the endogenous agonist of the cannabinoid receptor type 1 (CB1) in 2000. The discovery was 100 gram of porcine brain, (approximately a single brain) was added to a mixture of 200 mL of chloroform and 200 mL of methanol and mixed in a laboratory blender for 2 minutes. 100 mL of Water was then added, and the mixing process continued for another minute. After this, the mixture was filtered
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Anandamide
Anandamide (ANA), also known as N-arachidonoylethanolamine (AEA), is a fatty acid neurotransmitter derived from the non-oxidative metabolism of eicosatetraenoic acid (arachidonic acid), an essential omega-6 fatty acid. The name is taken from the Sanskrit word ananda, which means "joy, bliss, delight", and amide.[1][2] It is synthesized from N-arachidonoyl phosphatidylethanolamine by multiple pathways.[3] It is degraded primarily by the fatty acid amide hydrolase (FAAH) enzyme, which converts anandamide into ethanolamine and arachidonic acid. As such, inhibitors of FAAH lead to elevated anandamide levels and are being pursued for therapeutic use.[4][5] Anandamide was first described (and named) in 1992 by Raphael Mechoulam and his lab members W. A. Devane and Lumír Hanuš.[1] Anandamide's effects can occur in either the central or peripheral nervous system
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Cannabichromene
Cannabichromene (CBC), also called cannabichrome, cannanbichromene, pentylcannabichromene or cannabinochromene,[1] is one of the hundreds of cannabinoids found in the Cannabis plant,[2] and is therefore a phytocannabinoid. It bears structural similarity to the other natural cannabinoids, including tetrahydrocannabinol (THC), tetrahydrocannabivarin (THCV), cannabidiol (CBD), and cannabinol (CBN), among others.[2][3] CBC and its derivatives are as abundant as cannabinols in cannabis.[2] It is not scheduled by the Convention on Psychotropic Substances. Within the Cannabis plant, CBC occurs mainly as cannabichromenic acid (CBCA, 2-COOH-CBC, CBC-COOH). Geranyl pyrophosphate and olivetolic acid combine to produce cannabigerolic acid (CBGA; the sole intermediate for all other phytocannabinoids), which is cyclized by the enzyme CBCA synthase to form CBCA
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Virodhamine
Virodhamine (O-arachidonoyl ethanolamine; O-AEA) is an endocannabinoid and a nonclassic eicosanoid, derived from arachidonic acid. O-Arachidonoyl ethanolamine is arachidonic acid and ethanolamine joined by an ester linkage, the opposite of the amide linkage found in anandamide. Based on this opposite orientation, the molecule was named virodhamine from the Sanskrit word virodha, which means opposition. It acts as an antagonist of the CB1 receptor and agonist of the CB2 receptor. Concentrations of virodhamine in the human hippocampus are similar to those of anandamide, but they are 2- to 9-fold higher in peripheral tissues that express CB2
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Synthetic Cannabinoid
Synthetic cannabinoids are a class of molecules that bind to the same receptors to which cannabinoids (THC and CBD) in cannabis plants attach. They are designer drugs, commonly sprayed onto plant matter[1] and are usually smoked,[2] although they have also been ingested as a concentrated liquid form in the US and UK since 2016.[3] They have been marketed as herbal incense, or "herbal smoking blends",[2] and sold under common names like K2, Spice,[4] and Synthetic Marijuana.[1] They are often labeled "not for human consumption" for liability defense.[4] A large and complex variety of synthetic cannabinoids are designed in an attempt to avoid legal restrictions on cannabis, making synthetic cannabinoids designer drugs.[2] Most synthetic cannabinoids are agonists of the cannabinoid receptors
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AM-2201
AM-2201 (1-(5-fluoropentyl)-3-(1-naphthoyl)indole) is a recreational designer drug that acts as a potent but nonselective full agonist for the cannabinoid receptor.[1] It is part of the AM series of cannabinoids discovered by Alexandros Makriyannis at Northeastern University. Convulsions have been reported[2] including at doses as low as 10 mg.[3] AM-2201 is a full agonist for cannabinoid receptors
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