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Over 100 chemically and biosynthetically related cannabinoids have been identified in cannabis to date. There are two major components, cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC) along with several other less potent cannabinoids, Cannabichromene (CBC), Cannabichromevarin (CBCV), Δ9-tetra hydrocannabivarin (THCV), cannabigerol (CBG), cannabigerovarin (CBGV), cannabidivarin (CBDV), and Cannabinol (CBN).
Studies of THC effects on human being led to discovery of a cannabinoid receptor (CB1) gene and human endocannabinoid System (ECS). The ECS was defined as the ensemble of 1) two transmembrane and G protein-coupled receptors (GPCRs) proteins for THC—cannabinoid receptor type 1(CB1) and cannabinoid receptor type 2 (CB2); 2) 2 endogenous ligands, the “endocannabinoids” N-arachidonoylethanolamine (anandamide) and 2-arachidonoylglycerol (2-AG); and 3) the enzymes are responsible for endocannabinoid biosynthesis [i.e., N-acyl-phosphatidyl-ethanolamine-selective phospholipase D (NAPE-PLD) and diacylglycerol lipases (DAGL) α and β, for anandamide and 2-AG, respectively] and hydrolytic inactivation [i.e., fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), for anandamide and 2-AG, respectively]. Endocannabinoids and ECS regulate synaptic plasticity in central nervous system to modulate brain functions such as memory, mood and emotions, and pain perceptions. ECS may promote both non-rapid-eye movement and rapid-eye-movement sleep by interacting with melanin-concentrating hormone neurons in the lateral hypothalamus.
THC and THCV were uniquely binding with high affinity to CB1 and CB2 (with agonist and antagonist activity for THC and THCV, respectively). CBD, on the other hand, may “indirectly” active CB1/CB2 by weakly inhibiting AEA enzymatic hydrolysis (i.e., fatty acid amide hydrolase (FAAH)) to regulate the ECS and effect the pain, anxiety, and insomnia conditions. Cannabinoids also exhibit moderate activity on a wide array of molecular target, i.e. orphan G protein-coupled receptors (GPCRs), several channel proteins belonging to the transient receptor potential (TRP) family, namely, rat and human TRPV1, as well as serotonin receptors (HT1A) to modulate brain functions, i.e. pain perceptions etc.
The therapeutic efficacy of cannabinoids may be impacted the genetic variations of receptor genes (CB1, CB2, TRPV1, and HT1A), transport and signaling genes, i.e. serotonin transporter (SLC6A4), metabolism genes that activating or inactivating cannabinoids, such as Catechol-O-Methyltransferase (COMT) and Cytochrome P450 genes (CYP2C9 and CYP3A4), as well as interactions of the genetic variations between these genes. Pharmacogenomic and pharmacogenetic test-guided target therapy likely provides cost effective personalized treatments, and it is particularly attractive for complex diseases or disorders of difficult in tailoring their treatments, i.e. chronic pain, insomnia, and anxiety.