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CBD heated to 175, [13] or 250–300 °C may partially be converted into THC. [14] Even at room temperature, trace amounts of THC can be formed as a contaminant in CBD stored for long periods in the presence of moisture and carbon dioxide in the air, with storage under inert gas required to maintain analytically pure CBD.
Sodium channel blockers are also used as local anesthetics and anticonvulsants. [5] Sodium channel blockers have been proposed for use in the treatment of cystic fibrosis, [6] but current evidence is mixed. [7] It has been suggested that the analgesic effects of some antidepressants may be mediated in part via sodium channel blockade. [8]
An equianalgesic chart is a conversion chart that lists equivalent doses of analgesics (drugs used to relieve pain). Equianalgesic charts are used for calculation of an equivalent dose (a dose which would offer an equal amount of analgesia) between different analgesics. [1]
The oral bioavailability of cannabidiol is approximately 6% in fasting state and 36.5—57.3% in fed-state [71] in humans, while its bioavailability via inhalation is 11 to 45% (mean 31%). [11] [12] [71] [72] The oral bioavailability of cannabidiol varies based on several factors such as formulation, [72] dose, and food intake. [71]
However, other research has found that CBG does inhibit FAAH and DGL, as well as monoacylglycerol lipase (MAGL), although it is less potent as an inhibitor of FAAH than cannabidiol (CBD). Aside from endocannabinoid-metabolizing enzymes, CBG is a weak inhibitor of the cyclooxygenase COX-1 and COX-2 enzymes (30% inhibition of each at 25,000 nM). [1]
[5] [6] Nabiximols is a combination drug standardized in composition, formulation, and dose. Its principal active components are the cannabinoids: tetrahydrocannabinol (THC) and cannabidiol (CBD). Each spray delivers a dose of 2.7 mg THC and 2.5 mg CBD. In 2003, GW Pharmaceuticals partnered with Bayer to market the drug under the brand name ...
Cannabidiol has little affinity for CB 1 and CB 2 receptors but acts as an indirect antagonist of cannabinoid agonists. [25] It was found to be an antagonist at the putative new cannabinoid receptor, GPR55, a GPCR expressed in the caudate nucleus and putamen. [26] Cannabidiol has also been shown to act as a 5-HT 1A receptor agonist. [27]
[1] [2] Cannabidiol (CBD), a naturally occurring cannabinoid and a non-competitive CB 1 /CB 2 receptor antagonist, as well as Δ 9-tetrahydrocannabivarin (THCV), a naturally occurring cannabinoid, modulate the effects of THC via direct blockade of cannabinoid CB 1 receptors, thus behaving like first-generation CB 1 receptor inverse agonists ...