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CBD (cannabidiol) er et naturlig virkestoff som finnes i cannabisplanten og har en lang tradisjon i medisinsk sammenheng. Alle ekstrakter fra cannabisplante (uavhengig av THC) er regulert av FNs narkotikakonvensjon og narkotikaforskrift, og samtlige CBD-produkter basert på fra cannabisplanten regnes som narkotika (4).
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Interestingly, inspection of the chemical structures of the abundant 7-COOH-CBD derivatives, which account for about the half of the metabolites identified in the above study, reveals the branched alkyl chain of (2E)-2-propylpent-2-enoic acid (Δ 2(E) -valproate) embedded in the cyclohexenecarboxylic acid moiety of such acidic CBD metabolites. Δ 2(E) -Valproate is the major active metabolite of valproic acid, and unlike the parent saturated acid, its anticonvulsant properties are not compromised by hepatotoxicity and teratogenicity, and is well tolerated in humans. 61 Whether the 7-COOH-CBD metabolite species with a Δ 2(E) -valproate-like structure are involved in the antiepileptic activity of CBD remains to be established.
In 12 subjects, oral administration of chocolate cookies spiked with a blend of 40 mg CBD+20 mg THC resulted in low peak plasma levels of ∼5 ng/mL for each drug at 1.5–3 h. 33 Similar low peak plasma levels with a mean of 0.93 ng/mL (range: 0.3–2.6 ng/mL) were noted in 24 volunteers 1 h after oral ingestion of gelatin capsules with cannabis extract containing 5.4 mg CBD+10 mg THC. 34 Interesting results were obtained from experiments in which capsules filled with either unheated or heated cannabis extracts containing 10 mg THCtotal (THC+THCA) and 10–15 mg CBDtotal (CBD+CBDA) estimated when fresh: pharmacokinetic analysis of the blood of patients ingesting two such capsules showed mean peak plasma CBD concentrations four times higher in the unheated extract than in the heat-treated extract (1.24 ng/mL at 1.17 h vs. 0.30 ng/mL at 0.83 h, respectively). 35 The results suggest that the use of unheated cannabis extract rich in acidic phytocannabinoids may beneficially affect the uptake and metabolism of CBD or other phytocannabinoids.
The first demonstration of CB biotransformation in humans appears to be the study of Christiansen and Rafaelsen 56 who in 1969 reported the separation by thin layer chromatography several polar CB derivatives from the urine of 10 volunteers drinking cannabis “tea”; however, no attempts were made to identify the substances. Subsequently, the use of sophisticated analytical techniques, especially GC-MS and, occasionally, reliance on synthetic standards for structure confirmation allowed the unequivocal identification of CB metabolites in humans (see below).
The first CBD metabolites to be identified were isolated from rat liver homogenate and their structures were determined as a primary alcohol derived from the oxidation at the allylic C-7 methyl group on the cyclohexene moiety (7-OH-CBD) and a secondary alcohol resulting from the oxidation of the central (C-3′′) methylene group of the pentyl side chain (3′′-OH-CBD; for numbering, see Fig. 1 ) in 1973. 57,57a Since then, biotransformation studies in mammals, including humans, using various types of CBD administration have indicated considerable species variability. 26,58,59 All studies in vivo appear to have been restricted to the characterization of urinary CBD metabolites.
Human Metabolites of CBD
While first-pass metabolism could be avoided by rectal administration of suppository formulation of CBs, as it has been demonstrated for THC, 46,47 relevant studies with CBD appear to be lacking.
Although CBD was isolated and characterized first, THC has been investigated more thoroughly: THC is responsible for the unique psychoactivity of marijuana, or cannabis, which is an internationally controlled substance, nevertheless widely used for recreational purposes or, more recently, for self-medication. 6 Synthetic THC has been available for three decades as a medicine, and pharmaceutical-grade herbal cannabis, as well as formulations of cannabis extracts containing THC and CBD in well-defined ratios, has also been registered as medicines in several countries (see chapters of Part 3 of Pertwee 6 ). Due to its unique psychoactivity and therapeutic potential, both associated with the activation of cannabinoid (CB) receptors, as well as for forensic reasons, the pharmacokinetics and pharmacodynamics of THC is much better understood than those of the nonpsychoactive CBD, which for decades has been a neglected phytocannabinoid.
A recent study examined the safety and pharmacokinetics of 400 and 800 mg of CBD coadministered with various doses of the potent opioid analgesic fentanyl to 17 healthy individuals. 39 In a representative session, 3 h after the oral administration of 800 mg of CBD and 2 h after fentanyl injection (0.5 μg/kg i.v.), the highest plasma concentration of CBD was 221±36 ng/mL; the mean peak urinary CBD concentration was recorded at 4 h after CBD intake and estimated to be 3.7 ng/mL.
In an early study with healthy volunteers who were given 20 mg [ 3 H]CBD by intravenous (i.v.) injection, 7-COOH-CBD was the most abundant metabolite in the plasma, while 7-OH-CBD was only a minor biotransformation product (in the original publication, the compounds are referred to as 11-carboxy-CBD and 11-hydroxy-CBD, respectively). 32 In the urine, unchanged CBD and, to a lesser extent, conjugated CBD were the main excretion products and about 16% of the total radioactivity was eliminated in 72 h by this route of excretion. It was also observed that 33% of the total radioactivity, again mostly unchanged CBD accompanied by several oxygenated metabolites, including mono- and dihydroxylated and monocarboxylic derivatives of CBD, was excreted in the feces within 72 h. In a subsequent and more detailed investigation, five young marijuana smokers were given 20 mg [ 2 H]CBD by i.v. injection. 31 At 3 min following drug administration, the CBD plasma levels peaked at 686 ng/mL (range: 356–962 ng/mL), which rapidly dropped to 48 ng/mL (range: 37–61 ng/mL) after 1 h; the mean half-life was 24±6 h.
Experiments in vitro with seven recombinant human CYP450 isoforms indicated 6α-OH-, 6β-OH-, 7-OH-, and 4′′-OH-CBD as main monohydroxylated metabolites. 60 Specifically, CYP1A1 is involved in the formation of 6α/β-OH-, 7-OH-, and 1′′-OH-CBD; CYP1A2 is responsible for the formation of 6α/β-OH-CBD, as well as of 1′′-, 2′′-, 3′′-, and 4′′-OH-CBD species; CYP2C19 is involved in the formation mostly of 6α-OH-, 7-OH-, and 4′′-OH-CBD; CYP2D6 appears to be the main isoform responsible for the formation of 6α/β-OH-CBD as well as of 7-OH-, 4′′-OH-, and 5′′-OH-CBD; CYP3A4 efficiently catalyzes the formation of 6α/β-OH-CBD, although the 7-OH-, 2′′-OH-, 4′′-OH-, and 5′′-OH-CBD metabolites are also produced by this isoform; CYP3A5 is involved in the formation mainly of 6α/β-OH-CBD although the 7-OH-, 2′′-OH-, 3′′-OH-, and 4′′-OH-CBD metabolites are also produced. The role of CYP2A9 appears to be minor, but 6α/β-OH-, 7-OH-, 4′′-OH-, and 5′′-OH-CBD could be formed by this isoform.