WordNet
- psychoactive substance present in marijuana; used therapeutically to control nausea associated with cancer therapy
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/12/09 07:00:36」(JST)
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"THC" redirects here. For other uses, see THC (disambiguation).
| Systematic (IUPAC) name | |
|---|---|
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(−)-(6aR,10aR)-6,6,9-Trimethyl-3-pentyl-6a,7,8,10a-tetrahydro-6H-benzo[c]chromen-1-ol
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| Clinical data | |
| Trade names | Marinol |
| Licence data | US FDA:link |
| Pregnancy category |
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| Legal status |
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| Dependence liability |
8–10% (Relatively low risk of tolerance)[1] |
| Routes of administration |
Orally, local/topical, transdermal, sublingual, inhaled |
| Pharmacokinetic data | |
| Bioavailability | 10–35% (inhalation), 6–20% (oral)[3] |
| Protein binding | 97–99%[3][4][5] |
| Metabolism | Mostly hepatic by CYP2C[3] |
| Biological half-life | 1.6–59 h,[3] 25–36 h (orally administered dronabinol) |
| Excretion | 65–80% (feces), 20–35% (urine) as acid metabolites[3] |
| Identifiers | |
| CAS Number | 1972-08-3 Y |
| ATC code | A04AD10 |
| PubChem | CID: 16078 |
| IUPHAR/BPS | 2424 |
| DrugBank | DB00470 Y |
| ChemSpider | 15266 Y |
| UNII | 7J8897W37S Y |
| ChEBI | CHEBI:66964 N |
| ChEMBL | CHEMBL465 Y |
| Synonyms | Dronabinol |
| Chemical data | |
| Formula | C21H30O2 |
| Molecular mass | 314.469 g/mol |
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SMILES
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InChI
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| Physical data | |
| Boiling point | 157 °C (315 °F) [7] |
| Solubility in water | 0.0028,[6] (23 °C) mg/mL (20 °C) |
| Specific rotation | -152° (ethanol) |
| N (what is this?) (verify) | |
Tetrahydrocannabinol (THC), or more precisely its main isomer (−)-trans-Δ9-tetrahydrocannabinol ( (6aR,10aR)-delta-9-tetrahydrocannabinol), is the principal psychoactive constituent (or cannabinoid) of cannabis. First isolated in 1964 by Israeli scientists Prof. Raphael Mechoulam and Dr. Yechiel Gaoni at the Weizmann Institute of Science[8][9][10] it is a water-clear glassy solid when cold, which becomes viscous and sticky if warmed. A pharmaceutical formulation of (−)-trans-Δ9-tetrahydrocannabinol, known by its INN dronabinol, is available by prescription in the U.S. and Canada under the brand name Marinol. An aromatic terpenoid, THC has a very low solubility in water, but good solubility in most organic solvents, specifically lipids and alcohols.[6] THC, CBD, CBN, CBC, CBG and about 80 other molecules make up the phytocannabinoid family.
Like most pharmacologically-active secondary metabolites of plants, THC in Cannabis is assumed to be involved in self-defense, perhaps against herbivores.[11] THC also possesses high UV-B (280–315 nm) absorption properties, which, it has been speculated, could protect the plant from harmful UV radiation exposure.[12][13][14]
Tetrahydrocannabinol, along with its double bond isomers and their stereoisomers, is one of only three cannabinoids scheduled by the Convention on Psychotropic Substances (the other two are dimethylheptylpyran and parahexyl). Previously listed as a substance under Schedule I of the 1971 Convention on Psychotropic Substances, THC was reclassified to Schedule II in 1991 following a recommendation from the World Health Organization. Based on their subsequent studies, the WHO has recommended for the reclassification of THC to the less-stringent Schedule III.[15] Cannabis as a plant is scheduled by the Single Convention on Narcotic Drugs (Schedule I and IV).
Contents
- 1 Effects
- 1.1 Appetite and taste
- 2 Medical uses
- 2.1 Multiple sclerosis symptoms
- 2.2 Neurodegenerative disorders
- 2.3 Other neurological disorders
- 2.4 Other studies in humans
- 3 Adverse effects
- 3.1 Acute toxicity
- 3.2 Cognitive effects
- 3.3 Impact on psychosis
- 3.4 Other potential long-term effects
- 4 Interactions
- 5 Pharmacology
- 5.1 Mechanism of action
- 5.2 Pharmacokinetics
- 6 Physical and chemical properties
- 6.1 Discovery and structure identification
- 6.2 Isomerism
- 6.3 Biosynthesis
- 6.4 Detection in body fluids
- 7 History
- 8 Society and culture
- 8.1 Brand names
- 8.1.1 Comparisons with medical cannabis
- 8.1 Brand names
- 9 See also
- 10 References
- 11 External links
Effects
See also: Effects of cannabis, Long-term effects of cannabis and Cannabis in pregnancy
THC has mild to moderate analgesic effects, and cannabis can be used to treat pain by altering transmitter release on dorsal root ganglion of the spinal cord and in the periaqueductal gray.[16] Other effects include relaxation, alteration of visual, auditory, and olfactory senses, fatigue, and appetite stimulation. THC has marked antiemetic properties. It may acutely reduce aggression.[17]
Due to its partial agonistic activity, THC appears to result in greater downregulation of cannabinoid receptors than endocannabinoids, further limiting its efficacy over other cannabinoids. While tolerance may limit the maximal effects of certain drugs, evidence suggests that tolerance develops irregularly for different effects with greater resistance for primary over side-effects, and may actually serve to enhance the drug's therapeutic window.[18] However, this form of tolerance appears to be irregular throughout mouse brain areas. THC, as well as other cannabinoids that contain a phenol group, possesses mild antioxidant activity sufficient to protect neurons against oxidative stress, such as that produced by glutamate-induced excitotoxicity.[19]
Appetite and taste
A study in mice suggested that based on the connection between palatable food and stimulation of dopamine (DA) transmission in the shell of the nucleus accumbens (NAc), cannabis may not only stimulate taste, but possibly the hedonic (pleasure) value of food as well. The study later demonstrates habitual use of THC lessening this heightened pleasure response, indicating a possible similarity in humans.[20] The inconsistency between DA habituation and enduring appetite observed after THC application suggests that cannabis-induced appetite stimulation is not only mediated by enhanced pleasure from palatable food, but through THC stimulation of another appetitive response as well.[citation needed]
Medical uses
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In April 2014 the American Academy of Neurology published a systematic review of the efficacy and safety of medical marijuana and marijuana-derived products in certain neurological disorders.[21] The review identified 34 studies meeting inclusion criteria, of which 8 were rated as Class I quality.[21] The study found evidence supporting the effectiveness of cannabis extracts and THC in treating certain symptoms of multiple sclerosis, but found insufficient evidence to determine the effectiveness of cannabis products in treating several other neurological diseases.[21]
Multiple sclerosis symptoms
- Spasticity. Based on the results of 3 high quality trials and 5 of lower quality, oral cannabis extract was rated as effective, and THC as probably effective, for improving patient's subjective experience of spasticity. Oral cannabis extract and THC both were rated as possibly effective for improving objective measures of spasticity.[21]
- Centrally mediated pain and painful spasms. Based on the results of 4 high quality trials and 4 low quality trials, oral cannabis extract was rated as effective, and THC as probably effective in treating central pain and painful spasms.[21]
- Bladder dysfunction. Based on a single high quality study, oral cannabis extract and THC were rated as probably ineffective for controlling bladder complaints in multiple sclerosis[21]
Neurodegenerative disorders
- Huntington disease. No reliable conclusions could be drawn regarding the effectiveness of THC or oral cannabis extract in treating the symptoms of Huntington disease as the available trials were too small to reliably detect any difference[21]
- Parkinson disease. Based on a single study, oral cannabis extract was rated probably ineffective in treating levodopa-induced dyskinesia in Parkinson disease.[21]
- Alzheimer's disease. A 2011 Cochrane Review found insufficient evidence to conclude whether cannabis products have any utility in the treatment of Alzheimer's disease.[22]
Other neurological disorders
- Tourette syndrome. The available data was determined to be insufficient to allow reliable conclusions to be drawn regarding the effectiveness of oral cannabis extract or THC in controlling tics.[21]
- Cervical dystonia. Insufficient data was available to assess the effectiveness of oral cannabis extract of THC in treating cervical dystonia.[21]
- Epilepsy. Data was considered insufficient to judge the utility of cannabis products in reducing seizure frequency or severity.[21]
Other studies in humans
Evidence suggests that THC helps alleviate symptoms suffered both by AIDS patients, and by cancer patients undergoing chemotherapy, by increasing appetite and decreasing nausea.[23][24][25][26] It has also been shown to assist some glaucoma patients[medical citation needed] by reducing pressure within the eye, and is used in the form of cannabis by a number of multiple sclerosis patients, who use it to alleviate neuropathic pain and spasticity. The National Multiple Sclerosis Society is currently supporting further research into these uses.[27] THC has also shown antitumor activity in animal studies where it killed cancer cells.[28] Studies in humans have been limited by federal and state laws criminalizing marijuana.
In August 2009 a phase IV clinical trial by the Hadassah Medical Center in Jerusalem, Israel started to investigate the effects of THC on post-traumatic stress disorders.[29]
Studies have been conducted with spinal injury patients and THC.[30]
Both THC and CBD phytocannabinoids have been shown to decrease intestinal permeability.[31]
Adverse effects
A hybrid Cannabis strain (White Widow) (which contains one of the highest amounts of Cannabidiol), flower coated with trichomes, which contain more THC than any other part of the plant
Closeup of THC-filled trichomes on a Cannabis sativa leaf
Acute toxicity
There has never been a documented human fatality solely from overdosing on tetrahydrocannabinol.[32] However, numerous reports have suggested an association of cannabis smoking with an increased risk of myocardial infarction,[33][34] also known as a heart attack. Information about the toxicity of THC is primarily based on results from non-human studies. The toxicity depends on the route of administration and the laboratory animal.
The estimated lethal dose of intravenous dronabinol in humans is 30 mg/kg,[35] meaning lethality is unlikely. The typical medicinal dosage administered is two 2.5 mg capsules daily; for an 80 kg man (~170 lb). A lethal dose for such a person would be 960 of those capsules infused intravenously. Non-fatal overdoses have occurred: "Significant CNS symptoms in antiemetic studies followed oral doses of 0.4 mg/kg (28 mg/70 kg) of dronabinol capsules."[35]
-
- A meta analysis of cannabis and THC clinical trials conducted by the American Academy of Neurology found that of 1619 persons treated with cannabis products (including some treated with smoked cannabis and nabiximols), 6.9% discontinued due to side effects, compared to 2.2% of 1,118 treated with placebo. Detailed information regarding side effects was not available from all trials, but nausea, increased weakness, behavioral or mood changes, suicidal ideation, hallucinations, dizziness, and vasovagal symptoms, fatigue, and feelings of intoxication were each described as side effects in at least 2 trials. There was a single death rated by the investigator as "possibly related" to treatment. This person had a seizure followed by aspiration pneumonia. The paper does not describe whether this was one of the patients from the epilepsy trials.[21]
Cognitive effects
Its status as an illegal drug in most countries can make research difficult; for instance in the United States where the National Institute on Drug Abuse was the only legal source of cannabis for researchers until it recently became legalized in Colorado, Washington state, Oregon, Alaska, and Washington D.C.[36]
A 2011 systematic review evaluated published studies of the acute and long-term cognitive effects of cannabis. THC intoxication is well established to impair cognitive functioning on an acute basis, including effects on the ability to plan, organize, solve problems, make decisions, and control impulses. The extent of this impact may be greater in novice users, and paradoxically, those habituated to high level ingestion may have reduced cognition during withdrawal. Studies of long-term effects on cognition have provided conflicting results, with some studies finding no difference between long-term abstainers and never-users and others finding long-term deficits. The discrepancies between studies may reflect greater long-term effects among heavier users relative to occasional users, and greater duration of effect among those with heavy use as adolescents compared to later in life.[37] A second systematic review focused on neuroimaging studies found little evidence supporting an effect of cannabis use on brain structure and function.[38] A 2003 meta analysis concluded that any long-term cognitive effects were relatively modest in magnitude and limited to certain aspects of learning and memory.[39]
Impact on psychosis
A 2007 meta analysis concluded that cannabis use reduced the average age of onset of psychosis by 2.7 years relative to non-cannabis use.[40] A 2005 meta analysis concluded that adolescent use of cannabis increases the risk of psychosis, and that the risk is dose-related.[41] A 2004 literature review on the subject concluded that cannabis use is associated with a two-fold increase in the risk of psychosis, but that cannabis use is "neither necessary nor sufficient" to cause psychosis.[42] A French review from 2009 came to a conclusion that cannabis use, particularly that before age 15, was a factor in the development of schizophrenic disorders.[43]
Some studies have suggested that cannabis users have a greater risk of developing psychosis than non-users. This risk is most pronounced in cases with an existing risk of psychotic disorder.[44][45] A 2005 paper from the Dunedin study suggested an increased risk in the development of psychosis linked to polymorphisms in the COMT gene.[46] However, a more recent study cast doubt on the proposed connection between this gene and the effects of cannabis on the development of psychosis.[47]
A 2008 German review reported that cannabis was a causal factor in some cases of schizophrenia and stressed the need for better education among the public due to increasingly relaxed access to cannabis.[48]
Other potential long-term effects
A 2008 National Institutes of Health study of 19 chronic heavy marijuana users with cardiac and cerebral abnormalities (averaging 28 g to 272 g (1 to 9+ oz) weekly) and 24 controls found elevated levels of apolipoprotein C-III (apoC-III) in the chronic smokers.[49] An increase in apoC-III levels induces the development of hypertriglyceridemia.
Interactions
The effects of the drug can be reduced by the CB1 receptor inverse agonist rimonabant (SR141716A) as well as opioid receptor antagonists (opioid blockers) naloxone and naloxonazine.[20][50] The α7 nicotinic receptor antagonist methyllycaconitine can block self-administration of THC in rates comparable to the effects of varenicline on nicotine administration.[51]
Cannabidiol, the second most abundant cannabinoid found in cannabis, is an indirect antagonist against cannabinoid agonists; thus reducing the effects of anandamide and THC agonism on the CB1 and CB2 receptors.
Pharmacology
Mechanism of action
For a review of the mechanisms behind endocannabinoid synaptic transmission, see Endocannabinoid system.
The actions of THC result from its partial agonist activity at the cannabinoid receptor CB1 (Ki=10nM[52]), located mainly in the central nervous system, and the CB2 receptor (Ki=24nM[52]), mainly expressed in cells of the immune system.[19] The psychoactive effects of THC are primarily mediated by its activation of CB1G-protein coupled receptors, which result in a decrease in the concentration of the second messenger molecule cAMP through inhibition of adenylate cyclase.[16]
The presence of these specialized cannabinoid receptors in the brain led researchers to the discovery of endocannabinoids, such as anandamide and 2-arachidonoyl glyceride (2-AG). THC targets receptors in a manner far less selective than endocannabinoid molecules released during retrograde signaling, as the drug has a relatively low cannabinoid receptor efficacy and affinity. In populations of low cannabinoid receptor density, THC may act to antagonize endogenous agonists that possess greater receptor efficacy.[18] THC is a lipophilic molecule[53] and may bind non-specifically to a variety of entities in the brain and body, such as adipose tissue (fat).[54][55]
THC, similarly to cannabidiol, albeit less potently, is an allosteric modulator of the μ- and δ-opioid receptors.[56]
Pharmacokinetics
THC is metabolized mainly to 11-OH-THC by the body. This metabolite is still psychoactive and is further oxidized to 11-nor-9-carboxy-THC (THC-COOH). In humans and animals, more than 100 metabolites could be identified, but 11-OH-THC and THC-COOH are the dominating metabolites. Metabolism occurs mainly in the liver by cytochrome P450 enzymes CYP2C9, CYP2C19, and CYP3A4.[57] More than 55% of THC is excreted in the feces and ~20% in the urine. The main metabolite in urine is the ester of glucuronic acid and THC-COOH and free THC-COOH. In the feces, mainly 11-OH-THC was detected.[58]
Physical and chemical properties
Discovery and structure identification
The discovery of THC by a team of researchers from Hebrew University Pharmacy School was first described in "Isolation, structure and partial synthesis of an active constituent of hashish", published in the Journal of the American Chemical Society in 1964.[8] Research was also published in the academic journal Science, with "Marijuana chemistry" by Raphael Mechoulam in June 1970.[59]
Isomerism
| This section does not cite any references (sources). Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (January 2014) |
| 7 double bond isomers and their 30 stereoisomers | ||||||||
|---|---|---|---|---|---|---|---|---|
| Dibenzopyran numbering | Monoterpenoid numbering | Number of stereoisomers | Natural occurrence | Convention on Psychotropic Substances Schedule | Structure | |||
| Short name | Chiral centers | Full name | Short name | Chiral centers | ||||
| Δ6a,7-tetrahydrocannabinol | 9 and 10a | 8,9,10,10a-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol | Δ4-tetrahydrocannabinol | 1 and 3 | 4 | No | Schedule I | |
| Δ7-tetrahydrocannabinol | 6a, 9 and 10a | 6a,9,10,10a-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol | Δ5-tetrahydrocannabinol | 1, 3 and 4 | 8 | No | Schedule I | |
| Δ8-tetrahydrocannabinol | 6a and 10a | 6a,7,10,10a-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol | Δ6-tetrahydrocannabinol | 3 and 4 | 4 | Yes | Schedule I | |
| Δ9,11-tetrahydrocannabinol | 6a and 10a | 6a,7,8,9,10,10a-hexahydro-6,6-dimethyl-9-methylene-3-pentyl-6H-dibenzo[b,d]pyran-1-ol | Δ1,7-tetrahydrocannabinol | 3 and 4 | 4 | No | Schedule I | |
| Δ9-tetrahydrocannabinol | 6a and 10a | 6a,7,8,10a-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol | Δ1-tetrahydrocannabinol | 3 and 4 | 4 | Yes | Schedule II | |
| Δ10-tetrahydrocannabinol | 6a and 9 | 6a,7,8,9-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol | Δ2-tetrahydrocannabinol | 1 and 4 | 4 | No | Schedule I | |
| Δ6a,10a-tetrahydrocannabinol | 9 | 7,8,9,10-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol | Δ3-tetrahydrocannabinol | 1 | 2 | No | Schedule I | |
| 4 stereoisomers of Δ9-tetrahydrocannabinol | ||||
|---|---|---|---|---|
| Names | Description | Natural occurrence | Structure | |
| (−)-trans-Δ9-tetrahydrocannabinol | (6aR,10aR)-Δ9-tetrahydrocannabinol | levorotary trans | Yes | |
| (−)-cis-Δ9-tetrahydrocannabinol | (6aS,10aR)-Δ9-tetrahydrocannabinol | levorotary cis | Yes | |
| (+)-trans-Δ9-tetrahydrocannabinol | (6aS,10aS)-Δ9-tetrahydrocannabinol | dextrorotary trans | No | |
| (+)-cis-Δ9-tetrahydrocannabinol | (6aR,10aS)-Δ9-tetrahydrocannabinol | dextrorotary cis | No | |
Note that 6H-dibenzo[b,d]pyran-1-ol is the same as 6H-benzo[c]chromen-1-ol.
- Further reading on cannabanoid isomerism: John C. Leffingwell (May 2003). "Chirality & Bioactivity I.: Pharmacology" (PDF). pp. 18–20. Retrieved 12 January 2014.
Biosynthesis
Biosynthesis of THC
In the Cannabis plant, THC occurs mainly as tetrahydrocannabinolic acid (THCA, 2-COOH-THC). Geranyl pyrophosphate and olivetolic acid react, catalysed by an enzyme to produce cannabigerolic acid,[60] which is cyclized by the enzyme THC acid synthase to give THCA. Over time, or when heated, THCA is decarboxylated, producing THC. The pathway for THCA biosynthesis is similar to that which produces the bitter acid humulone in hops.[61][62]
Detection in body fluids
Main article: Cannabis drug testing
THC, 11-OH-THC and THC-COOH can be detected and quantified in blood, urine, hair, oral fluid or sweat using a combination of immunoassay and chromatographic techniques as part of a drug use testing program or in a forensic investigation of a traffic or other criminal offense or suspicious death.[63][64][65]
History
For more details on this topic, see Removal of cannabis from Schedule I of the Controlled Substances Act.
Since at least 1986, the trend has been for THC in general, and especially the Marinol preparation, to be downgraded to less and less stringently-controlled schedules of controlled substances, in the U.S. and throughout the rest of the world.[citation needed]
On May 13, 1986, the Drug Enforcement Administration (DEA) issued a Final Rule and Statement of Policy authorizing the "Rescheduling of Synthetic Dronabinol in Sesame Oil and Encapsulated in Soft Gelatin Capsules From Schedule I to Schedule II" (DEA 51 FR 17476-78). This permitted medical use of Marinol, albeit with the severe restrictions associated with Schedule II status.[66] For instance, refills of Marinol prescriptions were not permitted. At its 1045th meeting, on April 29, 1991, the Commission on Narcotic Drugs, in accordance with article 2, paragraphs 5 and 6, of the Convention on Psychotropic Substances, decided that Δ9-tetrahydrocannabinol (also referred to as Δ9-THC) and its stereochemical variants should be transferred from Schedule I to Schedule II of that Convention. This released Marinol from the restrictions imposed by Article 7 of the Convention (See also United Nations Convention Against Illicit Traffic in Narcotic Drugs and Psychotropic Substances).[citation needed]
An article published in the April–June 1998 issue of the Journal of Psychoactive Drugs found that "Healthcare professionals have detected no indication of scrip-chasing or doctor-shopping among the patients for whom they have prescribed dronabinol". The authors state that Marinol has a low potential for abuse.[67]
In 1999, Marinol was rescheduled from Schedule II to III of the Controlled Substances Act, reflecting a finding that THC had a potential for abuse less than that of cocaine and heroin. This rescheduling constituted part of the argument for a 2002 petition for removal of cannabis from Schedule I of the Controlled Substances Act, in which petitioner Jon Gettman noted, "Cannabis is a natural source of dronabinol (THC), the ingredient of Marinol, a Schedule III drug. There are no grounds to schedule cannabis in a more restrictive schedule than Marinol".[68]
At its 33rd meeting, in 2003, the World Health Organization Expert Committee on Drug Dependence recommended transferring THC to Schedule IV of the Convention, citing its medical uses and low abuse potential.[69]
Society and culture
Brand names
Not to be confused with Droperidol.
Dronabinol is the INN for a pure isomer of THC, (–)-trans-Δ9-tetrahydrocannabinol,[70] which is the main isomer found in cannabis. Synthesized dronabinol is marketed as Marinol[71] (a registered trademark of Solvay Pharmaceuticals). Dronabinol is also marketed, sold, and distributed by PAR Pharmaceutical Companies under the terms of a license and distribution agreement with SVC pharma LP, an affiliate of Rhodes Technologies. Synthesized THC may be generally referred to as dronabinol. It is available as a prescription drug (under Marinol[72]) in several countries including the United States, Germany, South Africa and Australia.[73] In the United States, Marinol is a Schedule III drug, available by prescription, considered to be non-narcotic and to have a low risk of physical or mental dependence. Efforts to get cannabis rescheduled as analogous to Marinol have not succeeded thus far, though a 2002 petition has been accepted by the DEA. As a result of the rescheduling of Marinol from Schedule II to Schedule III, refills are now permitted for this substance. Marinol has been approved by the U.S. Food and Drug Administration (FDA) in the treatment of anorexia in HIV/AIDS patients, as well as for refractory nausea and vomiting of patients undergoing chemotherapy, which has raised much controversy[74] as to why natural THC is considered a schedule I drug.[75]
An overdose usually presents with lethargy, decreased motor coordination, slurred speech, and postural hypotension. The FDA estimates the lethal human dose of intravenous dronabinol to be 30 mg/kg (2100 mg/ 70 kg).[76]
An analog of dronabinol, nabilone, is available commercially in Canada under the trade name Cesamet, manufactured by Valeant Pharmaceuticals. Cesamet has also received FDA approval and began marketing in the U.S. in 2006. Nabilone is a Schedule II drug.[77]
Comparisons with medical cannabis
Further information: Medical cannabis
Female cannabis plants contain more than 60 cannabinoids, including cannabidiol (CBD), thought to be the major anticonvulsant that helps multiple sclerosis patients;[78] and cannabichromene (CBC), an anti-inflammatory which may contribute to the pain-killing effect of cannabis.[79]
It takes over one hour for Marinol to reach full systemic effect,[80] compared to seconds or minutes for smoked or vaporized cannabis.[81] Some patients accustomed to inhaling just enough cannabis smoke to manage symptoms have complained of too-intense intoxication from Marinol's predetermined dosages[citation needed]. Many patients have said that Marinol produces a more acute psychedelic effect than cannabis, and it has been speculated that this disparity can be explained by the moderating effect of the many non-THC cannabinoids present in cannabis.[citation needed] For that reason, alternative THC-containing medications based on botanical extracts of the cannabis plant such as nabiximols are being developed. Mark Kleiman, director of the Drug Policy Analysis Program at UCLA's School of Public Affairs said of Marinol, "It wasn't any fun and made the user feel bad, so it could be approved without any fear that it would penetrate the recreational market, and then used as a club with which to beat back the advocates of whole cannabis as a medicine."[82] Mr. Kleiman's opinion notwithstanding, clinical trials comparing the use of cannabis extracts with Marinol in the treatment of cancer cachexia have demonstrated equal efficacy and well-being among patients in the two treatment arms.[83] United States federal law currently registers dronabinol as a Schedule III controlled substance, but all other cannabinoids remain Schedule I, except synthetics like nabilone.[84]
See also
| Cannabis portal | |
| Chemistry portal |
- Anandamide
- Cannabis (drug)
- Psychoactive drug
- Cannabinoids
- 11-Hydroxy-THC, metabolite of THC
- Anandamide, 2-Arachidonoylglycerol, endogenous cannabinoid agonists
- Cannabidiol (CBD), an isomer of THC
- Cannabinol (CBN), a metabolite of THC
- Dimethylheptylpyran
- Parahexyl
- Tetrahydrocannabinolic acid, the biosynthetic precursor for THC
- HU-210, WIN 55,212-2, JWH-133, synthetic cannabinoid agonists
- Medical cannabis
- War on Drugs
- Cannabis rescheduling in the United States
- Health issues and the effects of cannabis
References
- ^ Marlowe, Douglas B. (December 2010). "The Facts On Marijuana". NADCP.
Based upon several nationwide epidemiological studies, marijuana’s dependence liability has been reliably determined to be 8 to 10 percent.
- ^ http://www.fda.gov/ohrms/dockets/dockets/05n0479/05N-0479-emc0004-04.pdf
- ^ a b c d e Grotenhermen, F (2003). "Pharmacokinetics and pharmacodynamics of cannabinoids". Clin Pharmacokinet 42 (4): 327–60. doi:10.2165/00003088-200342040-00003. PMID 12648025. (subscription required (help)).
- ^ The Royal Pharmaceutical Society of Great Britain (30 November 2006). "Cannabis". In Sean C. Sweetman. Martindale: The Complete Drug Reference: Single User (35th ed.). Pharmaceutical Press. ISBN 978-0-85369-703-9. [page needed]
- ^ "Tetrahydrocannabinol – Compound Summary". National Center for Biotechnology Information. PubChem. Retrieved 12 January 2014.
Dronabinol has a large apparent volume of distribution, approximately 10 L/kg, because of its lipid solubility. The plasma protein binding of dronabinol and its metabolites is approximately 97%.
- ^ a b Garrett ER, Hunt CA (July 1974). "Physicochemical properties, solubility, and protein binding of Δ9-tetrahydrocannabinol". J. Pharm. Sci. 63 (7): 1056–64. doi:10.1002/jps.2600630705. PMID 4853640.
- ^ McPartland JM, Russo EB (2001). "Cannabis and cannabis extracts: greater than the sum of their parts?" (PDF). Journal of Cannabis Therapeutics 1 (3/4): 103–132. doi:10.1300/J175v01n03_08.
- ^ a b Gaoni Y, Mechoulam R (1964). "Isolation, structure and partial synthesis of an active constituent of hashish". Journal of the American Chemical Society 86 (8): 1646–1647. doi:10.1021/ja01062a046.
- ^ "Interview with the winner of the first ECNP Lifetime Achievement Award: Raphael Mechoulam, Israel". February 2007.
- ^ Geller, Tom (2007). "Cannabinoids: A Secret History". Chemical Heritage Newsmagazine 25 (2). Archived from the original on 19 June 2008.
- ^ Pate, David W. (1994). "Chemical ecology of Cannabis". Journal of the International Hemp Association 1 (29): 32–37.
- ^ Pate, David W. (1983). "Possible role of ultraviolet radiation in evolution of Cannabis chemotypes". Economic Botany 37 (4): 396–405. doi:10.1007/BF02904200.
- ^ Lydon, John; Teramura, Alan H. (1987). "Photochemical decomposition of cannabidiol in its resin base". Phytochemistry 26 (4): 1216–1217. doi:10.1016/S0031-9422(00)82388-2.
- ^ Lydon J, Teramura AH, Coffman CB (1987). "UV-B radiation effects on photosynthesis, growth and cannabinoid production of two Cannabis sativa chemotypes". Photochemistry and Photobiology 46 (2): 201–206. doi:10.1111/j.1751-1097.1987.tb04757.x. PMID 3628508.
- ^ A Primer on the UN Drug Control Conventions. Transnational Institute
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|chapter=ignored (help) - ^ "Cannabis and Cannabinoids". National Cancer Institute. Retrieved 12 January 2014.
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The only approved preparations to date, Marinol (dronabinol, Δ9-THC) and Cesamet (nabilone), are approved for the indication of nausea and vomiting associated with cancer chemotherapy. Marinol is also approved for anorexia and cachexia in HIV/AIDS.
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...to date, there are no deaths known to have resulted from overdose of cannabis. (p. 128)
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The estimated lethal human dose of intravenous dronabinol is 30 mg/kg (2100 mg/70 kg). Significant CNS symptoms in antiemetic studies followed oral doses of 0.4 mg/kg (28 mg/70 kg) of dronabinol capsules.
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- ^ a b "PDSP Database – UNC". NIMH Psychoactive Drug Screening Program. Retrieved 11 June 2013.
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Δ9-THC and many of its derivatives are highly lipophilic and poorly water soluble. Calculations of the n-octanol/water partition coefficient (Ko/w) of Δ9-THC at neutral pH vary between 6,000, using the shake flask method, and 9.44 × 106, by reverse-phase high-performance liquid chromatography estimation.
- ^ Ashton CH (February 2001). "Pharmacology and effects of cannabis: a brief review". Br J Psychiatry 178 (2): 101–106. doi:10.1192/bjp.178.2.101. PMID 11157422.
Because they are extremely lipid soluble, cannabinoids accumulate in fatty tissues, reaching peak concentrations in 4–5 days. They are then slowly released back into other body compartments, including the brain. ... Within the brain, THC and other cannabinoids are differentially distributed. High concentrations are reached in neocortical, limbic, sensory and motor areas.
- ^ Huestis MA (August 2007). "Human cannabinoid pharmacokinetics". Chem Biodivers 4 (8): 1770–804. doi:10.1002/cbdv.200790152. PMC 2689518. PMID 17712819.
THC is highly lipophilic and initially taken up by tissues that are highly perfused, such as the lung, heart, brain, and liver.
- ^ Kathmann M, Flau K, Redmer A, Tränkle C, Schlicker E (February 2006). "Cannabidiol is an allosteric modulator at mu- and delta-opioid receptors". Naunyn Schmiedebergs Arch. Pharmacol. 372 (5): 354–61. doi:10.1007/s00210-006-0033-x. PMID 16489449.
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- ^ Marks MD, Tian L, Wenger JP, Omburo SN, Soto-Fuentes W, He J, Gang DR, Weiblen GD, Dixon RA (2009). "Identification of candidate genes affecting Δ9-tetrahydrocannabinol biosynthesis in Cannabis sativa". Journal of Experimental Botany 60 (13): 3715–26. doi:10.1093/jxb/erp210. PMC 2736886. PMID 19581347.
- ^ Baker PB, Taylor BJ, Gough TA (June 1981). "The tetrahydrocannabinol and tetrahydrocannabinolic acid content of cannabis products". J Pharm Pharmacol. 33 (6): 369–72. doi:10.1111/j.2042-7158.1981.tb13806.x. PMID 6115009.
- ^ Schwilke EW, Schwope DM, Karschner EL, Lowe RH, Darwin WD, Kelly DL, Goodwin RS, Gorelick DA, Huestis MA (2009). "Δ9-Tetrahydrocannabinol (THC), 11-Hydroxy-THC, and 11-Nor-9-carboxy-THC Plasma Pharmacokinetics during and after Continuous High-Dose Oral THC". Clinical Chemistry 55 (12): 2180–2189. doi:10.1373/clinchem.2008.122119. PMC 3196989. PMID 19833841.
- ^ Röhrich J, Schimmel I, Zörntlein S, Becker J, Drobnik S, Kaufmann T, Kuntz V, Urban R (2010). "Concentrations of Δ9-Tetrahydrocannabinol and 11-Nor-9-Carboxytetrahydrocannabinol in Blood and Urine After Passive Exposure to Cannabis Smoke in a Coffee Shop". Journal of Analytical Toxicology 34 (4): 196–203. doi:10.1093/jat/34.4.196. PMID 20465865.
- ^ Baselt, R. (2011). Disposition of Toxic Drugs and Chemicals in Man (9th ed.). Seal Beach, CA: Biomedical Publications. pp. 1644–8.
- ^ 51 Fed. Reg. 17476 (1986), Tuesday, May 13, 1986, pages 17476-17478
- ^ Calhoun SR, Galloway GP, Smith DE (1998). "Abuse potential of dronabinol (Marinol)". Journal of Psychoactive Drugs 30 (2): 187–96. doi:10.1080/02791072.1998.10399689. PMID 9692381. [better source needed]
- ^ "Petition to Reschedule Cannabis (Marijuana)" (PDF). Coalition for Rescheduling Cannabis. 9 October 2002. [better source needed]
- ^ "WHO Expert Committee on Drug Dependence". World Health Organization. Retrieved 12 January 2014.
- ^ "List of psychotropic substances under international control" (PDF). International Narcotics Control Board. p. 5. Archived from the original (PDF) on 7 September 2005. Retrieved 20 April 2011.
This international non-proprietary name refers to only one of the stereochemical variants of delta-9-tetrahydrocannabinol, namely (−)-trans-delta-9-tetrahydrocannabinol
- ^ EMCDDA, ELDD Comparative Study, May 2002.
- ^ "Marinol – the Legal Medical Use for the Marijuana Plant". Drug Enforcement Administration. Archived from the original on 21 October 2002. Retrieved 20 April 2011.
- ^ Alchimia Blog, Marijuana and Medicine: Cesamet, Marinol, Sativex
- ^ Downs, David (21 October 2014). "War on marijuana unconstitutional, doctors testify in federal court Monday". sfgate.com. Retrieved 21 October 2014.
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- ^ MARINOL (dronabinol) capsule drug label/data at Daily Med from U.S. National Library of Medicine, National Institutes of Health.
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- ^ "Government eases restrictions on pot derivative". Online Athens. Retrieved 12 January 2014.
External links
- U.S. National Library of Medicine: Drug Information Portal – Tetrahydrocannabinol
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UpToDate Contents
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- 1. 緩和ケア：悪液質と食欲不振の評価および管理 palliative care assessment and management of anorexia and cachexia
- 2. 高齢者における衰弱：管理 failure to thrive in elderly adults management
- 3. 制吐剤の特性 characteristics of antiemetic drugs
- 4. 癌における食欲不振および悪液質の薬理学的マネージメント pharmacologic management of cancer anorexia cachexia
- 5. 癌疼痛のマネージメント：鎮痛補助剤（鎮痛剤） cancer pain management adjuvant analgesics coanalgesics
English Journal
- The effects of dronabinol during detoxification and the initiation of treatment with extended release naltrexone.
- Bisaga A1, Sullivan MA2, Glass A3, Mishlen K4, Pavlicova M5, Haney M6, Raby WN7, Levin FR8, Carpenter KM9, Mariani JJ10, Nunes EV11.
- Drug and alcohol dependence.Drug Alcohol Depend.2015 Sep 1;154:38-45. doi: 10.1016/j.drugalcdep.2015.05.013. Epub 2015 Jul 8.
- BACKGROUND: Evidence suggests that the cannabinoid system is involved in the maintenance of opioid dependence. We examined whether dronabinol, a cannabinoid receptor type 1 partial agonist, reduces opioid withdrawal and increases retention in treatment with extended release naltrexone (XR-naltrexone
- PMID 26187456
- A 4-Week Pilot Study With the Cannabinoid Receptor Agonist Dronabinol and Its Effect on Metabolic Parameters in a Randomized Trial.
- Zachary RW1, Sloan J2, Rizvi-Toner A3, Bayman L3, Valestin J3, Schey R4.
- Clinical therapeutics.Clin Ther.2015 Aug 14. pii: S0149-2918(15)00972-8. doi: 10.1016/j.clinthera.2015.07.023. [Epub ahead of print]
- PURPOSE: Dronabinol (synthetic Δ9- tetrahydrocannabinol) is used in patients with nausea and vomiting from chemotherapy and in AIDS patients for appetite stimulation. Recently, dronabinol was used to successfully treat visceral hypersensitivity causing noncardiac chest pain. With widening uses of t
- PMID 26283236
- Cannabinoids for the Treatment of Agitation and Aggression in Alzheimer's Disease.
- Liu CS1, Chau SA, Ruthirakuhan M, Lanctôt KL, Herrmann N.
- CNS drugs.CNS Drugs.2015 Aug 14. [Epub ahead of print]
- Alzheimer's disease (AD) is frequently associated with neuropsychiatric symptoms (NPS) such as agitation and aggression, especially in the moderate to severe stages of the illness. The limited efficacy and high-risk profiles of current pharmacotherapies for the management of agitation and aggression
- PMID 26271310
Japanese Journal
- Δ9-Tetrahydrocannabinol Targeting Estrogen Receptor Signaling: The Possible Mechanism of Action Coupled with Endocrine Disruption
- Takeda Shuso
- Biological and Pharmaceutical Bulletin 37(9), 1435-1438, 2014
- … dronabinol), it is important to investigate the mechanistic basis underlying the anti-estrogenic activity of Δ9-THC. …
- NAID 130004684788
- Preliminary observation with dronabinol in patients with intractable pruritus secondary to cholestatic liver disease
- NEFF GW
- Am J Gastroenterol. 97, 2117-2119, 2002
- NAID 30010259390
Related Links
- Dronabinol may cause side effects. Tell your doctor if any of these symptoms are severe or do not go away: weakness sudden warm feeling stomach pain nausea vomiting memory loss anxiety confusion dizziness
- Tetrahydrocannabinol
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