11-Nor-9-carboxy-Δ9-tetrahydrocannabinol (11-COOH-THC orTHC-COOH), often referred to as11-nor-9-carboxy-THC orTHC-11-oic acid, is the main secondarymetabolite oftetrahydrocannabinol (THC) which is formed in the body aftercannabis is consumed.
11-COOH-THC is formed in the body byoxidation of the active metabolite11-hydroxy-THC (11-OH-THC) by liver enzymes. It is then metabolized further by conjugation withglucuronide,[2] forming a water-soluble congener which can be more easily excreted by the body.[3]
11-COOH-THC has a long half-life in the body of up to several days (or even weeks in very heavy users),[4][5][6] making it the main metabolite tested forblood or urine testing for cannabis use. More selective tests are able to distinguish between 11-OH-THC and 11-COOH-THC, which can help determine how recently cannabis was consumed;[7][8] if only 11-COOH-THC is present then cannabis was used some time ago and any impairment in cognitive ability or motor function will have dissipated, whereas if both 11-OH-THC and 11-COOH-THC are present then cannabis was consumed more recently and motor impairment may still be present.[9]
Recent studies highlight that individual factors such as metabolism, body fat percentage, and frequency of use significantly impact the detection window of 11-COOH-THC in drug testing.[10]
Some jurisdictions where cannabis use is decriminalized or permitted under some circumstances use such tests when determining whether drivers werelegally intoxicated and therefore unfit to drive, with the comparative levels of THC, 11-OH-THC and 11-COOH-THC being used to derive a "blood cannabis level" analogous to the blood alcohol level used in prosecuting impaired drivers.[11] On the other hand, in jurisdictions where cannabis is completely illegal, any detectable levels of 11-COOH-THC may be deemed to constitute driving while intoxicated, even though this approach has been criticized as tantamount to prohibition of "driving whilst being a recent user of cannabis" regardless of the presence or absence of any actual impairment that might impact driving performance.
While 11-COOH-THC does not have any psychoactive effects in its own right, it may still have a role in theanalgesic andanti-inflammatory effects of cannabis,[12][13][14] and has also been shown to moderate the effects of THC itself which may help explain the difference in subjective effects seen between occasional and regular users of cannabis.[15][16]
11-COOH-THC is aSchedule 8 prohibited substance inWestern Australia under thePoisons Standard (July 2016).[17] A schedule 8 substance is a controlled Drug – Substances which should be available for use but require restriction of manufacture, supply, distribution, possession and use to reduce abuse, misuse and physical or psychological dependence.[17]
Because 11-COOH-THC is substantially similar to the Schedule I controlled substance THC, possession or sale of 11-COOH-THC could be subject to prosecution under theFederal Analog Act.
^Law B, Mason PA, Moffat AC, King LJ (1984). "Confirmation of cannabis use by the analysis of delta 9-tetrahydrocannabinol metabolites in blood and urine by combined HPLC and RIA".Journal of Analytical Toxicology.8 (1):19–22.doi:10.1093/jat/8.1.19.PMID6323852.
^Huestis MA, Mitchell JM, Cone EJ (October 1995). "Detection times of marijuana metabolites in urine by immunoassay and GC-MS".Journal of Analytical Toxicology.19 (6):443–449.doi:10.1093/jat/19.6.443.PMID8926739.
^Dietz L, Glaz-Sandberg A, Nguyen H, Skopp G, Mikus G, Aderjan R (June 2007). "The urinary disposition of intravenously administered 11-nor-9-carboxy-delta-9-tetrahydrocannabinol in humans".Therapeutic Drug Monitoring.29 (3):368–372.doi:10.1097/FTD.0b013e31805ba6fd.PMID17529896.S2CID25321236.
^Huestis MA, Henningfield JE, Cone EJ (1992). "Blood cannabinoids. II. Models for the prediction of time of marijuana exposure from plasma concentrations of delta 9-tetrahydrocannabinol (THC) and 11-nor-9-carboxy-delta 9-tetrahydrocannabinol (THCCOOH)".Journal of Analytical Toxicology.16 (5):283–290.doi:10.1093/jat/16.5.283.PMID1338216.
^Huestis MA, Elsohly M, Nebro W, Barnes A, Gustafson RA, Smith ML (August 2006). "Estimating time of last oral ingestion of cannabis from plasma THC and THCCOOH concentrations".Therapeutic Drug Monitoring.28 (4):540–544.doi:10.1097/00007691-200608000-00009.PMID16885722.S2CID22536528.
^Doyle SA, Burstein SH, Dewey WL, Welch SP (August 1990). "Further studies on the antinociceptive effects of delta 6-THC-7-oic acid".Agents and Actions.31 (1–2):157–163.doi:10.1007/bf02003237.PMID2178317.S2CID23310488.
^Burstein S, Hunter SA, Latham V, Renzulli L (April 1987). "A major metabolite of delta 1-tetrahydrocannabinol reduces its cataleptic effect in mice".Experientia.43 (4):402–403.doi:10.1007/BF01940427.PMID3032669.S2CID22153383.
^Burstein S, Hunter SA, Latham V, Renzulli L (August 1986). "Prostaglandins and cannabis--XVI. Antagonism of delta 1-tetrahydrocannabinol action by its metabolites".Biochemical Pharmacology.35 (15):2553–2558.doi:10.1016/0006-2952(86)90053-5.PMID3017356.
N
Y (what is this?) (verify)