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THC-11-oic acid molecule
Clinical data
  • Inconclusive
Routes of
Pharmacokinetic data
Elimination half-life5.2 to 6.2 days [1]
CAS Number
PubChem CID
CompTox Dashboard (EPA)
Chemical and physical data
Molar mass344.451 g·mol−1
3D model (JSmol)
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11-Nor-9-carboxy-Δ9-tetrahydrocannabinol (11-COOH-THC or THC-COOH), often referred to as 11-nor-9-carboxy-THC or THC-11-oic acid, is the main secondary metabolite of tetrahydrocannabinol (THC), which is formed in the body after cannabis is consumed.

Metabolism and detection[edit]

11-COOH-THC is formed in the body by oxidation of the active metabolite 11-hydroxy-THC (11-OH-THC) by liver enzymes. It is then metabolized further by conjugation with glucuronide,[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 for blood 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.[citation needed]

Some jurisdictions where cannabis use is decriminalized or permitted under some circumstances use such tests when determining whether drivers were legally 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.[9] 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 the analgesic and anti-inflammatory effects of cannabis,[10][11][12] 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.[13][14]

Legal status[edit]

The legal status of 11-nor-9-carboxy-THC varies among jurisdictions.


11-COOH-THC is a Schedule 8 prohibited substance in Western Australia under the Poisons Standard (July 2016).[15] 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.[15]

United States[edit]

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 the Federal Analog Act.

See also[edit]

Ajulemic acid, a synthetic analog of 11-nor-9-carboxy-THC


  1. ^ Schwilke, E. W; Schwope, D. M; Karschner, E. L; Lowe, R. H; Darwin, W. D; Kelly, D. L; Goodwin, R. S; Gorelick, D. A; Huestis, M. A (2009). "9-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.
  2. ^ Skopp, G; Pötsch, L (2002). "Stability of 11-nor-delta(9)-carboxy-tetrahydrocannabinol glucuronide in plasma and urine assessed by liquid chromatography-tandem mass spectrometry". Clinical Chemistry. 48 (2): 301–6. PMID 11805011.
  3. ^ 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. PMID 6323852.
  4. ^ Huestis, MA; Mitchell, JM; Cone, EJ (1995). "Detection times of marijuana metabolites in urine by immunoassay and GC-MS". Journal of Analytical Toxicology. 19 (6): 443–9. doi:10.1093/jat/19.6.443. PMID 8926739.
  5. ^ Pope Jr, HG; Gruber, AJ; Hudson, JI; Huestis, MA; Yurgelun-Todd, D (2001). "Neuropsychological performance in long-term cannabis users". Archives of General Psychiatry. 58 (10): 909–15. doi:10.1001/archpsyc.58.10.909. PMID 11576028.
  6. ^ Dietz, L; Glaz-Sandberg, A; Nguyen, H; Skopp, G; Mikus, G; Aderjan, R (2007). "The urinary disposition of intravenously administered 11-nor-9-carboxy-delta-9-tetrahydrocannabinol in humans". Therapeutic Drug Monitoring. 29 (3): 368–72. doi:10.1097/FTD.0b013e31805ba6fd. PMID 17529896.
  7. ^ 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): 283–90. doi:10.1093/jat/16.5.283. PMID 1338216.
  8. ^ Huestis, MA; Elsohly, M; Nebro, W; Barnes, A; Gustafson, RA; Smith, ML (2006). "Estimating time of last oral ingestion of cannabis from plasma THC and THCCOOH concentrations". Therapeutic Drug Monitoring. 28 (4): 540–4. doi:10.1097/00007691-200608000-00009. PMID 16885722.
  9. ^ Ménétrey, A; Augsburger, M; Favrat, B; Pin, MA; Rothuizen, LE; Appenzeller, M; Buclin, T; Mangin, P; Giroud, C (2005). "Assessment of driving capability through the use of clinical and psychomotor tests in relation to blood cannabinoids levels following oral administration of 20 mg dronabinol or of a cannabis decoction made with 20 or 60 mg Delta9-THC". Journal of Analytical Toxicology. 29 (5): 327–38. doi:10.1093/jat/29.5.327. PMID 16105257.
  10. ^ Burstein, SH; Hull, K; Hunter, SA; Latham, V (1988). "Cannabinoids and pain responses: a possible role for prostaglandins". The FASEB Journal. 2 (14): 3022–6. doi:10.1096/fasebj.2.14.2846397. PMID 2846397.
  11. ^ Doyle, SA; Burstein, SH; Dewey, WL; Welch, SP (1990). "Further studies on the antinociceptive effects of delta 6-THC-7-oic acid". Agents and Actions. 31 (1–2): 157–63. doi:10.1007/bf02003237. PMID 2178317.
  12. ^ Ujváry, I; Grotenhermen, F (2014). "11-Nor-9-carboxy-Δ9-tetrahydrocannabinol – a ubiquitous yet underresearched cannabinoid. A review of the literature" (PDF). Cannabinoids. 9 (1): 1–8.
  13. ^ Burstein, S; Hunter, SA; Latham, V; Renzulli, L (1987). "A major metabolite of delta 1-tetrahydrocannabinol reduces its cataleptic effect in mice". Experientia. 43 (4): 402–3. doi:10.1007/BF01940427. PMID 3032669.
  14. ^ Burstein, S; Hunter, SA; Latham, V; Renzulli, L (1986). "Prostaglandins and cannabis--XVI. Antagonism of delta 1-tetrahydrocannabinol action by its metabolites". Biochemical pharmacology. 35 (15): 2553–8. doi:10.1016/0006-2952(86)90053-5. PMID 3017356.
  15. ^ a b Poisons Standard July 2016 Comlaw.gov.au