Systematic (IUPAC) name
Clinical data
Pregnancy cat.  ?
Legal status Prescription only
Routes Oral, Smoked
Pharmacokinetic data
Half-life 20 hours
CAS number 486-56-6 YesY
ATC code None
PubChem CID 854019
ChemSpider 746405 YesY
UNII K5161X06LL YesY
Chemical data
Formula C10H12N2O 
Mol. mass 176.22 g/mol
SMILES eMolecules & PubChem
 YesY(what is this?)  (verify)

Cotinine is an alkaloid found in tobacco and is also a metabolite of nicotine.[1][2] The word "cotinine" is an anagram of "nicotine". Cotinine is used as a biomarker for exposure to tobacco smoke and has also been sold as an antidepressant under the brand name Scotine.[1]

Similarly to nicotine, cotinine binds to, activates, and desensitizes neuronal nicotinic acetylcholine receptors, though at much lower potency in comparison.[2][3][4][5] It has demonstrated nootropic and antipsychotic-like effects in scientific research.[6][7]

Measure of nicotine exposure

Cotinine has an in vivo half-life of approximately 20 hours, and is typically detectable for several days (up to one week) after the use of tobacco. The level of cotinine in the blood is proportionate to the amount of exposure to tobacco smoke, so it is a valuable indicator of tobacco smoke exposure, including secondary (passive) smoke.[8] People who smoke menthol cigarettes may retain cotinine in the blood for a longer period because menthol can compete with enzymatic metabolism of cotinine.[9] Genetic encoding of liver enzymes may also play a role, as people of African descent routinely register higher blood cotinine levels than Caucasians.[10] Several variable factors (such as menthol cigarette preference and puff size) suggest that the explanation for this difference may be more complex than gender or race.[citation needed]

Cotinine levels <10 ng/mL are considered to be consistent with no active smoking. Values of 10 ng/mL to 100 ng/mL are associated with light smoking or moderate passive exposure, and levels above 300 ng/mL are seen in heavy smokers - more than 20 cigarettes a day. In urine, values between 11 ng/mL and 30 ng/mL may be associated with light smoking or passive exposure, and levels in active smokers typically reach 500 ng/mL or more. Cotinine assays provide an objective quantitative measure that is more reliable than smoking histories or counting the number of cigarettes smoked per day. Cotinine also permits the measurement of exposure to second-hand smoke (passive smoking).

Drug tests can detect cotinine in the blood, urine, or saliva.

However, some smoking cessation programs contain Nicotine which will result in a positive for Cotinine presence. Therefore, the presence of Cotinine is not a conclusive indication of tobacco use.[11]


  1. ^ a b David J. Triggle (1996). Dictionary of Pharmacological Agents. Boca Raton: Chapman & Hall/CRC. ISBN 0-412-46630-9. 
  2. ^ a b Dwoskin LP, Teng L, Buxton ST, Crooks PA (March 1999). "(S)-(-)-Cotinine, the major brain metabolite of nicotine, stimulates nicotinic receptors to evoke [3Hdopamine release from rat striatal slices in a calcium-dependent manner"]. The Journal of Pharmacology and Experimental Therapeutics 288 (3): 905–11. PMID 10027825. 
  3. ^ Anderson DJ, Arneric SP (March 1994). "Nicotinic receptor binding of [3Hcytisine, [3H]nicotine and [3H]methylcarbamylcholine in rat brain"]. European Journal of Pharmacology 253 (3): 261–7. doi:10.1016/0014-2999(94)90200-3. PMID 8200419. 
  4. ^ Briggs CA, McKenna DG (September 1998). "Activation and inhibition of the human alpha7 nicotinic acetylcholine receptor by agonists". Neuropharmacology 37 (9): 1095–102. doi:10.1016/S0028-3908(98)00110-5. PMID 9833639. 
  5. ^ Buccafusco JJ, Shuster LC, Terry AV (February 2007). "Disconnection between activation and desensitization of autonomic nicotinic receptors by nicotine and cotinine". Neuroscience Letters 413 (1): 68–71. doi:10.1016/j.neulet.2006.11.028. PMID 17157984. 
  6. ^ Buccafusco JJ, Terry AV (October 2009). "A reversible model of the cognitive impairment associated with schizophrenia in monkeys: potential therapeutic effects of two nicotinic acetylcholine receptor agonists". Biochemical Pharmacology 78 (7): 852–62. doi:10.1016/j.bcp.2009.06.102. PMID 19577545. 
  7. ^ Buccafusco JJ, Beach JW, Terry AV (February 2009). "Desensitization of nicotinic acetylcholine receptors as a strategy for drug development". The Journal of Pharmacology and Experimental Therapeutics 328 (2): 364–70. doi:10.1124/jpet.108.145292. PMC 2682277. PMID 19023041. 
  8. ^ Florescu A, Ferrence R , Einarson T, Selby P, Soldin O, Koren G (February 2009). "Methods for quantification of exposure to cigarette smoking and environmental tobacco smoke: focus on developmental toxicology". Therapeutic Drug Monitoring 31 (1): 14–30. doi:10.1097/FTD.0b013e3181957a3b. PMID 19125149. 
  9. ^ Ham, Becky (December 2002). "Signs of smoking linger longer in menthol smokers". Center for the Advancement of Health. Science Blog. Archived from the original on 17 March 2010. Retrieved 17 March 2010. 
  10. ^ News, BBC (2007-03-17). "'Race role' in tobacco smoke risk". BBC NEWS. Retrieved 2007-03-18. 
  11. ^ Hewitt, Doug. "Reasons for False Positives for Nicotine on a Blood Test". Retrieved 21 October 2011.