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Anatabine is an alkaloid compound found in tobacco and plants in the nightshade family, which includes eggplant and peppers. Anatabine possesses anti-inflammatory properties but further research is needed to determine if supplementation is practical.

Our evidence-based analysis on anatabine features 20 unique references to scientific papers.

Research analysis led by and reviewed by the Examine team.
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Research Breakdown on Anatabine

1Sources and Structure


Anatabine is an alkaloid found in tobacco and the solanaceae family of plants. This alkaloid is structurally similar to nicotine, and is an analogue of both nornicotine and anabasine (other alkaloids in the same plant family).[1]

It is found in:

  • Tobacco in the range of 927-1390μg/g[2] or on average 554μg per cigarette (range of 130-1120μg; American cigarettes containing 500-550μg)[1]

Anatabine is a tobacco alkaloid similar to nicotine, and is found in the same plants

1.2Structure and Properties

Anatabine is an alkaloid with structural similarity to nicotine, and closer structure similarity to anabasine (which is anatabine without the double bond in the right ring pictured below).


2.1Cholinergic Neurotransmission

In vitro, anatabine has been noted to have bind to the α3β4 receptor with similar affinity as nicotine.[3]

May interact with nicotinic cholinergic receptors, although this is not well researched

2.2Alzheimer's Disease

Anatabine has been found to reduce Aβ production (both Aβ1–40 and Aβ1–42) with an IC50 of around 640µg/mL, and it appeared to mostly inhibit β-cleavage of APP.[4] As this is known to occur with NF-kB inhibition[5][6] anatabine was then tested on the protein and it was found to inhibit NF-kB activation from TNF-α with a similar IC50 value[4] and nicotine was found to be inactive at the same concentrations tested. It has been noted elsewhere that this inhibitory effect on NF-kB is secondary to inhibiting STAT3 phosphorylation at 600-800µg/mL[7] although concnetrations as low as 10µg/mL can inhibit LPS-induced NF-kB activity and 400µg/mL can fully abolish IL-1β secretion induced by LPS.[7]

Nicotine has been found to inhibit Aβ production by regulating BACE-1 transcription in cells that express its receptor (α4β2 nicotinic acetylcholine receptor)[8] and anatabine has also been found to downregulate BACE-1 mRNA, which was credited to NF-kB inhibition (known to regulate BACE-1[9]). Activation of the nicotinic receptors can inhibit NF-kB[10] via STAT3[11] but nicotine seems to require a cholinergic receptor whereas anatabine does not.[4]

When injected into mice at 0.5-2mg/kg, only the higher dose was able to reduce brain and plasma Aβ concentrations to near control levels (in plasma) and by about 25% (brain)[4] and this dose has been noted to exert anti-inflammatory effects by reducing C-reactive protein[4] as well as IL-1β, IL-6, and TNF-α.[7]

Anatabine is a STAT3 inhibitor, which then inhibits NF-kB and exerts an anti-inflammatory effect. This appears to be active following injections of anatabine and may be of therapeutic benefit to Alzheimer's Disease

3Cardiovascular Health

3.1Blood Pressure

Anatabine has structural similarity to nicotine, and since nicotine is able to acutely increase heart rate and blood pressure[12] anatabine has been investigated for its ability to do the same; it has since failed to significantly influence blood pressure or heart rate.[13]

Currently no significant interactions between anatabine and cardiovascular function are known

4Inflammation and Immunology


Incubation of macrophages with 250-350μM was able to inhibit an IFN-γ and LPS induced increases in iNOS and COX-2 mRNA levels, suggesting antiinflammatory effects.[14]

May have general antiinflammatory properties at moderately high concentrations

4.2Autoimmune Diseases

Despite the large amount of adverse health effects associated with tobacco smoking, both ulcerative colitis[15][16] and autoimmune (Hashimoto's) thyroiditis[17][18] have noted benefits associated with smoking. This is currently thought to be due to the antiinflammatory properties of nicotine via the α7 nicotinic receptor[19] (inhibits STAT3 and then NF-kB), but anatabine is also being tested.

In mice inflicted with experimental autoimmune thyroiditis and concurrently supplemented orally with approximately 12.5mg/kg anatabine, occurrence of thyroiditis and the antibody response were significantly reduced.[14] Autoimmune encephalomyelitis (research model for Multiple sclerosis) also sees clinical benefit in response to 20mg/kg anatabine in mice, although antibodies were not affected in this study.[20]

Appears to be beneficial for rodents with autoimmune diseases in high oral doses

5Physical Exercise and Skeletal Muscle

5.1Muscle Soreness and Damage

Supplementation of 6-12mg anatabine (via lozenges that also conferred 834-1668IU vitamin A and 66-132IU Vitamin D) for ten days prior to physical exercise testing in otherwise healthy young men failed to outperform placebo (which contained the vitamins) in reducing muscle soreness or power output when measured over the next three days.[13]

The lone study in humans assessing the antiinflammatory properties of anatabine failed to find any significant influence of supplementation


  1. ^ a b Wu W, Ashley DL, Watson CH. Determination of nicotine and other minor alkaloids in international cigarettes by solid-phase microextraction and gas chromatography/mass spectrometry. Anal Chem. (2002)
  2. ^ Lisko JG, et al. Application of GC-MS/MS for the analysis of tobacco alkaloids in cigarette filler and various tobacco species. Anal Chem. (2013)
  3. ^ Screening of Tobacco Smoke Condensate for Nicotinic Acetylcholine Receptor Ligands using Cellular Membrane Affinity Chromatography Columns and Missing Peak Chromatography.
  4. ^ a b c d e Paris D, et al. Anatabine lowers Alzheimer's Aβ production in vitro and in vivo. Eur J Pharmacol. (2011)
  5. ^ Paris D, et al. Inhibition of Abeta production by NF-kappaB inhibitors. Neurosci Lett. (2007)
  6. ^ Paris D, et al. Reduction of beta-amyloid pathology by celastrol in a transgenic mouse model of Alzheimer's disease. J Neuroinflammation. (2010)
  7. ^ a b c Paris D, et al. Anti-inflammatory activity of anatabine via inhibition of STAT3 phosphorylation. Eur J Pharmacol. (2013)
  8. ^ Nicotine decreases beta-amyloid through regulating BACE1 transcription in SH-EP1-α4β2 nAChR-APP695 cells.
  9. ^ Buggia-Prevot V, et al. NFkappaB-dependent control of BACE1 promoter transactivation by Abeta42. J Biol Chem. (2008)
  10. ^ Yoshikawa H, et al. Nicotine inhibits the production of proinflammatory mediators in human monocytes by suppression of I-kappaB phosphorylation and nuclear factor-kappaB transcriptional activity through nicotinic acetylcholine receptor alpha7. Clin Exp Immunol. (2006)
  11. ^ Peña G, et al. Unphosphorylated STAT3 modulates alpha 7 nicotinic receptor signaling and cytokine production in sepsis. Eur J Immunol. (2010)
  12. ^ Haass M, Kübler W. Nicotine and sympathetic neurotransmission. Cardiovasc Drugs Ther. (1997)
  13. ^ a b Jenkins ND, et al. The effects of anatabine on non-invasive indicators of muscle damage: a randomized, double-blind, placebo-controlled, crossover study. J Int Soc Sports Nutr. (2013)
  14. ^ a b Caturegli P, et al. Anatabine ameliorates experimental autoimmune thyroiditis. Endocrinology. (2012)
  15. ^ Boyko EJ, et al. Effects of cigarette smoking on the clinical course of ulcerative colitis. Scand J Gastroenterol. (1988)
  16. ^ Calabrese E, et al. Low-dose smoking resumption in ex-smokers with refractory ulcerative colitis. J Crohns Colitis. (2012)
  17. ^ Belin RM, et al. Smoke exposure is associated with a lower prevalence of serum thyroid autoantibodies and thyrotropin concentration elevation and a higher prevalence of mild thyrotropin concentration suppression in the third National Health and Nutrition Examination Survey (NHANES III). J Clin Endocrinol Metab. (2004)
  18. ^ Pedersen IB, et al. Smoking is negatively associated with the presence of thyroglobulin autoantibody and to a lesser degree with thyroid peroxidase autoantibody in serum: a population study. Eur J Endocrinol. (2008)
  19. ^ Bencherif M, et al. Alpha7 nicotinic receptors as novel therapeutic targets for inflammation-based diseases. Cell Mol Life Sci. (2011)
  20. ^ Paris D, et al. Amelioration of experimental autoimmune encephalomyelitis by anatabine. PLoS One. (2013)