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Yohimbine structure.svg
Clinical data
Routes of
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability7-86% (mean 33%)
Elimination half-life0.25-2.5 hours[1]
ExcretionUrine (as metabolites)
CAS Number
PubChem CID
ECHA InfoCard100.005.157 Edit this at Wikidata
Chemical and physical data
Molar mass354.44 g/mol (base)
390.90 g/mol (hydrochloride)
3D model (JSmol)

Yohimbine (/jˈhɪmbn/)[2] is an indole alkaloid derived from the bark of the Pausinystalia yohimbe tree in Central Africa. It is a veterinary drug used to reverse sedation in dogs and deer. Yohimbine has been studied as a potential treatment for erectile dysfunction but there is insufficient evidence to rate its effectiveness.[3] Extracts from yohimbe have been marketed as dietary supplements for improving sexual function.[4]


Yohimbine is a drug used in veterinary medicine to reverse the effects of xylazine in dogs and deer.[5]

Yohimbe extracts, which contain yohimbine, have been used in traditional medicine and marketed as dietary supplements.[4]


Depending on dosage, yohimbine can either increase or decrease systemic blood pressure (through vasoconstriction or vasodilation, respectively). Because yohimbine has highest affinity for the α2 receptor, small doses can increase blood pressure by causing a relatively selective α2 blockade. Yohimbine also, however, interacts with α1 receptors, albeit with lower affinity; therefore, at higher doses an α1 blockade can occur and overwhelm the effects of the α2 blockade, leading to a potentially dangerous drop in blood pressure.[6] Higher doses of oral yohimbine may create numerous side effects, such as rapid heart rate, overstimulation, anomalous blood pressure, cold sweating, and insomnia.

Extracts and chemistry[edit]

Yohimbe (Pausinystalia johimbe) is a tree that grows in western and central Africa;[7] yohimbine was originally extracted from the bark of yohimbe in 1896 by Adolph Spiegel.[8] In 1943 the correct constitution of yohimbine was proposed by Witkop.[9] Fifteen years later, Van Tamelen used a 23-step synthesis to become the first person to achieve the synthesis of yohimbine.[10][11][12]


Yohimbine has high affinity for the α2-adrenergic receptor, moderate affinity for the α1 receptor, 5-HT1A, 5-HT1B, 5-HT1D, 5-HT1F, 5-HT2B, and D2 receptors, and weak affinity for the 5-HT1E, 5-HT2A, 5-HT5A, 5-HT7, and D3 receptors.[13][14] It behaves as an antagonist at α1-adrenergic, α2-adrenergic, 5-HT1B, 5-HT1D, 5-HT2A, 5-HT2B, and D2, and as a partial agonist at 5-HT1A.[13][15][16][17] Yohimbine interacts with serotonin and dopamine receptors in high concentrations.[18]

Pharmacologic profile
Molecular target Binding affinity
(Ki in nanomolar)[19]
Pharmacologic action
Species Source
SERT 1,000 Inhibitor Human Frontal cortex
5-HT1A 346 Partial agonist Human Cloned
5-HT1B 19.9 Antagonist Human Cloned
5-HT1D 44.3 Antagonist Human Cloned
5-HT1E 1,264 Unknown Human Cloned
5-HT1F 91.6 Unknown Human Cloned
5-HT2A 1,822 Antagonist Human Cloned
5-HT2B 143.7 Antagonist Human Cloned
5-HT7 2,850 Unknown Human Cloned
α1A 1,680 Antagonist Human Cloned
α1B 1,280 Antagonist Human Cloned
α1C 770 Antagonist Human Cloned
α1D 557 Antagonist Human Cloned
α2A 1.05 Antagonist Human Cloned
α2B 1.19 Antagonist Human Cloned
α2C 1.19 Antagonist Human Cloned
D2 339 Antagonist Human Cloned
D3 3,235 Antagonist Human Cloned


Yohimbine has been studied as a way to improve the effects of exposure therapy in people with post traumatic stress disorder.[21][22]

It has also been studied as a potential treatment for erectile dysfunction but there is insufficient evidence to rate its effectiveness.[6][3] It is illegal in the United States to market an over the counter product containing yohimbine as a treatment for erectile dysfunction without getting FDA approval to do so.[23] Yohimbine blocks the pre- and post-synaptic α2 receptors. Blockade of post-synaptic α2 receptors causes only minor corpus cavernosum smooth muscle relaxation, due to the fact that the majority of adrenoceptors in the corpus cavernosum are of the α1 type. Blockade of pre-synaptic α2 receptors facilitates the release of several neurotransmitters in the central and peripheral nervous system — thus in the corpus cavernosum — such as nitric oxide and norepinephrine. Whereas nitric oxide released in the corpus cavernosum is the major vasodilator contributing to the erectile process, norepinephrine is the major vasoconstrictor through stimulation of α1 receptors on the corpus cavernosum smooth muscle. Under physiologic conditions, however, nitric oxide attenuates norepinephrine vasoconstriction.[24]

See also[edit]


  1. ^ Hedner, T; Edgar, B; Edvinsson, L; Hedner, J; Persson, B; Pettersson, A (1992). "Yohimbine pharmacokinetics and interaction with the sympathetic nervous system in normal volunteers". European Journal of Clinical Pharmacology. 43 (6): 651–656. doi:10.1007/BF02284967. PMID 1493849.
  2. ^ yohimbine. (n.d.) Collins English Dictionary – Complete and Unabridged. (1991, 1994, 1998, 2000, 2003). Retrieved January 27, 2015 from http://www.thefreedictionary.com/yohimbine
  3. ^ a b Andersson KE (September 2001). "Pharmacology of penile erection". Pharmacological Reviews. 53 (3): 417–50. PMID 11546836.
  4. ^ a b Beille, P. E. (2013). "Scientific Opinion on the evaluation of the safety in use of Yohimbe (Pausinystalia yohimbe)". EFSA Journal. 11 (7): 3302. doi:10.2903/j.efsa.2013.3302.
  5. ^ 21 CFR Sec. 522.2670 Yohimbine
  6. ^ a b "Yohimbe Supplement". National Center for Complementary and Integrative Health. Retrieved 2017-08-28.
  7. ^ Kew World Checklist of Selected Plant Families, Pausinystalia johimbe
  8. ^ Year Book of the American Pharmaceutical Association. American Pharmaceutical Association. 1914. p. 564. Retrieved 2015-05-04.
  9. ^ Witkop, Bernhard (1943). "Zur Konstitution des Yohimbins und seiner Abbauprodukte". Justus Liebig's Annalen der Chemie. 554 (1): 83–126. doi:10.1002/jlac.19435540108. ISSN 0075-4617.
  10. ^ Liebig, Justus (1988). The Alkaloids: Chemistry and Pharmacology. Academic Press. p. 564. ISBN 978-0-12-469532-0.
  11. ^ van Tamelen; E. E. (1958). "The Total Synthesis of Yohimbine". J. Am. Chem. Soc. 80 (18): 5006–5007. doi:10.1021/ja01551a062.
  12. ^ Herle, B. (2011). "Total Synthesis of (+)-Yohimbine via an Enantioselective Organocatalytic Pictet–Spengler Reaction". J. Org. Chem. 76 (21): 8907–8912. doi:10.1021/jo201657n. PMID 21950549.
  13. ^ a b c Millan MJ, Newman-Tancredi A, Audinot V, et al. (February 2000). "Agonist and antagonist actions of yohimbine as compared to fluparoxan at alpha(2)-adrenergic receptors (AR)s, serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors. Significance for the modulation of frontocortical monoaminergic transmission and depressive states". Synapse. 35 (2): 79–95. doi:10.1002/(SICI)1098-2396(200002)35:2<79::AID-SYN1>3.0.CO;2-X. PMID 10611634.
  14. ^ "PDSP Ki Database".
  15. ^ a b Arthur JM, Casañas SJ, Raymond JR (June 1993). "Partial agonist properties of rauwolscine and yohimbine for the inhibition of adenylyl cyclase by recombinant human 5-HT1A receptors". Biochemical Pharmacology. 45 (11): 2337–41. doi:10.1016/0006-2952(93)90208-E. PMID 8517875.
  16. ^ a b Kaumann AJ (June 1983). "Yohimbine and rauwolscine inhibit 5-hydroxytryptamine-induced contraction of large coronary arteries of calf through blockade of 5 HT2 receptors". Naunyn-Schmiedeberg's Archives of Pharmacology. 323 (2): 149–54. doi:10.1007/BF00634263. PMID 6136920.
  17. ^ a b Baxter GS, Murphy OE, Blackburn TP (May 1994). "Further characterization of 5-hydroxytryptamine receptors (putative 5-HT2B) in rat stomach fundus longitudinal muscle". British Journal of Pharmacology. 112 (1): 323–31. doi:10.1111/j.1476-5381.1994.tb13072.x. PMC 1910288. PMID 8032658.
  18. ^ "Yohimbine (PIM 567)". Inchem.org. Retrieved 2013-05-26.
  19. ^ National Institute of Mental Health. "PDSP Ki Database". University of North Carolina. Archived from the original on November 8, 2013. Retrieved 5 July 2013.
  20. ^ "Yohimbine". DrugBank. University of Alberta. Archived from the original on January 30, 2013. Retrieved 12 April 2014.
  21. ^ Singewald, N; Schmuckermair, C; Whittle, N; Holmes, A; Ressler, KJ (May 2015). "Pharmacology of cognitive enhancers for exposure-based therapy of fear, anxiety and trauma-related disorders". Pharmacology & Therapeutics. 149: 150–90. doi:10.1016/j.pharmthera.2014.12.004. PMC 4380664. PMID 25550231.
  22. ^ McGuire, JF; Lewin, AB; Storch, EA (August 2014). "Enhancing exposure therapy for anxiety disorders, obsessive-compulsive disorder and post-traumatic stress disorder". Expert Review of Neurotherapeutics. 14 (8): 893–910. doi:10.1586/14737175.2014.934677. PMC 4125602. PMID 24972729.
  23. ^ FDA regulations on OTC products
  24. ^ Saenz De Tejada, I; Kim, NN; Goldstein, I; Traish, AM (2000). "Regulation of pre-synaptic alpha adrenergic activity in the corpus cavernosum". International Journal of Impotence Research. 12 Suppl 1: S20–25. doi:10.1038/sj.ijir.3900500. PMID 10845761.