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Yohimbine structure.svg
Systematic (IUPAC) name
carboxylic acid methyl ester
Clinical data
Trade names Actibine, Erex, Testomar, Yocon, Yohimar, Yohimbe
Pharmacokinetic data
Bioavailability 7-87% (mean 33%)
Half-life 0.25-2.5 hours[1]
Excretion Urine (as metabolites)
146-48-5 YesY
G04BE04 QV03AB93
PubChem CID 8969
IUPHAR ligand 102
DrugBank DB01392 YesY
ChemSpider 8622 YesY
ChEBI CHEBI:10093 YesY
Chemical data
Formula C21H26N2O3
354.44 g/mol (base)
390.90 g/mol (hydrochloride)
 YesY (what is this?)  (verify)

Yohimbine (/jˈhɪmbn/)[2] is an indole alkaloid derived from the bark of the Pausinystalia yohimbe tree in Central Africa. It is primarily used as a treatment for erectile dysfunction. Brand names include: Erex, Testomar, Yocon, Yohimar, Yohimbe. It is a stimulant with aphrodisiac and mild MAOI effects that primarily acts as an antagonist of α2 receptors.[3] It is available as a prescription medication in the standardized form, yohimbine hydrochloride, for the treatment of dry mouth and selective serotonin reuptake inhibitor induced sexual dysfunction. Yohimbine produces a profile similar to ADHD.[4]

Medical uses[edit]

SSRI side-effects[edit]

There is potential for yohimbine to be used as treatment for SSRI induced sexual dysfunction. One study has shown yohimbine's ability to increase physical functioning as well as desire in patients taking an SSRI.[5] Yohimbine has proved to be effective in treating dry mouth caused by anti-depressant use, however, much of the evidence has been centered around those taking a tricyclic antidepressant.[6][7]

Sexual dysfunction[edit]

Main article: Sexual dysfunction

The NIH states that yohimbine hydrochloride is the standardized form of yohimbine that is available as a prescription medicine in the United States, and that it has been shown in human studies to be effective in the treatment of male erectile dysfunction.[8] Yohimbine has been shown to be effective in the treatment of orgasmic dysfunction in men.[9] Yohimbine has also been used to treat hypoactive sexual desire disorder (under active libido) in women.[10]

Large doses of yohimbe have caused priapism.[11] Controlled studies suggest that it is not always an effective treatment for impotence, and evidence of increased sex drive (libido) is anecdotal.[12]

It cannot be excluded that orally administered yohimbine can have a beneficial effect in some patients with ED. The conflicting results available may be attributed to differences in drug design, patient selection, and definitions of positive response. Generally, however, available results of treatment are not impressive.[13]

Yohimbine blocks the pre- and post-synaptic α2 receptors. Blockade of post-synaptic α2 receptors causes minor corpus cavernosum smooth muscle relaxation. In fact, 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, nitric oxide attenuates norepinephrine vasoconstriction. Continuous administration of yohimbine, as opposed to on-demand administration, might result in increased norepinephrine reuptake and thereby reduced vasoconstriction from reduced α1 adrenergic receptors stimulation by its feedback down regulation mechanism -unlike on-demand administration that produces excessive norepinephrine release and bottlenecked reuptake. And α1 blockers on-demand reduce vasoconstriction caused by excessive norepinephrine release.[14]

Weight loss[edit]

There is no good evidence yohimbine is useful as an aid to weight loss.[15]

Other uses[edit]

Yohimbine has been used to facilitate recall of traumatic memories in the treatment of post traumatic stress disorder (PTSD).[16] Use of yohimbine outside of therapeutic settings may not be appropriate for persons suffering from PTSD.[17]

Side effects[edit]

Depending on dosage, yohimbine can either increase or decrease systemic blood pressure (through vasoconstriction or vasodilation, respectively); small amounts of yohimbine can increase blood pressure, while large amounts can dangerously lower blood pressure.[18]

The therapeutic index of yohimbine is quite low; the range between an effective dose and a dangerous dose is very narrow.[19] Perceptible effects begin under half a miligram. A typical dose for sexual dysfunction would be 15–30 mg, whereas 100 mg would be considered dangerous. Overdose may also precipitate panic-type reactions, heart attack, and possibly death. Some have experienced severe adverse effects under 5 mg.[citation needed]

Hallucinations or paralysis may occur with doses greater than 40 mg.[20] Higher doses of oral yohimbine may create numerous side effects, such as rapid heart rate, overstimulation, anomalous blood pressure, cold sweating, and insomnia. In rare cases panic attacks, hallucinations, headaches, dizziness, and skin flushing have occurred.[19]

Overdoses of yohimbine can cause priapism. There is little evidence for the use of pseudoephedrine in the treatment of priapism. The America Urology Association recommends phenylephrine intracavernous injection.[21]

Serious adverse effects of overdose may include seizures and kidney failure. Yohimbine should not be consumed by anyone with liver, kidney, or heart disease, or a psychological disorder.[19]

Precautions and contraindications[edit]

Yohimbe bark is on the FDA list of dangerous supplements.[22] The levels of yohimbine that are present in yohimbe bark extract are variable and often very low.[8] Therefore, although yohimbe bark has been used traditionally to alleviate male erectile dysfunction, there is not enough scientific evidence to form a definitive conclusion in this area.

In Africa, yohimbe has traditionally been used as an aphrodisiac.[23] However, it is important to note that while the terms yohimbine, yohimbine hydrochloride, and yohimbe bark extract are related, they are not interchangeable.[8]

In addition to the main active chemical, yohimbine, Pausinystalia yohimbe contains approximately 55 other alkaloids, of which yohimbine accounts for 1% to 20% of total alkaloids. Among them, corynanthine is an α1 receptor blocker. Hence the use of yohimbe extract in sufficient dosages may provide concomitant α1 and α2 receptors blockade and thus may better enhance erections than yohimbine alone.[14]

Pausinystalia yohimbe is currently threatened with extinction in its native habitat due to international demand.[citation needed] Its conservation is difficult because the bioactivity of the tree has led many Western governments to declare it a proscribed species.


At least 14 days should elapse between discontinuation of MAOI therapy and initiation of treatment with yohimbine.[24]

Research on cats suggests that yohimbine increases the effects of catecholaminergic stimulants, namely amphetamine and modafinil.[25]


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.[26][27] 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.[26][28][29][30] Yohimbine interacts with serotonin and dopamine receptors in high concentrations.[31]

Pharmacologic profile
Molecular Target Binding Affinity
(Ki in nanomoles)[32]
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


Additionally, it inhibits the function of monoamine oxidase enzymes, although it is not clear if it is a RIMA, MAOA, or MAOB inhibitor.

MAOIs are normally contraindicated for use with tyramine-rich food (see the cheese effect). Some companies have combined yohimbine with tyramine in their energy products.[34] However, tyramine failed to potentiate the effect of yohimbine except for somewhat augmenting the increase in DHPG.[35]

Despite its MAOI properties, it does not spare the degradation of tryptamines, (e.g. DMT) which remain orally inactive upon coadministration, suggesting that yohimbine is potentially a selective inhibitor of MAOB.

Yohimbine was explored as a remedy for type 2 diabetes in animal and human models carrying polymorphisms of the α2A-adrenergic receptor gene.[36]

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. ^ Verwaerde, P; Tran, MA; Montastruc, JL; Senard, JM; Portolan, G (1997). "Effects of yohimbine, an α2 receptors antagonist, on experimental neurogenic orthostatic hypotension.". Fundamental & clinical pharmacology 11 (6): 567–75. doi:10.1111/j.1472-8206.1997.tb00862.x. PMID 9444525. 
  4. ^ Arnsten, Amy F.T. (September 2009). "Toward a New Understanding of Attention-Deficit Hyperactivity Disorder Pathophysiology". CNS Drugs 23 (Supplement 1): 33–41. doi:10.2165/00023210-200923000-00005. PMID 19621976. 
  5. ^ Jacobsen, FM (April 1992). "Fluoxetine-induced sexual dysfunction and an open trial of yohimbine.". The Journal of clinical psychiatry 53 (4): 119–22. PMID 1564046. 
  6. ^ Rispail, Y; Schmitt, L; Berlan, M; Montastruc, JL; Montastruc, P (1990). "Yohimbine increases salivary secretion in depressed patients treated with tricyclic antidepressants.". European journal of clinical pharmacology 39 (4): 425–6. doi:10.1007/bf00315426. PMID 2076732. 
  7. ^ Bagheri, H; Schmitt, L; Berlan, M; Montastruc, JL (December 1992). "Effect of 3 weeks treatment with yohimbine on salivary secretion in healthy volunteers and in depressed patients treated with tricyclic antidepressants.". British journal of clinical pharmacology 34 (6): 555–8. doi:10.1111/j.1365-2125.1992.tb05661.x. PMID 1362888. 
  8. ^ a b c "Yohimbe: MedlinePlus Supplements". nlm.nih.gov. November 19, 2010. Retrieved December 13, 2010. 
  9. ^ Adeniyi AA, Brindley GS, Pryor JP, Ralph DJ (May 2007). "Yohimbine in the treatment of orgasmic dysfunction". Asian Journal of Andrology 9 (3): 403–7. doi:10.1111/J.1745-7262.2007.00276.x. PMID 17486282. 
  10. ^ http://onlinelibrary.wiley.com.wwwproxy0.library.unsw.edu.au/doi/10.1111/j.1745-7262.2007.00276.x/pdf
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