Last Updated: January 3, 2024

Yohimbine is promoted for its fat-burning properties and benefits for male sexual dysfunction. Though yohimbine is effective, side effects may include anxiety, nervousness, and an elevated heart rate, and the reported dose of yohimbine in many supplement formulas doesn’t match the actual dose.

Yohimbine is most often used for.

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Sources and Composition



Yohimbine is found naturally occurring primarily as an alkaloid in the Pausinystalia yohimbe tree (sometimes referred to as Corynanthe yohimbe), and can be found in the plant known as Rauwolfia Serpentina,[1] as well as the Rauwolfia family of plants in general.

Yohimbine, as a molecule, is sometimes also referred to as aphordine, corynine, hydroaergotocin, and quebrachine.[2]


Structure and Diastereoisomers

Yohimbine is one molcule that has three different molecules as diastereoisomers, and four molecules tend to exist together in sources of Yohimbine. These 4 molecules are yohimbine, 3-epi-α-yohimbine, corynanthine, and rauwolscine.[3] Of these, 3-epi-α-yohimbine appears to be structurally similar to Reserpine (a molecule in Rauwolfia Serpentina) and does not tend to interact highly with the alpha-adrenergic receptors, which is seen as yohimbine's main mechanism of action.[4]



MSDS data for Yohimbine states that Yohimbine HCl has a molecular weight of 390.87g and a boiling point of 302°C/575.6°F (with Sigma Aldrich MSDS noting 288-290 °C and 550-554°F)[5] It is recommended to store Yohimbine HCl in a dry cool place, and is deemed stable under these conditions (Sigma Aldrich MSDS); yohimbine may be sensitive to excessive light,[6] similar to structurally related alkaloids.[7] Yohimbine is a crystalline white powder.




Enzymatic Interactions

Yohimbine interacts with the CYP2D6 enzyme and can inhibit its function. One study measuring Ki noted an apparent Ki of 0.23uM for microsomes and 0.52uM for purified CYP2D6 enzymes; this extends to Corynanthine with an apparent Ki of 0.08uM.[8] This enzyme is also the one that metabolizes Yohimbine into 11-hydroxy Yohimbine, and shows over a 1000-fold variation between individuals based on the genotype of CYP2D6 expressed (with some interaction with CYP3A4).[9] Those with lower metabolism rates of Yohimbine due to less CYP2D6 noted increased nervous system effects from stimulation[10][9] and the best predictive factor appears to be ethnicity.[9] Variants of underactive CYP2D6 (poor metabolizers of Yohimbine) appear to reach 7% in caucasians of European descent, while being 1% and 1.8% in Chinese and Blacks, respectively.[11]

Inhibition by competitive metabolism, CYP2D6 is a locus for interpersonal differences in Yohimbine metabolism rates and some persons do not metabolize Yohimbine to 11-hydroxy Yohimbine at all


Species differences

Yohimbine acts vicariously through the adrenergic system, of which inter-species differences have been noted. The dog has been identified as the most likely representative animal model for alpha-adrenergic antagonism, although caution should still be taken in extrapolating animal studies to humans in this scenario.[12]


Interactions with Neurology


Adrenergic Neurotransmission

The primary and most researched mechanism of yohimbine is antagonism (inactivation) of a class of receptors known as Alpha-2-Adrenergic receptors.

By inhibiting these autoreceptors on presynaptic noradrenergic neurons, Yohimbine can increase noradrenaline release as the negative feedback inhibition loop is disrupted.[13] This increase in noradrenaline is reliably seen in humans in a dose-dependent manner[14][15][16][17][18][19] although symptoms associated with noradrenaline (heart rate, arousal, anxiety) appear to be subject to variability in subjects.[20] For example, one study that measured anxiety via EEG (using the frontal midline theta pulse as biomarker) noted that participants with less anxiety at baseline that recieving 15mg yohimbine did not influence anxiety as measured by either EEG or self-report, while those with higher baseline anxiety experienced an exacerbation of anxiety on both measures; general arousal was increased in both groups.[21]

This increase in noradrenaline may be subject to resistance, as one study that noted serum increases of noradrenaline after acute administration failed to note these effects after 2 weeks of continuous administration.[18]

Yohimbine reliably increases noradrenaline levels by preventing their uptake into subsequent neurons


Melatonergic Neurotransmission

Oral supplementation of 10.8mg yohimbine to female subjects failed to alter serum levels of melatonin when taken at 6pm and measured until 10pm in a dim room, but there was an increase in urinary melatonin excretion.[22]

Yohimbine does not appear to alter plasma melatonin concentrations when taken in the evening



In regards to attention, increased firing of the neurons in the medial pre-frontal cortex is associated with the mechanism of action of many ADHD drugs such as Methylphenidate (Ritalin) and the noradreline-based ones such as Desipramine or Atomoxetine, where signalling via D1 receptors and involvement of A2A receptors appears to be critical.[23][24]

Yohimbine can augment the signalling of Methylphenidate in a synergistic manner, where 1mg/kg doubles the rate of firing in PCNs in rats.[25] Neither β1-adrenergic antagonists nor A1A antagonists were effective, yet yohimbine in isolation does not alter signalling of these neurons; blocking of D1 receptors abolishes the augmentation as well.[25]

Yohimbine preload has, however, been associated with an attenuation of the attentive effects of Nortriptyline.[26]

Yohimbine may increase the efficacy of ADHD medication secondary to its A2A antagonistic abilities, but does not appear to have efficacy by itself at standard concentrations



Yohimbine may be able to suppress appetite in both lean and obese mice with more efficacy in the latter, which may be inherent to its interactions with the alpha2-adrenergic recpetors as it appears to also extend to rauwolscine.[27] This study noted that 2.1-4.6mg/kg yohimbine was able to reduce food intake to 49-62% of control at the first dose in obese rats, gradually losing efficacy to 56-72% of food intake by day 13; appetite suppression in lean rats varied from 94.6-95.7% of control and tended to miss statistical significance, although it reached significance when increasing the dose to 5mg/kg, reducing food intake to 69.8-75.6% in lean mice.[27] Water intake was not affected, and rauwolscine was equally effective but required a higher dose (up to 10mg/kg in lean mice).[27]

May suppress appetite in animals, regardless of previous weight status

When measuring the rate of gastric emptying, a slowing correlated with appetite suppression, 15mg Yohimbine failed to influence gastric emptying, while 50mg ephedrine was effective.[28]



Yohimbine can reverse the anti-aphrodisiac effects of alpha-2-adrenergic agonists in rats (such as clonidine[29]) or can otherwise negate some chemicals that antagonize sexuality (such as Naloxone,[30]) while enhancing sexual motivation in otherwise healthy rats. This effect is independent of the state of the genitalia (working in models of genital anesthetization[31]), the state of exhaustion,[32] and works independently of the hormone [testosterone](still effective despite castration[33]), testosterone of which is known to be associated with enhanced libido in men[34] and women.[35]


Stress, Panic, and Anxiety

Interactions with yohimbine and stress (as well as panic) may be related to the locus coeruleus, a nucleus in the brainstem that is related to these responses; antagonism of the A2(A) receptors in this brain region increase noradrenaline levels via reducing the rate of degradation.[36]

This increase in anxiety may be a per se effect of yohimbine in excess, as 30mg yohimbine can induce anxiety acutely in otherwise healthy persons (assessed by the Visual Analogue Scale for Anxiety),[37] opioid dependent persons,[38] and in persons who are susceptable to panic attacks; where yohimbine may be able to induce panic attacks.[39]

Due to effectively increasing noradrenaline, the neural side-effects of excess noradrenaline may result if too high a dose is taken; the most common are anxiety and panic disorders, with the later affecting susceptable persons

The increase in anxiety can be abolished by diazepam (anxiolytic sedative)[37] and clonidine (activator of the A2A receptor that yohimbine inhibits).[37]

The increase in anxiety still exists but to a lesser degree in persons with good aerobic fitness, such as marathon runners;[40] this may be a benefit of aerobic fitness per se and merely generalized to yohimbine, as it has been noted in response to psychosocial stress.[40][41]



In persons with low baseline anxiety, 15 mg yohimbine is associated with an increase in arithmetic task performance secondary to its ability to increase arousal; this improvement was still noted in persons who experienced anxiety from yohimbine, but was accompanied by a greater amount of errors as well.[21]


Cerebral Blood Flow

In a study that aimed to assess the effects of adrenergic stimulation on cerebral blood flow, yohimbine was used to increase noradrenaline due to its reliability.[42] It was found that yohimbine reduced cerebral blood flow in most subjects (in a range of 4-29%, mean decrease of 14.5%), but one that subject who had a minor panic attack experienced an increase in blood flow (+23%) and in neither group were changes in blood flow selective for one brain region over another.[42]



Yohimbine appears to play a role in facilitating fear extinction, which is a psychological phenomena where repeated exposures to a fearful stimuli eventually results in desensitization to the stimuli and less fear associated with it; the most practical application of facilitating fear extinction is in phobia treatment, where yohimbine treamtent has been associated with improved fear extinction secondary to exposure therapy[43] and thought to be due to increasing noradrenaline levels.[43] That being said. a follow-up study that noted increased noradrenaline (assessed via salivary amlyase) noted that this increase was independent of any significant benefit to phobia treatment.[15] Currently, the evidence for yohimbine facilitating phobia treatment is mixed, with one preliminary study noting positive results with Claustrophobia[43] but another noting no benefit of yohimbine on the fear of flying.[15]

Currently, the evidence for yohimbine facilitating phobia treatment is mixed



Yohimbine does not appear to adversely affect sleep quality.[44]



Impulsivity appears to be correlated to noradrenergic signalling (initially seen due to correlations with the state of arousal[45]) and subsequent activation in the nuclear accumbens and the orbitofrontal cortex[46] and noradrenaline appears to have a link to impulsivity-like symptoms in some clinical situations such as ADHD[47] and PTSD.[48][49]

These effects have been noted in healthy human subjects in a dose-dependent manner[50] and may be mediated by activity (and CREB phosphorylation) in the orbitofrontal cortex. One rat study noted increased impulsivity following a U-shaped curve (with maximal effectiveness at 1-2mg/kg, within normal human doses of 14-28mg for a 200lb person) associated with increased CREB phosphorylation in the orbitofronal cortex, but not the nuclear accumbens, and the effects paralleling that seen in humans.[51]

Yohimbine has been found to increase impulsivity in humans in at least one trial, which may be mediated via noradrenergic signalling secondary to the basic alpha-2-adrenergic antagonism


Interactions with Sexuality


Erectile Dysfunction

Yohimbine, secondary to its alpha-2-adrenergic inhibitory potential, was commonly used as first-line treatment for erectile dysfunction previous to the advent of PDE5 inhibitors.[52] A review[52] that cited the following trials[53][54][55][56][57][58][59] notes a variable efficacy range of 34-73% exists and this may be due to efficacy in persons with psychogenic erectile dysfunction rather than other models of erectile dysfunction, such as organic.[52]

Combination therapy of Yohimbine with L-Arginine has shown preliminary benefits[60] with more efficacy in mild to moderate (rather than severe) erectile dysfunction.[61]


Fat Mass and Obesity



Yohimbine acts upon the adrenergic receptor system of fat cells, which regulate thermogenesis. The beta-subunits of the adrenergic receptors (targets of ephedrine) can be seen as stimulatory for fat loss as they increase the activity of the enzyme Adenyl Cyclase and subsequently cAMP levels (mainly via the b1 and b2 subunits; with b3 being less active in humans).[62][63] The alpha-subunits are more suppressive of fat metabolism, in which their activation reduces activity of Adenyl Cyclase and reduces cAMP levels (specifically alpha-2). Yohimbine is a selective alpha-2 adrenergic receptor antagonist (inactivator), which inhibits activation of the suppressive set of receptors and preserves Adenyl Cyclase activity and the effects mediated via the beta receptors.[64]

Antagonism (Inactivation) of the Alpha-2-Adrenergic receptors preserves fat burning effects mediated via other mechanisms, a negation of a suppressive effect that ultimately results in more lipolysis (fat burning)

When looking at the interactions of yohimbine at the receptor level, yohimbine was found to be as a selective alpha2-adrenergic antagonist with 44-fold higher affinity for the alpha2 subunit than it does for the alpha1 subunit when tested in rat anoccygeus and vas deferens; this differs from the related compound corynanthine and rauwolscine which are selective for the alpha1 receptor (33-fold) and mostly non-selective (3.3 fold); respectively.[65] These values were derived from in vitro experimentations, and a second test using competitive binding in brain slices noted that the selectivity was reduced from 45-fold to 5.7.[65]

When looking at the alpha2-receptor itself, yohimbine appears to further have selectivity for the alpha2C subunit rather than A or B; in the range of 4-15 times selectivity,[66] while rauwolscine appears to be nonselective among these three subunits.[67][66] Rauwolscine appears to be as effective on the level of the receptor as yohimbine,[68] with coynanthine being magnitudes less effective.[65]

Beyond being an 'Alpha-Adrenergic antagonist', yohimbine has selectivity for the Alpha-2C subunit more than other subunits.

Beyond that, yohimbine itself can potentially induce fat loss vicariously through the release of adrenaline; adrenaline itself is an activator of beta-adrenergic receptors.[69] However, this increase of adrenaline may fade with time reaching statistical insignificnace 2 weeks after daily ingestion.[18] Increases in plasma free fatty acids and the density of alpha2-adrenergic receptors remain similar at both time points, suggesting that yohimbine selectively loses the spike in adrenaline but not direct receptor fat burning effects.

May have indirect fat burning mechanisms secondary to adrenaline release from the brain, the positive fat burning effects may be lost after usage despite the 'anti-fat gain' effects of Alpha-2C Antagonism being preserved


Body Fat Distribution

Yohimbine was first investigated for its role in selective body fat removal due to its usage as a topical cream (being able to choose where to apply the yohimbine)[70][71] but also secondary to its usage to eliminate thigh size in women, as elevated estrogen levels increased alpha2-adrenergic receptor activity.[72] Due to increased amounts of alpha2-adrenergic activity in the thighs of women, antagonism of these receptors was thought to reduce selective adiposity; results with cream are mixed, with one trial coming back positive[71] and the other noted benefit with both forskolin (from Coleus Forskohlii) and aminophylline but not yohimbine.[70]

Investigated for the ability to selectively induce fat loss in the thighs of women (which express higher levels of the Alpha2-Adrenergic receptor due to estrogen) but results are mixed and confounded with other compounds



Ketogenesis, or the production of ketone bodies, is enhanced under the presence of noradrenaline under normal conditions. Blocking the alpha adrenergic receptors, via the blocking of the alpha-2 adrenergic receptor, augments the ketogenic effects of noradrenaline. [73]


Interactions with Fed/Fasted states

One intervention that noted increased fat burning (biomarkers of increased NEFA and glycerol) also noted that this increase was abolished during a fed state.[74] It has been hypothesized that this interaction with the fasted state as well as apparently additive/synergistic effects of yohimbine and exercise on lipolysis[74] could result in timing of yohimbine being prior to morning exercise.[75]

When paired with food acutely, yohimbine may actually augment glucose-induced insulin release from pancreatic cells[76][77] but does not occur in the fasted state after oral consumption of 0.2mg/kg.[19][74]

May not be effective in a fed state. This may be due to augmenting insulin release during a fed but not fasted state

If the mechanism is via stimulation of insulin release reducing lipolysis, it is theoretical that a carbohydrate-free and low-protein meal (to reduce glucose-induced stimulation) could be similar to the fasted state; this has not been investigated in trials.



One study has been conducted with Yohimbine in elite soccer players taking 10mg yohimbine twice a day (20mg total) for a period of 21 days noted that, after the diet was controlled for, that fat percentage was decreased from 9.3+/-1.1% to 7.1+/-2.2% (assessed via calipers), while placebo experienced a nonsignificant increase.[78]

0.2mg/kg Yohimbine in otherwise healthy men appears to enhance the fat burning effects of endogenous noradrenaline, and appears to be more effective during periods of exercise and attenuated if given beta-blockers;[74] another study noted this attenuation to be measured at 70%.[19]

In athletes or in persons with conjunction with exercise or in a fasted state, yohimbine appears to be able to induce lipolysis (fat loss)

However, at least one study has noted null results, in that yohimbine did not decrease weight in healthy volunteers.[79]


Cardiovascular and Blood Health


Orthostatic Hypotension

Orthostatic hypotension is a benign condition where, upon standing, lightheadedness results due to a temporarily reduced cerebral blood pressure. Yohimbine appears to be capable of enhancing sympathetic tone due to its ability to increase blood pressure[80] and is a more potent treatment of orthostatic hypotension than pyridostigmine (60mg) when yohimbine is used at 5.4mg.[81]


Interactions with Lean Mass



One study in elite soccer players noted that, after 21 days of supplementation at 20mg daily (two doses of 10mg) that no influence was found on lean mass nor exercise performance despite a decrease in fat mass.[78]


Interactions with Glucose Metabolism



One study investigating the interaction of yohimbine and diabetes (based on the observation that alpha2-adrenoreceptors are overexpressed in rat pancreatic cells during diabetes[82] where they act to suppress excess insulin secretion[83]) noted that yohimbine at 2.5mg/kg bodyweight injected was able to normalize pancreatic blood flow (impaired during the diabetic state) and increased serum insulin levels in diabetic but not non-diabetic control rats.[82]


Interactions with Hormones



Yohimbine intervention at 5.4 or 10.8mg in otherwise healthy men with organic erectile dysfunction failed to influence testosterone.[84]

The increase in sexual desire seen from Yohimbine does not appear to be related to testosterone,[33] although at least one human study has noted that the response to pro-erectile properties of yohimbine is weakly associated with free testosterone.[84]



Yohimbine in isolation (at 30mg) does not seem to increase cortisol nor related stress hormone levels in vivo[85], although increases were noted at this level when injected[86][87] and particularily when paired with caffeine at 10mg/kg bodyweight.[88]


Nutrient-Nutrient Interactions


PDE5 inhibitors (Viagra)

Yohimbine appears to synergistically enhance the pro-erectile effects of Viagra, assessed by stimulation of the cavernosal nerve in rats given the agent.[89] This study noted that 1umol/kg injections of yohimbine increased the efficacy of administered Viagra despite not being significantly effective on its own.[89]



Sibutramine (not to be confused with Sulbutiamine) is an appetite supressing pharmaceutical that has been withdrawn from the market due to associations with cardiovascular incidents. Yohimbine and Sibutramine has the potential to interact as the side-effects of Sibutramine are mediated via adrenaline and yohimbine can increase systemic adrenaline levels.[90]


MethylPhenidate (Ritalin)

In anaesthetised rats given intravenous Methylphenidate (MPH) to test its effects on neuronal firing, the activation of firing in the prefrontal cortex appears to be augmented under the influence of alpha-2-adrenergic antagonism by yohimbine (1mg/kg).[25] Stimulation of these neurons was not seen with yohimbine in isolation, and were mediated via dopaminergic activation (blocking of D1 receptors blocks this augmentation).[25]



Relative to consuming Ephedrine at 25mg and Caffeine at 200mg (components of the ECA stack), adding Yohimbine at 5mg appears to attenuate cardiac work at rest, but augment cardiac work during exercise in obese women.[91] This study did use a significantly low-calorie diet (400kcal for 10 days), but the results were compared to a control also on the same diet.[91]



Alcohol also appears to increase noradrenaline levels, and 1.1mL/kg of 95% ethanol (100-120mg/dL BAC[92]) appears to increase noradrenaline (measured via serum MHPG) to a greater level than does 0.4mg/kg yohimbine (double the usual dose); they had additive effects on increasing serum MHPG yet alcohol attenuated the increase of sitting blood pressure nonsignificantly.[87] Despite the higher levels or MHPG with alcohol, subjective anxiety was greater with Yohimbine while alcohol had no effect on yohimbine-induced cortisol spikes.[87]


Safety and Toxicology



Adverse drug events in persons taking the recommended dosage (for erectile dysfunction, 5.4mg thrice a day) include nausea, abdominal pain, dizziness, and nervousness.[93] Higher acute dosages in the 15-20mg range some persons may experience tachycardia (irregular heartbeat) and hypertension.[94][95]

There are also issues surrounding indeterminate or inaccurate labeling of the dose of yohimbine in many US supplements. One study of 49 supplements purchased in the US which claimed to contain yohimbine found that the actual dose ranged from 0 to 12.9 mg per recommended serving. The latter dose is greater than the highest prescription strength dose formally available in the US. Furthermore, the actual dose in supplements that contained yohimbine and had a dose on the label was 23-147% of that listed on the supplement, and only 22% of the supplements listed the quantity of yohimbine at all. 18% of the supplements examined did not warn the consumer of possible adverse effects of yohimbine.[96]

Adverse effects for yohimbine occur even at recommended dosages, including nausea, abdominal pain, dizziness, and nervousness. Also, many supplements in containing yohimbine in the US either do not have the dosages labelled or the doses on the label are inaccurate.


Case Studies

Acute neurotoxicity has been reported in man in a dose of 5,000mg (far above the recommended dosage of 0.2mg/kg) in an isolated case study.[97]

Other case studies include a man (24 and otherwise healthy) who experienced elevated blood pressure, heart rate, and glucose as well as agitation and anxiety in response to a single bolus of 300mg yohimbine with symptoms being significantly attenuated to a healthy status one week later at followup.[2]

Yohimbine, in isolation and when excessive amounts are consumed, are causative of toxicity symptoms that appear to be related to the ability of yohimbine to increase adrenaline levels

In adverse event report has been published with data from the California Poison Control System.[93] This study was retrospective in nature and looked for cases between 2000 and 2006 assessing 18 year old persons where yohimbine was assessed as 'probably causing the results' (Naranjo causality score of 1 or more) and had 238 cases meet this criteria (350 in total, but 32% excluded for either underage or not likely related to yohimbine).[93] The majority of cases were in males (77%) using non-prescription yohimbine (98.7%), and 59.7% of cases had nutrient confounds (with fat burners, caffeine and ephedrine were commonly associated; for penile health, saw palmetto and panax ginseng) and 29.5% had pharmaceutical or alcohol interactions. Of the 238 cases, 7 were deemed to be of serious magnitude (where symptoms as a result of the exposure which were lifethreatening) and most common side effects were anxiety/agitation, hypertension or cardiac ailments, and gastrointestinal problems.[93] There was not enough evidence to conclude what the average dose exposure was.

Problems seem to arise more often with nutrient-nutrient interactions than with yohimbine in isolation, although some cases have surfaced with yohimbine in isolation and these tend to result in cardiac arrythmia and/or hypertension when the dose is exceeded or the person is susceptable

2.^Cimolai N, Cimolai TYohimbine use for physical enhancement and its potential toxicityJ Diet Suppl.(2011 Dec)
6.^Asker AF, Helal MA, Motawi MMLight stability of some parenteral solutions of reserpinePharmazie.(1971 Feb)
7.^Jamil N, Afrozrizvi H, Ahmed I, Beg AEStudies on the photostability of reserpine in parenteral solutionsPharmazie.(1983 Jul)
8.^Strobl GR, von Kruedener S, Stöckigt J, Guengerich FP, Wolff TDevelopment of a pharmacophore for inhibition of human liver cytochrome P-450 2D6: molecular modeling and inhibition studiesJ Med Chem.(1993 Apr 30)
9.^Le Corre P, Parmer RJ, Kailasam MT, Kennedy BP, Skaar TP, Ho H, Leverge R, Smith DW, Ziegler MG, Insel PA, Schork NJ, Flockhart DA, O'connor DTHuman sympathetic activation by alpha2-adrenergic blockade with yohimbine: Bimodal, epistatic influence of cytochrome P450-mediated drug metabolismClin Pharmacol Ther.(2004 Aug)
10.^Bharucha AE, Skaar T, Andrews CN, Camilleri M, Philips S, Seide B, Burton D, Baxter K, Zinsmeister ARRelationship of cytochrome P450 pharmacogenetics to the effects of yohimbine on gastrointestinal transit and catecholamines in healthy subjectsNeurogastroenterol Motil.(2008 Aug)
11.^Ozawa S, Soyama A, Saeki M, Fukushima-Uesaka H, Itoda M, Koyano S, Sai K, Ohno Y, Saito Y, Sawada JEthnic differences in genetic polymorphisms of CYP2D6, CYP2C19, CYP3As and MDR1/ABCB1Drug Metab Pharmacokinet.(2004 Apr)
12.^Taouis M, Berlan M, Montastruc P, Lafontan MMechanism of the lipid-mobilizing effect of alpha-2 adrenergic antagonists in the dogJ Pharmacol Exp Ther.(1988 Dec)
13.^Szemeredi K, Komoly S, Kopin IJ, Bagdy G, Keiser HR, Goldstein DSSimultaneous measurement of plasma and brain extracellular fluid concentrations of catechols after yohimbine administration in ratsBrain Res.(1991 Feb 22)
14.^Ehlert U, Erni K, Hebisch G, Nater USalivary alpha-amylase levels after yohimbine challenge in healthy menJ Clin Endocrinol Metab.(2006 Dec)
16.^Hedner T, Edgar B, Edvinsson L, Hedner J, Persson B, Pettersson AYohimbine pharmacokinetics and interaction with the sympathetic nervous system in normal volunteersEur J Clin Pharmacol.(1992)
17.^Grossman E, Rosenthal T, Peleg E, Holmes C, Goldstein DSOral yohimbine increases blood pressure and sympathetic nervous outflow in hypertensive patientsJ Cardiovasc Pharmacol.(1993 Jul)
18.^Galitzky J, Rivière D, Tran MA, Montastruc JL, Berlan MPharmacodynamic effects of chronic yohimbine treatment in healthy volunteersEur J Clin Pharmacol.(1990)
19.^Berlan M, Galitzky J, Riviere D, Foureau M, Tran MA, Flores R, Louvet JP, Houin G, Lafontan MPlasma catecholamine levels and lipid mobilization induced by yohimbine in obese and non-obese womenInt J Obes.(1991 May)
20.^Sturgill MG, Grasing KW, Rosen RC, Thomas TJ, Kulkarni GD, Trout JR, Maines M, Seibold JRYohimbine elimination in normal volunteers is characterized by both one- and two-compartment behaviorJ Cardiovasc Pharmacol.(1997 Jun)
21.^Mizuki Y, Suetsugi M, Ushijima I, Yamada MDifferential effects of noradrenergic drugs on anxiety and arousal in healthy volunteers with high and low anxietyProg Neuropsychopharmacol Biol Psychiatry.(1996 Nov)
22.^Kennedy SH, Gnam W, Ralevski E, Brown GMMelatonin responses to clonidine and yohimbine challengesJ Psychiatry Neurosci.(1995 Jul)
26.^Roychowdhury S, Peña-Contreras Z, Tam J, Yadlapalli A, Dinh L, Nichols JA, Basu D, Atzori Mα₂- and β-adrenoceptors involvement in nortriptyline modulation of auditory sustained attention and impulsivityPsychopharmacology (Berl).(2012 Jul)
27.^Callahan MF, Beales M, Oltmans GAYohimbine and rauwolscine reduce food intake of genetically obese (obob) and lean micePharmacol Biochem Behav.(1984 Apr)
29.^Clark JT, Smith ER, Davidson JMEvidence for the modulation of sexual behavior by alpha-adrenoceptors in male ratsNeuroendocrinology.(1985 Jul)
30.^Koskinen I, Hendricks S, Yells D, Fitzpatrick D, Graber BYohimbine and naloxone: effects on male rat sexual behaviorPhysiol Behav.(1991 Sep)
31.^Clark JT, Smith ER, Davidson JMEnhancement of sexual motivation in male rats by yohimbineScience.(1984 Aug 24)
32.^Rodríguez-Manzo G, Fernández-Guasti AReversal of sexual exhaustion by serotonergic and noradrenergic agentsBehav Brain Res.(1994 Jun 30)
33.^Clark JT, Smith ER, Davidson JMTestosterone is not required for the enhancement of sexual motivation by yohimbinePhysiol Behav.(1985 Oct)
34.^Travison TG, Morley JE, Araujo AB, O'Donnell AB, McKinlay JBThe relationship between libido and testosterone levels in aging menJ Clin Endocrinol Metab.(2006 Jul)
38.^Stine SM, Southwick SM, Petrakis IL, Kosten TR, Charney DS, Krystal JHYohimbine-induced withdrawal and anxiety symptoms in opioid-dependent patientsBiol Psychiatry.(2002 Apr 15)
40.^Sommer M, Braumann M, Althoff T, Backhaus J, Kordon A, Junghanns K, Ehrenthal D, Bartmann U, Hohagen F, Broocks APsychological and neuroendocrine responses to social stress and to the administration of the alpha-2-receptor antagonist, yohimbine, in highly trained endurance athletes in comparison to untrained healthy controlsPharmacopsychiatry.(2011 Jun)
41.^Rimmele U, Zellweger BC, Marti B, Seiler R, Mohiyeddini C, Ehlert U, Heinrichs MTrained men show lower cortisol, heart rate and psychological responses to psychosocial stress compared with untrained menPsychoneuroendocrinology.(2007 Jul)
42.^Cameron OG, Zubieta JK, Grunhaus L, Minoshima SEffects of yohimbine on cerebral blood flow, symptoms, and physiological functions in humansPsychosom Med.(2000 Jul-Aug)
44.^Gentili A, Godschalk MF, Gheorghiu D, Nelson K, Julius DA, Mulligan TEffect of clonidine and yohimbine on sleep in healthy men: a double-blind, randomized, controlled trialEur J Clin Pharmacol.(1996)
49.^Casada JH, Roache JDBehavioral inhibition and activation in posttraumatic stress disorderJ Nerv Ment Dis.(2005 Feb)
50.^Swann AC, Birnbaum D, Jagar AA, Dougherty DM, Moeller FGAcute yohimbine increases laboratory-measured impulsivity in normal subjectsBiol Psychiatry.(2005 May 15)
51.^Sun H, Green TA, Theobald DE, Birnbaum SG, Graham DL, Zeeb FD, Nestler EJ, Winstanley CAYohimbine increases impulsivity through activation of cAMP response element binding in the orbitofrontal cortexBiol Psychiatry.(2010 Apr 1)
52.^Shamloul RNatural aphrodisiacsJ Sex Med.(2010 Jan)
54.^Morales A, Condra M, Owen JA, Surridge DH, Fenemore J, Harris CIs yohimbine effective in the treatment of organic impotence? Results of a controlled trialJ Urol.(1987 Jun)
55.^Mann K, Klingler T, Noe S, Röschke J, Müller S, Benkert OEffects of yohimbine on sexual experiences and nocturnal penile tumescence and rigidity in erectile dysfunctionArch Sex Behav.(1996 Feb)
56.^Reid K, Surridge DH, Morales A, Condra M, Harris C, Owen J, Fenemore JDouble-blind trial of yohimbine in treatment of psychogenic impotenceLancet.(1987 Aug 22)
57.^Vogt HJ, Brandl P, Kockott G, Schmitz JR, Wiegand MH, Schadrack J, Gierend MDouble-blind, placebo-controlled safety and efficacy trial with yohimbine hydrochloride in the treatment of nonorganic erectile dysfunctionInt J Impot Res.(1997 Sep)
58.^Susset JG, Tessier CD, Wincze J, Bansal S, Malhotra C, Schwacha MGEffect of yohimbine hydrochloride on erectile impotence: a double-blind studyJ Urol.(1989 Jun)
59.^Rowland DL, Kallan K, Slob AKYohimbine, erectile capacity, and sexual response in menArch Sex Behav.(1997 Feb)
62.^Carmen GY, Víctor SMSignalling mechanisms regulating lipolysisCell Signal.(2006 Apr)
64.^Lafontan M, Berlan M, Galitzky J, Montastruc JLAlpha-2 adrenoceptors in lipolysis: alpha 2 antagonists and lipid-mobilizing strategiesAm J Clin Nutr.(1992 Jan)
65.^Doxey JC, Lane AC, Roach AG, Virdee NKComparison of the alpha-adrenoceptor antagonist profiles of idazoxan (RX 781094), yohimbine, rauwolscine and corynanthineNaunyn Schmiedebergs Arch Pharmacol.(1984 Feb)
66.^Lalchandani SG, Lei L, Zheng W, Suni MM, Moore BM, Liggett SB, Miller DD, Feller DRYohimbine dimers exhibiting selectivity for the human alpha 2C-adrenoceptor subtypeJ Pharmacol Exp Ther.(2002 Dec)
67.^MacDonald E, Kobilka BK, Scheinin MGene targeting--homing in on alpha 2-adrenoceptor-subtype functionTrends Pharmacol Sci.(1997 Jun)
69.^Reiner S, Ambrosio M, Hoffmann C, Lohse MJDifferential signaling of the endogenous agonists at the beta2-adrenergic receptorJ Biol Chem.(2010 Nov 12)
70.^Greenway FL, Bray GA, Heber DTopical fat reductionObes Res.(1995 Nov)
74.^Galitzky J, Taouis M, Berlan M, Rivière D, Garrigues M, Lafontan MAlpha 2-antagonist compounds and lipid mobilization: evidence for a lipid mobilizing effect of oral yohimbine in healthy male volunteersEur J Clin Invest.(1988 Dec)
76.^Ito K, Hirose H, Kido K, Koyama K, Maruyama H, Saruta TAdrenoceptor antagonists, but not guanethidine, reduce glucopenia-induced glucagon secretion from perfused rat pancreasDiabetes Res Clin Pract.(1995 Dec)
77.^Ribes G, Hillaire-Buys D, Gross R, Blayac JP, Loubatières-Mariani MMInvolvement of a central nervous pathway in yohimbine-induced insulin secretionEur J Pharmacol.(1989 Mar 21)
80.^Biaggioni I, Robertson RM, Robertson DManipulation of norepinephrine metabolism with yohimbine in the treatment of autonomic failureJ Clin Pharmacol.(1994 May)
81.^Shibao C, Okamoto LE, Gamboa A, Yu C, Diedrich A, Raj SR, Robertson D, Biaggioni IComparative efficacy of yohimbine against pyridostigmine for the treatment of orthostatic hypotension in autonomic failureHypertension.(2010 Nov)
82.^Sandberg M, Pettersson U, Henriksnäs J, Jansson LThe α2-Adrenoceptor Antagonist Yohimbine Normalizes Increased Islet Blood Flow in GK Rats: A Model of Type 2 DiabetesHorm Metab Res.(2012 Sep 26)
84.^Guay AT, Spark RF, Jacobson J, Murray FT, Geisser MEYohimbine treatment of organic erectile dysfunction in a dose-escalation trialInt J Impot Res.(2002 Feb)
85.^Cuneo RC, Livesey JH, Nicholls MG, Espiner EA, Donald RAEffects of alpha-2 adrenoreceptor blockade by yohimbine on the hormonal response to hypoglycaemic stress in normal manHorm Metab Res.(1989 Jan)
87.^McDougle CJ, Krystal JH, Price LH, Heninger GR, Charney DSNoradrenergic response to acute ethanol administration in healthy subjects: comparison with intravenous yohimbinePsychopharmacology (Berl).(1995 Mar)
89.^Senbel AM, Mostafa TYohimbine enhances the effect of sildenafil on erectile process in ratsInt J Impot Res.(2008 Jul-Aug)
90.^Jordan J, Sharma AMPotential for sibutramine-yohimbine interactionLancet.(2003 May 24)
94.^Linden CH, Vellman WP, Rumack BYohimbine: a new street drugAnn Emerg Med.(1985 Oct)
95.^HOLMBERG G, GERSHON SAutonomic and psychic effects of yohimbine hydrochloridePsychopharmacologia.(1961)
96.^Cohen PA, Yang Y-H, Maller G, DeSouza R, Khan IAPharmaceutical quantities of yohimbine found in dietary supplements in the USADrug Test Anal.(2015 Sep)
97.^Giampreti A, Lonati D, Locatelli C, Rocchi L, Campailla MTAcute neurotoxicity after yohimbine ingestion by a body builderClin Toxicol (Phila).(2009 Sep)