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Clinical data
Pronunciation /ˈbjuːsprn/ (BEW-spi-rohn)
Trade names Buspar
AHFS/Drugs.com Monograph
MedlinePlus a688005
  • AU: B1
  • US: B (No risk in non-human studies)
Routes of
By mouth
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability 3.9%[3]
Protein binding 86–95%[4]
Metabolism Hepatic (via CYP3A4)[1][2]
Biological half-life 2.5 hours[1]
Excretion Urine: 29–63%[4]
Feces: 18–38%[4]
CAS Number
PubChem CID
ECHA InfoCard 100.048.232
Chemical and physical data
Formula C21H31N5O2
Molar mass 385.50314 g/mol
3D model (Jmol)

Buspirone, brand name Buspar, is an anxiolytic drug that is primarily used to treat generalized anxiety disorder (GAD).[5] It is also commonly used to augment antidepressants in the treatment of major depressive disorder.[6] Unlike most anxiolytics, the pharmacology of buspirone is not related to that of benzodiazepines, barbiturates, or carbamates (it is not a GABA receptor agonist), and so buspirone does not carry the risk of physical dependence and withdrawal symptoms for which those drug classes are known. Buspirone is not considered to be a drug-of-abuse, is safer in overdose than traditional anxiolytics, and is significantly less impairing at therapeutic doses.

Medical uses[edit]


Buspirone is approved in the United States by the Food and Drug Administration (FDA) for the short- or long-term treatment of anxiety disorders or can also be used for the short-term relief of the symptoms of anxiety.[7] Likewise in Australia, buspirone is licensed for the treatment of anxiety disorders.[8][9] In the United Kingdom, buspirone is indicated only for the short-term treatment of anxiety.[10][11]

Buspirone has no immediate anxiolytic effects, and hence has a delayed onset of action; its full clinical effectiveness may require 2 to 4 weeks to manifest.[12] The drug has been shown to be similarly effective in the treatment of GAD to benzodiazepines including diazepam, alprazolam, lorazepam, and clorazepate.[3] Buspirone is not known to be effective in the treatment of other anxiety disorders besides GAD,[6] although there is some limited evidence that it may be useful in the treatment of social phobia as an adjunct to selective serotonin reuptake inhibitors (SSRIs).[13][3] Buspirone allows fast-acting anxiety medications such as benzodiazepines to be effective at a much lower dose which greatly reduces the physical and mental side-effects of their use, making them feasible options for immediately treating anxiety when full cognitive function is required. Its lack of GABA-ergic activity also makes it a much safer option than traditional anxiolytics when used along with pain and seizure medications, and it is a first-line anxiety treatment for patients with chronic pain complaints.

Due to buspirone's unique method of action, it is not a viable rescue-medication to immediately abort anxiety episodes, it is taken daily to exert a constant effect (in the same manner as traditional antidepressant medications); the full effect of buspirone generally does not become apparent for up to a month after the patient initiates the full dose for long-term daily use, and continues to work for at least 1-2 weeks after discontinuation due to the presence of a constant quantity of the drug in the patient's blood plasma (therefore missing one or two consecutive doses will not compromise the benefit of buspirone therapy once plasma-levels of the drug have been stabilized within the therapeutic range). It is not uncommon for a very low-dose benzodiazepine to be prescribed in addition to buspirone, for treating acute episodes if/when they occur (buspirone's constant anxiolytic effect greatly reduces the minimum effective dose of benzodiazepines and barbiturates and therefore makes them significantly more-tolerable for use at work/driving/performing other activities which require the patient's full cognitive capacity).


Although not approved for this indication, studies such as STAR*D have shown buspirone to be an effective augmentation agent alongside treatment with selective serotonin reuptake inhibitors (SSRIs) for clinical depression and is also used to counter the sexual dysfunction (anorgasmia and erectile dysfunction) associated with SSRIs.[14][15][16][17] The drug has also been found to be effective in the treatment of depression as a standalone drug.[6]

Other uses[edit]

Sexual dysfunction[edit]

There is some evidence that buspirone on its own may be useful in the treatment of hypoactive sexual desire disorder (HSDD) in women.[18]


Several clinical trials, most randomized double-blind trials (and in one buspirone was used as an adjunct to atomoxetine) and one open-label, have been conducted to evaluate the utility of buspirone in the treatment of attention deficit hyperactivity disorder (ADHD), with mostly positive results.[19][20][21][22]


Buspirone may be useful in the management of irritability, agitation, and aggression in older patients with dementia and in pediatrics, although further research is necessary to more clearly establish its effectiveness.[6]

Buspirone is not effective as a treatment for benzodiazepine withdrawal, barbiturate withdrawal, or alcohol withdrawal/delirium tremens.[23]


Buspirone has these contraindications:[24][25]


For GAD: 15–30 mg. Starting dose is 5 mg, 3 times daily, average dosage being 20–30 mg a day. If symptoms still persist after several weeks then the dose may be titrated up to 30 mg. Due to the short elimination half-life and linear pharmacokinetics of buspirone,[26] dosage can be increased by 5 mg every two to three days.[27][28][29][30][31][32][33]


Buspirone has been shown in vitro to be metabolized by the enzyme CYP3A4.[2] This finding is consistent with the in vivo interactions observed between buspirone and these inhibitors or inducers of cytochrome P450 3A4 (CYP3A4), among others:[24]

Elevated blood pressure has been reported when buspirone has been administered to patients taking monoamine oxidase inhibitors (MAOIs).[24]

Side effects[edit]

Buspar (buspirone) 10-mg tablets.

Known side effects associated with buspirone include dizziness, headaches, nausea, nervousness, and paresthesia.[3] Unlike benzodiazepines, buspirone is relatively well-tolerated, and is not associated with sedation, cognitive and psychomotor impairment, muscle relaxation, physical dependence, or anticonvulsant effects.[3] In addition, buspirone does not produce euphoria,[12] and is not a drug of abuse.[8]

Extensive list of side effects[edit]

Adverse effects by incidence[4][7][8][10] include:

Very common (>10% incidence)

  • Dizziness/light-headedness
  • Headache
  • Somnolence (sleepiness)

Common (1–10% incidence)

  • Nervousness
  • Insomnia
  • Sleep disorder
  • Disturbance in attention
  • Depression
  • Confusional state
  • Anger
  • Tachycardia (fast heart rate)
  • Chest pain
  • Sinusitis (nasal congestion)
  • Pharyngolaryngeal pain
  • Paraesthesia (tingling skin)
  • Blurred vision
  • Abnormal coordination
  • Tremor
  • Cold sweat
  • Rash
  • Nausea
  • Abdominal pain
  • Dry mouth
  • Diarrhea
  • Constipation
  • Vomiting
  • Fatigue
  • Musculoskeletal pain

Uncommon (0.1–1%)

  • Syncope
  • Hypotension
  • Hypertension
  • Redness and itching of the eyes
  • Altered taste
  • Conjunctivitis
  • Flatulence
  • Anorexia
  • Increased appetite
  • Salivation
  • Rectal bleeding
  • Urinary frequency
  • Urinary hesitancy
  • Menstrual irregularity or spotting
  • Dysuria
  • Muscle cramps
  • Muscle spasms
  • Muscle rigidity/stiffness
  • Involuntary movements
  • Shortness of breath
  • Chest congestion
  • Changes in libido
  • Oedema
  • Pruritus
  • Flushing
  • Easy bruising
  • Dry skin
  • Facial oedema
  • Mild increases in hepatic aminotransferases (AST, ALT)
  • Weight gain
  • Fever
  • Roaring sensation in the head
  • Weight loss
  • Malaise
  • Depersonalisation
  • Noise intolerance
  • Euphoria
  • Akathisia
  • Fearfulness
  • Loss of interest
  • Dissociative reaction

Rare (<0.1% incidence)


Activated charcoal is believed to be an effective treatment for overdose, provided the patient is treated promptly.  Expected symptoms (based on symptoms in male healthy volunteers treated with 375 mg/day — compared to the maximum daily licensed dosage in Australia, the UK, and the US):[7][8][10]

  • Nausea
  • Vomiting
  • Dizziness
  • Drowsiness
  • Miosis
  • Gastric distress

Buspirone appears to be relatively benign in cases of single-drug overdose, although no definitive data on this subject appear to be available.[35]


Binding profile of buspirone[36]
Binding site Affinity (Ki)
5-HT1A 20 nM
5-HT1B > 100 μM
5-HT1D > 100 μM
5-HT2A 1,300 nM
5-HT2C 1,100 nM
D1 33,000 nM
D2 240 nM
α1-Adrenergic 1,000 nM
α2-Adrenergic 6,000 nM
β-Adrenergic 8,800 nM
mACh 38,000 nM
GABAA/BDZ > 100 μM

Buspirone acts as an agonist of the serotonin 5-HT1A receptor with high affinity (Ki = 20 nM).[3][36] It is a preferential full agonist of presynaptic 5-HT1A receptors, which are inhibitory autoreceptors, and is a partial agonist of postsynaptic 5-HT1A receptors.[3] In accordance, an animal study found that buspirone dose-dependently decreases serotonin levels, while increasing dopamine and norepinephrine levels.[3] It is thought that the main effects of buspirone are mediated via its interaction with the 5-HT1A receptor.[3] Some of its effects may be mediated via oxytocin release secondary to 5-HT1A receptor agonism.[37][38][non-primary source needed] Buspirone additionally possesses weak affinity for the serotonin 5-HT2A and 5-HT2C receptors (Ki = 1,300 nM and 1,100 nM; ~60-fold less than for 5-HT1A), although this probably isn't clinically significant.[3][36]

In addition to the 5-HT1A receptor, buspirone is a weak antagonist of the dopamine D2 receptor (Ki = 240 nM), with approximately 15-fold lower affinity for this receptor relative to the 5-HT1A receptor.[3][36] It preferentially blocks inhibitory presynaptic D2 autoreceptors, and antagonizes postsynaptic D2 receptors only at higher doses.[3] In accordance, buspirone has been found to increase dopaminergic neurotransmission in the nigrostriatal pathway at low doses, whereas at higher doses, postsynaptic D2 receptors are blocked and antidopaminergic effects such as hypoactivity and reduced stereotypy, though notably not catalepsy, are observed in animals.[3] Buspirone has also been found to bind with high affinity to the D3 and D4 receptors (Ki = 98 nM and 29 nM, respectively).[39]

The major metabolite of buspirone, 1-(2-pyrimidinyl)piperazine (1-PP), occurs at higher circulating levels than buspirone itself, and is known to act as a potent α2-adrenergic receptor antagonist.[40] It may be responsible for the increased noradrenergic activity observed with buspirone in animals.[40] In addition, it may be involved in the antidepressant effects of buspirone.[citation needed]

Buspirone has weak affinity for the α1-adrenergic receptor (Ki = 1,000 nM), the clinical significance of which is uncertain.[36][39] Notably, buspirone has been reported to have shown "significant and selective intrinsic efficacy" at the α1-adrenergic receptor expressed in a "tissue- and species-dependent".[39]

Unlike benzodiazepines, buspirone does not interact with the GABAA receptor complex.[3][41]


Buspirone has a low oral bioavailability of 3.9% relative to intravenous injection due to extensive first-pass metabolism.[3] The time to peak plasma levels following ingestion is 0.9 to 1.5 hours.[3] It is reported to have an elimination half-life of 2.8 hours,[3] although a review of 14 studies found that the mean terminal half-life ranged between 2 and 11 hours, and one study even reported a terminal half-life of 33 hours.[42] Buspirone is metabolized primarily by CYP3A4, and prominent drug interactions with inhibitors and inducers of this enzyme have been observed.[1][2] Major metabolites of buspirone include 5-hydroxybuspirone, 6-hydroxybuspirone, 8-hydroxybuspirone, and 1-(2-pyrimidinyl)piperazine (1-PP).[42][43][44] 6-Hydroxybuspirone has been identified as the predominant hepatic metabolite of buspirone, with plasma levels that are 40-fold greater than those of buspirone after oral administration of buspirone to humans.[43] The metabolite is a high-affinity partial agonist of the 5-HT1A receptor (Ki = 25 nM) similarly to buspirone, and has demonstrated occupancy of the 5-HT1A receptor in vivo.[43] As such, it is likely to play a significant role in the therapeutic effects of buspirone.[43]


Buspirone is a member of the azapirone chemical class, and consists of azaspirodecanedione and pyrimidinylpiperazine components linked together.


Alkylation of 1-(2-pyrimidyl)piperazine (1) with 3-chloro-1-cyanopropane (2, 4-chlorobutyronitrile) gives 3, which is reduced either by hydrogenation over Raney nickel catalyst, or with LAH. The resulting 1° amine (4) from the previous step is then reacted with 3,3-tetramethyleneglutaric anhydride (5, 8-Oxaspiro[4.5]decane-7,9-dione) in order to yield buspirone (6).


Structural analogues of buspirone include tandospirone, gepirone, and perospirone.


Buspirone was first synthesized, by a team at Mead Johnson, in 1968,[6] but was not patented until 1975.[46][47][additional citation needed] It was initially developed as an antipsychotic drug acting on the D2 receptor, but was found to be ineffective in the treatment of psychosis and was repurposed as an anxiolytic.[3] In 1986, Bristol-Myers Squibb gained FDA approval for buspirone in the treatment of GAD.[6] The patent placed on buspirone expired in 2001 and it is now available as a generic drug.

Society and culture[edit]

Generic name[edit]

Buspirone is the INN, BAN, DCF, and DCIT of buspirone, while buspirone hydrochloride is its USAN, BANM, and JAN.[48][49][50][51]

Brand name[edit]

Buspirone is primarily sold under the brand name Buspar.[49][51]


Female sexual dysfunction[edit]

Buspirone/testosterone (tentative brand name Lybridos) is a combination formulation of buspirone and testosterone which is under development by a pharmaceutical company called Emotional Brain for the treatment of female sexual dysfunction.[52]


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