Buspirone
- Molecular FormulaC21H31N5O2
- Average mass385.503 Da
-
буспиронبوسبيرون丁螺酮
- 8-[4-[4-(2-Pyrimidinyl)-1-piperazinyl]butyl]-8-azaspiro[4.5]decane-7,9-dione
- Buspin
- Buspirone
- Spitomin
Buspirone, sold under the brand name Buspar, among others, is a medication primarily used to treat anxiety disorders, particularly generalized anxiety disorder.[9][10] Benefits support its short term use.[11] It has not been found to be effective in treating psychosis.[9] It is taken by mouth, and it may take up to four weeks to have an effect.[9][10]
Common side effects of buspirone include nausea, headaches, dizziness, and difficulty concentrating.[9][11] Serious side effects may include hallucinations, serotonin syndrome, and seizures.[11] Its use in pregnancy appears to be safe but has not been well studied, while use during breastfeeding is not recommended.[11][12] It is a serotonin 5-HT1A receptor agonist.[2]
Buspirone was first made in 1968 and approved for medical use in the United States in 1986.[9][10] It is available as a generic medication.[11] In 2018, it was the 92nd most-commonly prescribed medication in the United States, with more than 8 million prescriptions.[13][14]
Medical uses
Anxiety
Buspirone is used for the short-term treatment of anxiety disorders or symptoms of anxiety.[15][16][17][18][19] It is generally less preferred than selective serotonin reuptake inhibitors (SSRIs).[10]
Buspirone has no immediate anxiolytic effects, and hence has a delayed onset of action; its full clinical effectiveness may require 2–4 weeks to manifest itself.[20] The drug has been shown to be similarly effective in the treatment of generalized anxiety disorder (GAD) to benzodiazepines including diazepam, alprazolam, lorazepam, and clorazepate.[2] Buspirone is not known to be effective in the treatment of other anxiety disorders besides GAD,[21] 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).[2][22]
Other uses
Sexual dysfunction
There is some evidence that buspirone on its own may be useful in the treatment of hypoactive sexual desire disorder (HSDD) in women.[23]
Miscellaneous
Buspirone is not effective as a treatment for benzodiazepine withdrawal, barbiturate withdrawal, or alcohol withdrawal/delirium tremens.[24]
SSRI and SNRI antidepressants such as paroxetine and venlafaxine may cause jaw pain/jaw spasm reversible syndrome (although it is not common), and buspirone appears to be successful in treating bruxism on SSRI/SNRI-induced jaw clenching.[25][26]
Contraindications
Buspirone has these contraindications:[27][28]
- Hypersensitivity to buspirone
- Metabolic acidosis, as in diabetes
- Should not be used with MAO inhibitors
- Severely compromised liver and/or kidney function
Side effects
Known side effects associated with buspirone include dizziness, headaches, nausea, nervousness, and paresthesia.[2] Buspirone is relatively well tolerated, and is not associated with sedation, cognitive and psychomotor impairment, muscle relaxation, physical dependence, or anticonvulsant effects.[2] In addition, buspirone does not produce euphoria[20] and is not a drug of abuse.[16]
It is unclear if there is a risk of tardive dyskinesia or other movement disorders with buspirone.[9]
Overdose
Buspirone appears to be relatively benign in cases of single-drug overdose, although no definitive data on this subject appear to be available.[29] In one clinical trial, buspirone was administered to healthy male volunteers at a dosage of 375 mg/day, and produced side effects including nausea, vomiting, dizziness, drowsiness, miosis, and gastric distress.[15][16][18] In early clinical trials, buspirone was given at dosages even as high as 2,400 mg/day, with akathisia, tremor, and muscle rigidity observed.[30] Deliberate overdoses with 250 mg and up to 300 mg buspirone have resulted in drowsiness in about 50% of individuals.[30] One death has been reported in association with 450 mg buspirone together with alprazolam, diltiazem, alcohol, cocaine.[30]
Interactions
Buspirone has been shown in vitro to be metabolized by the enzyme CYP3A4.[8] This finding is consistent with the in vivo interactions observed between buspirone and these inhibitors or inducers of cytochrome P450 3A4 (CYP3A4), among others:[27]
- Itraconazole: Increased plasma level of buspirone
- Rifampicin: Decreased plasma levels of buspirone
- Nefazodone: Increased plasma levels of buspirone
- Haloperidol: Increased plasma levels of haloperidol
- Carbamazepine: Decreased plasma levels of buspirone
- Grapefruit: Significantly increases the plasma levels of buspirone.[31] See grapefruit–drug interactions.
- Fluvoxamine: Moderately increase plasma levels of buspirone.[32]
Elevated blood pressure has been reported when buspirone has been administered to patients taking monoamine oxidase inhibitors (MAOIs).[27]
Pharmacology
Pharmacodynamics
Site | Ki (nM) | Species | Ref |
---|---|---|---|
5-HT1A | 3.98–214 21 (median) |
Human | [33][34] |
5-HT1B | >100,000 | Rat | [35] |
5-HT1D | 22,000–42,700 | Human | [36][37] |
5-HT2A | 138 759–1,300 |
Human Rat |
[38] [35][38] |
5-HT2B | 214 | Human | [38] |
5-HT2C | 490 1,100–6,026 |
Human Rat/pig |
[38] [35][38] |
5-HT3 | >10,000 | Rat | [39][40] |
5-HT4 | >10,000 | Rat | [40] |
5-HT6 | 398 | Mouse | [41] |
5-HT7 | 375–381 | Rat | [42][43] |
α1 | 1,000 | Rat | [35] |
α2 | 6,000 | Rat | [44] |
α2A | 7.3 (1-PP) | Human | [35] |
β | 8,800 | Rat | [35] |
D1 | 33,000 | Rat | [35] |
D2 | 484 240 |
Human Rat |
[45] [35] |
D3 | 98 | Human | [45] |
D4 | 29 | Human | [45] |
mACh | 38,000 | Rat | [35] |
GABAA (BDZ) |
>100,000 | Rat | [35] |
Values are Ki (nM). The smaller the value, the more strongly the drug binds to the site. |
Buspirone acts as an agonist of the serotonin 5-HT1A receptor with high affinity.[2][35] It is a partial agonist of both presynaptic 5-HT1A receptors, which are inhibitory autoreceptors, and postsynaptic 5-HT1A receptors.[2] It is thought that the main effects of buspirone are mediated via its interaction with the presynaptic 5-HT1A receptor, thus reducing the firing of serotonin-producing neurons.[2] Buspirone also has lower affinities for the serotonin 5-HT2A, 5-HT2B, 5-HT2C, 5-HT6, and 5-HT7 receptors.[33]
In addition to binding to serotonin receptors, buspirone is an antagonist of the dopamine D2 receptor with weak affinity.[2][35] It preferentially blocks inhibitory presynaptic D2 autoreceptors, and antagonizes postsynaptic D2 receptors only at higher doses.[2] 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.[2] Buspirone has also been found to bind with much higher affinity to the dopamine D3 and D4 receptors, where it is similarly an antagonist.[45]
A 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.[44][46][47] This metabolite may be responsible for the increased noradrenergic and dopaminergic activity observed with buspirone in animals.[46][48] In addition, 1-PP may play an important role in the antidepressant effects of buspirone.[48] Buspirone also has very weak and probably clinically unimportant affinity for the α1-adrenergic receptor.[35][49] However, buspirone has been reported to have shown “significant and selective intrinsic efficacy” at the α1-adrenergic receptor expressed in a “tissue- and species-dependent manner”.[49]
Unlike benzodiazepines, buspirone does not interact with the GABAA receptor complex.[2][50]
Pharmacokinetics
Buspirone has a low oral bioavailability of 3.9% relative to intravenous injection due to extensive first-pass metabolism.[2] The time to peak plasma levels following ingestion is 0.9 to 1.5 hours.[2] It is reported to have an elimination half-life of 2.8 hours,[2] 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.[4] Buspirone is metabolized primarily by CYP3A4, and prominent drug interactions with inhibitors and inducers of this enzyme have been observed.[7][8] Major metabolites of buspirone include 5-hydroxybuspirone, 6-hydroxybuspirone, 8-hydroxybuspirone, and 1-PP.[4][5][6] 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.[5] 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.[5] As such, it is likely to play an important role in the therapeutic effects of buspirone.[5] 1-PP has also been found to circulate at higher levels than those of buspirone itself and may similarly play a significant role in the clinical effects of buspirone.[46][48]
History
Buspirone was first synthesized, by a team at Mead Johnson, in 1968,[21] but was not patented until 1975.[54][55] It was initially developed as an antipsychotic drug acting on the D2 receptor, but was found to be ineffective in the treatment of psychosis; it was then used as an anxiolytic instead.[2] In 1986, Bristol-Myers Squibb gained FDA approval for buspirone in the treatment of GAD.[21][56] The patent placed on buspirone expired in 2001 and it is now available as a generic drug.
Society and culture
Generic names
Buspirone is the INN, BAN, DCF, and DCIT of buspirone, while buspirone hydrochloride is its USAN, BANM, and JAN.[1][57][58][59]
Brand name
Buspirone was primarily sold under the brand name Buspar.[57][59] Buspar is currently listed as discontinued by the US Federal Drug Administration.[60] In 2010, in response to a citizen petition, the US FDA determined that Buspar was not withdrawn for sale because of reasons of safety or effectiveness.[61]
2019 shortage
Due to interrupted production at a Mylan Pharmaceuticals plant in Morgantown, West Virginia, the United States experienced a shortage of buspirone in 2019.[62]
Research
Some tentative research supports other uses such as the treatment of depression and behavioral problems following brain damage.[2]
Chemistry
Buspirone is a member of the azapirone chemical class, and consists of azaspirodecanedione and pyrimidinylpiperazine components linked together by a butyl chain.
Analogues
Structural analogues of buspirone include other azapirones like gepirone, ipsapirone, perospirone, and tandospirone.[53]
Synthesis
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).
PAPERS
- Koziol, Anna E.; Acta Crystallographica, Section E: Structure Reports Online 2006, V62(12), Po5616-o5618
- Mou, Jie; Organic Preparations and Procedures International 2008, V40(4), P391-394
- Kairisalo, Pekka Juhani; FI 72975 B 1987
- Journal of medicinal chemistry (1983), 26(2), 194-203
- Journal of medicinal chemistry (1986), 29(8), 1476-82.
- Medicinal research reviews (1990), 10(3), 283-326.
- Heterocycles (1993), 36(7), 1463-9
- Journal of medicinal chemistry (1996), 39(5), 1125-9.
- Journal of medicinal chemistry (1996), 39(16), 3195-202.
- Nature Catalysis, 3(10), 843-850; 2020
PAPER
https://pubs.rsc.org/en/content/articlelanding/2019/GC/C8GC03328E#!divAbstract
- Green Chemistry, 21(1), 59-63; 2019
Abstract
A continuous flow method for the direct conversion of alcohols to amines via a hydrogen borrowing approach is reported. The method utilises a low loading (0.5%) of a commercial catalyst system ([Ru(p-cymene)Cl2]2 and DPEPhos), reagent grade solvent and is selective for primary alcohols. Successful methylation of amines using methanol and the direct dimethylamination of alcohols using commercial dimethylamine solution are reported. The synthesis of two pharmaceutical agents Piribedil (5) and Buspirone (25) were accomplished in good yields employing these new methods.
PAPER
Organic Preparations and Procedures International, 40(4), 391-394; 2008
https://www.tandfonline.com/doi/abs/10.1080/00304940809458099
PATENTS
US 3907801
ES 526304
EP 395192
EP 565274
EP 634411
EP 680961
US 5521313
Indian Pat. Appl., 2011MU01860,
PATENTS
WO 2014152737
https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2014152737
Syn
J Med Chem 1972,15(5),477-479
DE 2057845; FR 2073406; GB 1332194; US 3717634
The condensation of 1-(2-pyrimidinyl)piperazine (I) with 3-chloro-1-cyanopropane (II) by means of Na2CO3 in n-butanol gives 4-(2-pyrimidinyl)-1-(3-cyanopropyl)piperazine (III). This product is reduced with LiAlH4 or with H2 and Raney-Ni yielding 4-(2-pyrimidinyl)-1-(4-aminobutyl)piperazine (IV), which is finally condensed with 8-oxaspiro[4.5]decane-7,9-dione-(3,3-tetramethylene-glutaric anhydride) (V) in pyridine.
CLIP
Anxiolytics (Tranquilizers)
R.S. Vardanyan, V.J. Hruby, in Synthesis of Essential Drugs, 2006
Buspirone
Buspirone, 8-[4-[4-(2-pyrimidyl)-1-piperazinyl]butyl]-8-azaspiro [4,5] decan-7,9-dione (5.2.6), is synthesized by the reaction of 1-(2-pyrimidyl)-4-(4-aminobutyl)piperazine (5.2.4) with 8-oxaspiro[4,5]decan-7,9-dione (5.2.5). In turn, 1-(2-pyrimidyl)-4-(4-aminobutyl)piperazine (5.2.4) is synthesized by the reaction of 1-(2-pyrimidyl)piperazine with 4-chlorobutyronitrile, giving 4-(2-pyrimidyl)-1-(3-cyanopropyl)piperazine (5.2.3), which is hydrogenated with Raney nickel into buspirone (5.2.4) [51–55].
Buspirone is an extremely specific drug that could possibly represent a new chemical class of anxiolytics—azaspirones. As an anxiolytic, its activity is equal to that of benzodiazepines; however, it is devoid of anticonvulsant and muscle relaxant properties, which are characteristic of benzodiazepines. It does not cause dependence or addiction. The mechanism of its action is not conclusively known. It does not act on the GABA receptors, which occurs in benzodiazepine use; however, it has a high affinity for seratonin (5-HT) receptors and a moderate affinity for dopamine (D2) receptors. Buspirone is effective as an anxiolytic. A few side effects of buspirone include dizziness, drowsiness, headaches, nervousness, fatigue, and weakness. This drug is intended for treatment of conditions of anxiety in which stress, muscle pain, rapid heart rate, dizziness, fear, etc. are observed; in other words, conditions of anxiety not associated with somewhat common, usual, and everyday stress. Synonyms for buspirone are anizal, axoren, buspar, buspimen, buspinol, narol, travin, and others.
CLIP
Applications of Biocatalysis for Pharmaceuticals and Chemicals
Ramesh N. Patel, in Organic Synthesis Using Biocatalysis, 2016
5.2 Enzymatic Preparation of 6-Hydroxybuspirone
Buspirone (Buspar®, 59, Figure 11.17) is a drug used for the treatment of anxiety and depression, thought to produce its effects by binding to the serotonin 5HT1A receptor [114–116]. Mainly as a result of hydroxylation reactions, it is extensively converted to various metabolites and blood concentrations return to low levels a few hours after dosing [117]. A major metabolite, 6-hydroxybuspirone, produced by the action of liver cytochrome P450 CYP3A4, was present at much higher concentrations in human blood than buspirone itself. For development of 6-hydroxybuspirone as a potential antianxiety drug, preparation and testing of the two enantiomers as well as the racemate was of interest. An enantioselective microbial reduction process was developed for the reduction of 6-oxobuspirone 60 to (R)-6-hydroxybuspirone 61a or (S)-6-hydroxybuspitone 61b. About 150 microbial cultures were screened for the enantioselective reduction of 60. Rhizopus stolonifer SC 13898, Neurospora crassa SC 13816, Mucor racemosus SC 16198, and Pseudomonas putida SC 13817 gave >50% reaction yields and >95% ee of (S)-6-hydroxybuspirone 61a. The yeast strains Hansenula polymorpha SC 13845 and Candida maltosa SC 16112 gave (R)-6-hydroxybuspirone in >60% reaction yield and >97% ee [118]. The NADPH-dependent (R)-reductase (RHBR) from H. polymorpha SC 13845 was purified to homogeneity, its N-terminal and internal amino acid sequences were determined and the corresponding gene was cloned and expressed in E. coli. To regenerate the NADPH required for reduction, glucose-6-phosphate dehydrogenase gene from Saccharomyces cerevisiae was cloned and coexpressed in the same E. coli strain. Recombinant cultures coexpressing (R)-reductase (RHBR) and glucose 6-phosphate dehydrogenase catalyzed the reduction of 6-ketobuspirone to (R)-6-hydroxybuspirone 61a in 99% yield and 99.9% ee at 50 g/L substrate input [119].
The NADH-dependent (S)-reductase (SHBR) from P. putida SC 16269 was also purified to homogeneity, its N-terminal and internal amino acid sequences were determined and the corresponding gene was cloned and expressed in E. coli. To regenerate the NADH required for reduction, the NAD+ dependent formate dehydrogenase gene from Pichia pastoris was also cloned and co-expressed in the same E. coli strain. Recombinant E. coli coexpressing (S)-reductase and formate dehydrogenase was used to catalyze the reduction of 6-ketobuspirone to (S)-6-hydroxybuspirone 61b, in >98% yield and >99.8% ee at 50 g/L substrate input [119].
PATENT
https://patents.google.com/patent/US6686361
The present invention relates to methods of treating anxiety and depression using R-6-hydroxy-buspirone and pharmaceutical compositions containing R-6-hydroxy-buspirone.
Buspirone, chemically: 8-[4-[4-(2-pyrimidinyl)1-piperazinyl]butyl-8-azaspiro(4,5)-decane-7,9-dione, is approved for the treatment of anxiety disorders and depression by the United States Food and Drug Administration. It is available under the trade name BUSPAR® from Bristol-Myers Squibb Company.
Studies have shown that buspirone is extensively metabolized in the body. (See, for example, Mayol, et al., Clin. Pharmacol. Ther., 37, p. 210, 1985). One of the metabolites is 6-hydroxy-8-[4-[4-(2-pyrimidinyl)1-piperazinyl]butyl-8-azaspiro(4,5)-decane-7,9-dione having Formula I. This metabolite is also known as BMS 28674, BMS 442608, or
as 6-hydroxy-buspirone. This compound is believed to be the active metabolite of buspirone and its use in treating anxiety disorders and depression is disclosed in U.S. Pat. No. 6,150,365. The specific stereochemistry of 6-hydroxy-buspirone has not been described previously. Neither racemic 6-hydroxy-buspirone nor its enantiomers are commercially available at the present time.
Preclinical studies demonstrate that 6-hydroxy-buspirone, like buspirone, demonstrates a strong affinity for the human 5-HT1A receptor. In functional testing, 6-hydroxy-buspirone produced a dose-dependent anxiolytic response in the rat pup ultrasonic vocalization test, a sensitive method for assessment of anxiolytic and anxiogenic effects (Winslow and Insel, 1991, Psychopharmacology, 105:513-520).
Clinical studies in volunteers orally dosed with buspirone demonstrate that 6-hydroxy-buspirone blood plasma levels were not only 30 to 40 times higher but were sustained compared to buspirone blood plasma levels. The time course of 6-hydroxy-buspirone blood plasma levels, unlike buspirone blood plasma levels, correlate more closely with the sustained anxiolytic effect seen following once or twice a day oral dosing with buspirone.
Although buspirone is an effective treatment for anxiety disorders and depression symptomatology in a significant number of patients treated, about a third of patients get little to no relief from their anxiety and responders often require a week or more of buspirone treatment before experiencing relief from their anxiety symptomatology. Further, certain adverse effects are reported across the patient population. The most commonly observed adverse effects associated with the use of buspirone include dizziness, nausea, headache, nervousness, lightheadedness, and excitement. Also, since buspirone can bind to central dopamine receptors, concern has been raised about its potential to cause unwanted changes in dopamine-mediated neurological functions and a syndrome of restlessness, appearing shortly after initiation of oral buspirone treatment, has been reported in small numbers of patients. While buspirone lacks the prominent sedative effects seen in more typical anxiolytics such as the benzodiazepines, patients are nonetheless advised against operating potentially dangerous machinery until they experience how they are affected by buspirone.
It can be seen that it is desirable to find a medicament with buspirone’s advantages but which demonstrates more robust anxiolytic potency with a lack of the above described adverse effects.
Formation of 6-hydroxy-buspirone occurs in the liver by action of enzymes of the P450 system, specifically CYP3A4. Many substances such as grapefruit juice and certain other drugs; e.g. erythromycin, ketoconazole, cimetidine, etc., are inhibitors of the CYP3A4 isozyme and may interfere with the formation of this active metabolite from buspirone. For this reason it would be desirable to find a compound with the advantages of buspirone but without the drug—drug interactions when coadministered with agents affecting the activity level of the CYP3A4 isozyme.
EXAMPLE 3One-Step Synthesis of 6-Hydroxy-buspirone (I)
Buspirone (19.3 g, 50 mmole) was dissolved in dry THF (400 mL) and the resulting solution was cooled to −78° C. A solution of KN(SiMe3)2 in toluene (100 mL, 1 M) was added slowly. After the reaction mixture was stirred at −78° C. for 1 h, a solution of 2-(phenylsulfonyl)-3-phenyloxaziridine (Davis reagent, prepared according to literature method: F. A. Davis, et al., Org. Synth., 1988, 66, 203) (17.0 g, 65 mmole) in dry THF (150 mL, precooled to −78° C.) was added quickly via a cannular. After stirred for 30 mins at −78° C., the reaction was quenched with 1 N HCl solution (500 mL). It was extracted with EtOAc (3×500 mL). The aqueous layer was separated, neutralized with saturated sodium bicarbonate solution, and extracted with EtOAc (3×500 mL). The combined organic extracts were dried over Na2SO4, filtered, and concentrated under reduced pressure to give a white solid residue which was subjected to column chromatography using CH2Cl2/MeOH/NH4OH (200:10:1) as the eluent to give pure 6-hydroxy-buspirone (I, 7.2 g) and a mixture of buspirone and 6-hydroxy-buspirone (I). The mixture was purified by above column chromatography to afford another 3.3 g of pure 6-hydroxy-buspirone (I).
1H NMR (CDCl3) δ8.30 (d, J=4.7 Hz, 2H), 6.48 (t, J=4.7 Hz, 1H), 4.20 (s, 1H), 3.83-3.72 (m, 5H), 3.55 (s, 1H), 2.80 (d, J=17.5 Hz, 1H), 2.55-2.40 (m, 7H), 2.09-2.03 (m, 1H), 1.76-1.54 (m, 10 H), 1.41-1.36 (m, 1H), 1.23-1.20 (m, 1H).
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External links
- Media related to Buspirone at Wikimedia Commons
- “Buspirone”. Drug Information Portal. U.S. National Library of Medicine.
Clinical data | |
---|---|
Pronunciation | /ˈbjuːspɪroʊn/ (BEW-spi-rohn) |
Trade names | Buspar, Namanspin |
Other names | MJ 9022-1[1] |
AHFS/Drugs.com | Monograph |
MedlinePlus | a688005 |
Pregnancy category |
|
Routes of administration |
By mouth |
ATC code | |
Legal status | |
Legal status | |
Pharmacokinetic data | |
Bioavailability | 3.9%[2] |
Protein binding | 86–95%[3] |
Metabolism | Liver (via CYP3A4)[7][8] |
Metabolites | 5-OH-Buspirone; 6-OH-Buspirone; 8-OH-Buspirone; 1-PP[4][5][6] |
Elimination half-life | 2.5 hours[7] |
Excretion | Urine: 29–63%[3] Feces: 18–38%[3] |
Identifiers | |
CAS Number |
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PubChem CID | |
IUPHAR/BPS | |
DrugBank | |
ChemSpider | |
UNII | |
KEGG | |
ChEBI | |
ChEMBL | |
CompTox Dashboard (EPA) | |
ECHA InfoCard | 100.048.232 |
Chemical and physical data | |
Formula | C21H31N5O2 |
Molar mass | 385.512 g·mol−1 |
3D model (JSmol) | |
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#Buspirone, #буспирон , #بوسبيرون , #丁螺酮 , #Anxiolytic, #Arylpiperazines, #Serotonin Receptor Agonist, #Ansial, #Vita, #Ansiced, #Abello, #Axoren, #Glaxo Wellcome, #Bespar, #BMS, #Buspar, #Buspimen, Menarini, Buspinol, Zdravlje, Buspisal, Lesvi, Narol, Almirall,