World Library  
Flag as Inappropriate
Email this Article


Systematic (IUPAC) name
(±)-4-amino-3-phenyl-butyric acid
Clinical data
Trade names Noofen
Legal status
  • US: Not FDA approved
Routes of
Pharmacokinetic data
Bioavailability 64–65%[1][2]
Biological half-life 5.3 hours[1]
CAS Registry Number  N
ATC code N06
PubChem CID:
ChemSpider  Y
Synonyms Fenibut, Fenigam, Phenigam, Phenybut, Phenygam, Phenylgamma, PHG, PhGABA[3]
Chemical data
Formula C10H13NO2
Molecular mass 179.216 g/mol
Physical data
Melting point 253 °C (487 °F)

Phenibut (or, alternatively, fenibut, phenybut) (brand name Noofen, Citrocard), contracted from β-phenyl-γ-aminobutyric acid (β-phenyl-GABA), is a central depressant and derivative of the naturally occurring inhibitory neurotransmitter γ-aminobutyric acid (GABA). The addition of a phenyl ring allows phenibut to cross the blood–brain barrier.[1] Phenibut was developed in the Soviet Union in the 1960s, and has since been used there as a pharmaceutical drug to treat a wide range of ailments, including posttraumatic stress disorder, anxiety, depression, asthenia, insomnia, alcoholism, stuttering, and vestibular disorders, among other conditions.[4][5][1] In the rest of the world, phenibut is not approved for clinical use, and is instead sold as a nutritional supplement.[6] It has been reported by some researchers to possess nootropic actions for its ability to improve neurological functions,[4] but others have not observed these effects.[7] It is generally accepted that phenibut has anxiolytic effects in both animal models and in humans.[1]

Phenibut is a close structural analogue of GABA, as well as of baclofen (β-(4-chlorophenyl)-GABA), pregabalin (β-isobutyl-GABA), and GABOB (β-hydroxy-GABA).[8] Originally thought to act as a selective GABAB receptor agonist, phenibut has since been found to act preferentially as a blocker of α2δ subunit-containing voltage-gated calcium channels, similarly to gabapentin and pregabalin.[9] As such, phenibut is a gabapentinoid.[10][11]


  • History 1
  • Chemistry 2
    • Physical properties 2.1
  • Pharmacology 3
  • Dosage 4
  • Adverse reactions 5
    • Side effects 5.1
    • Overdose effects 5.2
    • Withdrawal effects 5.3
    • Interactions 5.4
  • See also 6
  • References 7
  • External links 8


Phenibut was synthesized at the A. I. Herzen Leningrad Pedagogical Institute (USSR) by Professor Vsevolod Perekalin's team and tested at the Institute of Experimental Medicine, USSR Academy of Medical Sciences.

Phenibut is mandated standard equipment in a Russian cosmonaut's medical kit. The use of "conventional" tranquilizers for stress and anxiety makes patients drowsy, which was deemed unacceptable for cosmonauts; phenibut, however, lowers stress levels without adversely affecting performance. In 1975 phenibut was included in the cosmonauts' kit for those who participated in the Apollo-Soyuz joint mission.[12]


In terms of chemical structure, phenibut is a derivative of GABA with a phenyl group in the β-position. It is a chiral molecule and thus has two potential configurations, an (R)- and (S)-enantiomer.[13] It has almost the same structure of baclofen (lacking only a chlorine atom in the para-position of the phenyl group)[4] and contains phenethylamine in its structure.[1] Pregabalin has the same structure as phenibut except that the phenyl group is instead an isobutyl group.

Physical properties

Phenibut hydrochloride is a white crystalline powder and the taste is very sour. It is readily soluble in water and in alcohol, and the pH of a 2.5% water solution is about 2.3–2.7.


Phenibut acts as an agonist of the GABAB receptor (specifically, a full agonist),[14] similarly to baclofen and γ-hydroxybutyric acid (GHB),[13] and at higher doses also of the GABAA receptor.[4][15] It has some 30- to 68-fold lower affinity for the GABAB receptor relative to baclofen, which is active at far lower doses in comparison.[14]

There is dispute in the literature about whether or not phenibut binds to the GABAA receptor, which is the receptor responsible for the actions of the benzodiazepines, barbiturates, and Z-drugs, and for the main effects of ethanol. According to Allikmets and Ryage (1983) and Shulgina (1986), phenibut does bind to the GABAA receptor,[4] but according to Lapin (2001), it does not.[1] In the case of the former, it is argued that the GABAA binding only occurs at higher concentrations.[4]

The literature that supports the nootropic effects of phenibut also suggest that it elicits tranquilizing effects,[1] reduction of stress and anxiety, improvement of impaired sleep, and the potentiation (enhancement) of the effects of tranquilizers, narcotics, and neuroleptics. It is also suggested to have an anticonvulsant effect,[4] though studies on other GABAB agonists, such as GHB and the phenibut analogue baclofen, have shown them to act as potential convulsants. It should be noted, however, that GHB acts on the convulsion-inducing GHB receptor,[16] which phenibut does not.

Recently, it has been found that phenibut binds to and blocks α2δ subunit-containing voltage-gated calcium channels (VGCCs), similarly to gabapentin and pregabalin.[9] Both enantiomers of phenibut show this action with similar efficacy.[9] Moreover, the R-enantiomer possesses five-fold greater affinity for this site relative to the GABAB receptor, while the S-enantiomer does not bind to the GABAB receptor.[9] As such, phenibut is likely to have much greater effect on α2δ subunit-containing VGCCs than on the GABAB receptor.[9] Notably, the antinociceptive effects of phenibut in rodents are mediated not by the GABAB receptor but by blockade of α2δ subunit-containing VGCCs.[9]

Phenibut has been found to reduce immobility time in the forced swim test, a measure of possible antidepressant activity, which was blocked by a GABAB receptor antagonist.[14]

Phenibut has been found to increase dopamine levels in the striatum.[1] It was suggested that phenibut may activate dopaminergic processes and that this may be involved in its effects.[1]

Anecdotal evidence indicates that phenibut can produce euphoria.[5] Recreational use of the drug has been reported.[17]


For medical use, phenibut is generally prescribed at a dosage of 250–1500 mg twice a day.[5]

Adverse reactions

Side effects

The side effects of phenibut are said to be similar to but milder than those of baclofen.[5] They include sleepiness and hangover-like effects such as headache and depression once the drug has worn off.[5]

Overdose effects

Symptoms of overdose (over 40 mg/kg) include lowered body temperature, muscle relaxation, and sleepiness.[5]

Withdrawal effects

Limited evidence indicates that withdrawal symptoms of phenibut include severe anxiety, nervousness, tremors, agitation, dizziness, irritation, fatigue, loss of appetite, rapid heartbeat, nausea, vomiting, tension, psychosis, hallucinations, and insomnia.[5] These effects may last for up to two weeks.[5] Tolerance may develop rapidly with repeated use.[5]


Phenibut should not be combined with alcohol, sedatives, monoamine oxidase inhibitors, anticonvulsants like carbamazepine, or other prescription drugs.[5] Persons on such medications should consult with their medical practitioners prior to taking phenibut. Evidence suggests that phenibut can modulate the function of some epilepsy medications.[4]

See also


  1. ^ a b c d e f g h i j Lapin, I. (2001). "Phenibut (beta-phenyl-GABA): A tranquilizer and nootropic drug" (pdf). CNS Drug Reviews 7 (4): 471–481.  
  2. ^ Smirnova LA, Perfilova VN, Tyurenkov IN, Ryabukha AF, Suchkov EA, Lebedeva SA (2013). "Study of the absolute bioavailability of citrocard, a new GABA derivative". Bull. Exp. Biol. Med. 155 (4): 458–60.  
  3. ^ J. Elks (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 69–.  
  4. ^ a b c d e f g h Shulgina, G. I. (1986). "On neurotransmitter mechanisms of reinforcement and internal inhibition". The Pavlovian journal of biological science 21 (4): 129–140.  
  5. ^ a b c d e f g h i j David W. Group (25 February 2015). Encyclopedia of Mind Enhancing Foods, Drugs and Nutritional Substances, 2d ed. McFarland. pp. 186–.  
  6. ^ Nelson, LS (2008). "'"Phenibut Withdrawal - A Novel 'Nutritional Supplement. Clinical Toxicology 46 (7): 605.  
  7. ^ Kovaleva, E. L. (1984). "Comparative characteristics of the nootropic action of fenibut and fepiron". Farmakologiia i toksikologiia 47 (1): 20–23.  
  8. ^ Lapin I (2001). "Phenibut (beta-phenyl-GABA): a tranquilizer and nootropic drug". CNS Drug Rev 7 (4): 471–81.  
  9. ^ a b c d e f Zvejniece, Liga; Vavers, Edijs; Svalbe, Baiba; Veinberg, Grigory; Rizhanova, Kristina; Liepins, Vilnis; Kalvinsh, Ivars; Dambrova, Maija (2015). "R-phenibut binds to the α2–δ subunit of voltage-dependent calcium channels and exerts gabapentin-like anti-nociceptive effects". Pharmacology Biochemistry and Behavior 137: 23–29.  
  10. ^ Elaine Wyllie; Gregory D. Cascino; Barry E. Gidal; Howard P. Goodkin (17 February 2012). Wyllie's Treatment of Epilepsy: Principles and Practice. Lippincott Williams & Wilkins. p. 423.  
  11. ^ Honorio Benzon; James P. Rathmell; Christopher L. Wu; Dennis C. Turk; Charles E. Argoff; Robert W Hurley (11 September 2013). Practical Management of Pain. Elsevier Health Sciences. p. 1006.  
  12. ^ Slava Lapin (30 July 2009). From the Inside. Luniver Press. p. 209.  
  13. ^ a b Dambrova, M.; Zvejniece, L.; Liepinsh, E.; Cirule, H.; Zharkova, O.; Veinberg, G.; Kalvinsh, I. (2008). "Comparative pharmacological activity of optical isomers of phenibut". European Journal of Pharmacology 583 (1): 128–134.  
  14. ^ a b c GABAb Receptor Pharmacology: A Tribute to Norman Bowery: A Tribute to Norman Bowery. Academic Press. 21 September 2010. pp. 25–.  
  15. ^ Zyablitseva, Evgeniya A.; Kositsyn, Nikolay S.; Shul'gina, Galina I. (2013). "The Effects of Agonists of Ionotropic GABAA and Metabotropic GABAB Receptors on Learning". The Spanish journal of psychology 12 (01): 12–20.  
  16. ^ Banerjee, P. K.; Snead Oc, 3. (1995). "Presynaptic gamma-hydroxybutyric acid (GHB) and gamma-aminobutyric acidB (GABAB) receptor-mediated release of GABA and glutamate (GLU) in rat thalamic ventrobasal nucleus (VB): A possible mechanism for the generation of absence-like seizures induced by GHB". The Journal of Pharmacology and Experimental Therapeutics 273 (3): 1534–1543.  
  17. ^ Wong A, Little M, Caldicott D, Easton C, Andres D, Greene SL (2015). "Analytically confirmed recreational use of Phenibut (β-phenyl-γ-aminobutyric acid) bought over the internet". Clin Toxicol (Phila) 53 (7): 783–4.  

External links

  • 4-Amino-3-phenylbutyric acid in the ChemIDplus database

This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.

Copyright © World Library Foundation. All rights reserved. eBooks from World eBook Library are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.