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Fatal overdose may occur when gabapentinoids are combined with other depressants such as opiates, benzodiazepines, barbiturates, thienodiazepines, alcohol or other GABAergic substances.[1]

It is strongly discouraged to combine these substances, particularly in common to heavy doses.

Summary sheet: Phenibut
Phenibut
Chemical Nomenclature
Common names Phenibut, Fenibut, Phenybut, PhGABA
Substitutive name β-Phenyl-γ-aminobutyric acid
Systematic name (RS)-4-Amino-3-phenyl-butyric acid
Class Membership
Psychoactive class Depressant
Chemical class Gabapentinoid
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.



Oral
Dosage
Threshold 0.25 g
Light 0.5 - 1 g
Common 1 - 2 g
Strong 2 - 3.5 g
Heavy 3.5 g +
Duration
Total 10 - 16 hours
Onset 1.5 - 3 hours
Come up 1.5 - 3 hours
Peak 3 - 4 hours
Offset 4 - 6 hours
After effects 6 - 24 hours









DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Interactions


β-Phenyl-γ-aminobutyric acid (also known as Fenibut, Phenybut, Noofen, Citrocard, and most commonly as Phenibut) is a central nervous system (CNS) depressant of the gabapentinoid chemical class[2][3] that produces anxiolytic, disinhibiting, relaxing, and euphoriant effects when administered.

Phenibut is a closely related structural analog of the naturally occurring inhibitory neurotransmitter gamma-aminobutyric acid (GABA). The addition of a phenyl ring to GABA allows it to cross the blood-brain barrier and produce psychoactive effects, a notable difference from GABA when taken exogenously.[4] It is also structurally related to baclofen, pregabalin, and GABOB.[4]

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 post-traumatic stress disorder, anxiety, depression, asthenia, insomnia, alcoholism, stuttering, and vestibular disorders, and other conditions.[5][6][4]

In the rest of the world, phenibut is not approved for clinical use and is instead sold as a nutritional supplement. It has been reported by some researchers to possess nootropic actions for its ability to improve neurological functions,[5] but others have not observed these effects.[7] It is generally accepted that phenibut has anxiolytic effects in both animal models and in humans.[4]

Chemistry

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, as (R)- and (S)-enantiomers.[8] It has almost the same structure of baclofen (lacking only a chlorine atom in the para-position of the phenyl group)[9] and contains phenethylamine in its structure.[10] Pregabalin has the same structure as phenibut, except that the phenyl group is instead an isobutyl group.

Most commercial phenibut is in the form of the hydrochloride salt (HCl). In this form, the phenibut is reacted with hydrochloric acid to form a stable, easily dissolvable, acidic, crystalline salt.

Alternatively, phenibut can exist as a Free Amino Acid (FAA). In this form, phenibut is close to pH neutral, non-crystalline, slow to dissolve and mildly bitter. The FAA form has about 20% more phenibut molecules on an equal mass basis compared to phenibut HCl. Phenibut FAA has the advantage of being suitable for sublingual, rectal, or intranasal use, which can be more efficient, faster acting, and predictable for some. Phenibut FAA is converted to phenibut HCl in the stomach. Equal masses of the two forms will have roughly equivalent effects when taken the same way (FAA may be slightly stronger).

Pharmacology

Phenibut is substantially more complex in its pharmacological profile than most other depressants. Unlike most depressants such as benzodiazepines, phenibut acts as a full agonist of the GABAB receptor, similar to baclofen and high doses of GHB.[11] At higher doses, phenibut loses its selectivity of GABAB, and acts as a GABAA agonist as well.[5] Phenibut's effects at the GABAB receptor are responsible for its sedating effects.

Recent research has shown that phenibut binds to and blocks α2δ subunit-containing voltage-dependent calcium channels (VDCCs), similarly to gabapentinoids such as gabapentin and pregabalin.[12] Both enantiomers of phenibut show this action with similar efficacy. The R-enantiomer possesses five-fold greater affinity for α2δ subunit-containing voltage-gated calcium channels relative to the GABAB receptor, whereas the S-entantiomer does not have any efficacy at the GABAB receptor.[12] The analgesic effects of phenibut in rodents are not mediated by the GABAB receptor but by the blockage of α2δ subunit-containing voltage-gated calcium channels.[12]

Additionally, phenibut has been found to increase dopamine levels within the brain. It is not known how this contributes to its effects[4].

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.

In comparison to other commonly used GABAergic depressants such as alcohol or benzodiazepines, this compound is reported to be longer lasting, more euphoric and more recreational at higher doses.

Physical effects

Visual effects

Cognitive effects

After effects

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential

Phenibut likely has a low toxicity relative to dose. However, it is [[Toxicity::potentially lethal when mixed with depressants like alcohol, benzodiazepines or opioids]].

Phenibut hydrochloride is highly caustic and in many sensitive users can cause intestinal discomfort and diarrhea with some lower digestive tract bleeding. The digestive issues can present themselves within an hour of dosing, or not occur until the next morning. This compound should therefore be taken on an empty stomach as the ionization state of the compound dictates its absorption. After dosing there will be an acute rise in stomach acidity and high doses can cause acid reflux, vomiting, and nausea.

Due to the extremely long come up of phenibut in comparison to other drugs, some users may have an urge to redose as they believe it is not working. This should be avoided to prevent overdose of the drug.

It is strongly recommended that one use harm reduction practices when using this substance.

Tolerance and addiction potential

Phenibut is moderately physically and psychologically addictive, although this usually only occurs with heavy abuse of the substance.

Tolerance will develop to the sedative-hypnotic effects within a couple of days of continuous use. After cessation, the tolerance returns to baseline in 7 - 14 days. Withdrawal symptoms or rebound symptoms may occur after ceasing usage abruptly following a few weeks or longer of steady dosing and may necessitate a gradual dose reduction.

Withdrawal symptoms include severe anxiety, nervousness, hallucinations, tremors, agitation, dizziness, tension, irritation, rapid heartbeat, fatigue, loss of appetite, nausea, vomiting, psychosis, and insomnia.[6]

Phenibut presents cross-tolerance with [[Cross-tolerance::all GABAgenic depressants]], meaning that after its consumption, most depressants will have a reduced effect.

Dangerous interactions

Although many drugs are safe on their own, they can become dangerous and even life-threatening when combined with other substances. The list below contains some common potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses of each but still increase the potential risk of death. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

  • Depressants (1,4-Butanediol, 2M2B, alcohol,[13] benzodiazepines, barbiturates, GHB/GBL, methaqualone, opioids) - This combination can result in dangerous or even fatal levels of respiratory depression. These substances potentiate the muscle relaxation, sedation and amnesia caused by one another and can lead to unexpected loss of consciousness at high doses. There is also an increased risk of vomiting during unconsciousness and death from the resulting suffocation. If this occurs, users should attempt to fall asleep in the recovery position or have a friend move them into it.
  • Dissociatives - This combination can result in an increased risk of vomiting during unconsciousness and dying from the resulting suffocation. If a sudden loss of consciousness occurs, users should attempt to fall asleep in the recovery position or have a friend move them into it.
  • Stimulants - It is dangerous to combine phenibut with stimulants due to the risk of excessive intoxication. Stimulants mask the sedative effect of phenibut, which is the main factor most people consider when determining their level of intoxication. Once the stimulant wears off, the effects of phenibut will be significantly increased, leading to intensified disinhibition as well as other effects. If combined, one should strictly limit themselves to only dosing a certain amount of phenibut per hour. This combination can also potentially result in severe dehydration if hydration is not monitored.

This legality section is a stub.

As such, it may contain incomplete or wrong information. You can help by expanding it.

  • United States - Phenibut is uncontrolled, meaning it is legal to possess without any sort of license or prescription.[14]
  • United Kingdom - Phenibut is uncontrolled and is legal to possess. It may be illegal to produce, supply, or import this drug under the Psychoactive Substance Act 2016, which blanketly applies the aforementioned restrictions on all "psychoactive substances" with exemptions for alcohol, nicotine and "medicinal products".[15]

See also

References

  1. Risks of Combining Depressants - TripSit 
  2. 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. | https://books.google.co.uk/books?id=j9t6Qg0kkuUC&pg=RA1-PA423&redir_esc=y#v=onepage&q&f=false
  3. 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. | https://books.google.co.uk/books?id=kfcDAQAAQBAJ&pg=PA1006&redir_esc=y#v=onepage&q&f=false
  4. 4.0 4.1 4.2 4.3 4.4 Lapin, I. (2001). "Phenibut (beta-phenyl-GABA): A tranquilizer and nootropic drug" (pdf). CNS Drug Reviews | http://onlinelibrary.wiley.com/doi/10.1111/j.1527-3458.2001.tb00211.x/pdf
  5. 5.0 5.1 5.2 Shulgina, G. I. (1986). "On neurotransmitter mechanisms of reinforcement and internal inhibition". The Pavlovian journal of biological science (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/2431377
  6. 6.0 6.1 David W. Group (25 February 2015). Encyclopedia of Mind Enhancing Foods, Drugs and Nutritional Substances, 2d ed. McFarland. pp. 186–. | https://books.google.co.uk/books?id=ZYqoBgAAQBAJ&pg=PA186&hl=en#v=onepage&q&f=false
  7. Kovaleva, E. L. (1984). "Comparative characteristics of the nootropic action of fenibut and fepiron". Farmakologiia i toksikologiia (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/6705902
  8. 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.
  9. Shulgina, G. I. (1986). On neurotransmitter mechanisms of reinforcement and internal inhibition. Integrative Physiological and Behavioral Science, 21(4), 129-140.
  10. https://www.ncbi.nlm.nih.gov/pubmed/11830761
  11. GABAb Receptor Pharmacology: A Tribute to Norman Bowery: A Tribute to Norman Bowery. Academic Press. | https://books.google.co.uk/books?id=_iMDQOA2UIsC&pg=PA25&redir_esc=y#v=onepage&q&f=false
  12. 12.0 12.1 12.2 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 (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/18275958
  13. Koski, A., Ojanperä, I., & Vuori, E. (2002). Alcohol and benzodiazepines in fatal poisonings. Alcoholism: Clinical and Experimental Research, 26(7), 956-959.
  14. Phenibut Legal Status by Erowid | https://erowid.org/smarts/phenibut/phenibut_law.shtml
  15. Psychoactive Substances Act 2016 (Legislation.gov.uk) | http://www.legislation.gov.uk/ukpga/2016/2/contents/enacted