
F-Phenibut
F-Phenibut | |||||||||||||||||||||||||||||||||
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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 | |||||||||||||||||||||||||||||||||
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Interactions | |||||||||||||||||||||||||||||||||
Stimulants | |||||||||||||||||||||||||||||||||
Depressants | |||||||||||||||||||||||||||||||||
Dissociatives |
Summary sheet: Phenibut |
Phenibut (also known as fenibut, phenybut, Noofen, Citrocard, or β-phenyl-γ-aminobutyric acid) 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 Post-traumatic stress disorder, anxiety, depression, asthenia, insomnia, alcoholism, stuttering, and vestibular disorders, among other conditions.[2][3][1] 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,[2] but others have not observed these effects.[4] 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, pregabalin, and GABOB.[1] In terms of its pharmacology, this compound is classified as a gabapentinoid.[5][6]
Chemistry
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, as (R)- and (S)-enantiomers.[7] It has almost the same structure of baclofen (lacking only a chlorine atom in the para-position of the phenyl group)[8] and contains phenethylamine in its structure.[9] Pregabalin has the same structure as phenibut, except that the phenyl group is instead an isobutyl group.
Phenibut HCL, being highly acidic, needs an acidic environment to become unionised and absorbed. Eating will dramatically increase (decrease acidity) of stomach pH. Caffeine promotes gastric acid/H+ secretion into the gut. Thus, an empty stomach coupled with increased gut acidity will dramatically increase the oral absorption of phenibut HCL.
Most commercial phenibut is in the form of the hydrochloride salt (HCL). In this form, the gamma-Aminobutyric acid 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[10]. At higher doses, phenibut loses its selectivity of GABAB, and acts as a GABAA agonist as well[2]. 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-gated calcium channels, similarly to gabapentinoids such as gabapentin and pregabalin[11]. 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 doses not have any efficacy at the GABAB receptor[11] . 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[11].
Additionally, phenibut has been found to increase dopamine levels within the brain. It is not known how this contributes to its effects[1].
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 GABAgenic depressants such as alcohol or benzodiazepines, this compound is longer lasting, more euphoric and more recreational.
Physical effects
- Stimulation and Sedation - At lower doses, phenibut has a mild physical and mental stimulation effect, encouraging movement, wakefulness, and productivity. At higher doses, however, it becomes physically sedating, encouraging sleep and lethargy. Sleeping after dosing a small amount results in a deep, restful sleep which can leave the user feeling refreshed and alert upon waking.
- Respiratory depression
- Nausea - Phenibut can induce mild to extreme nausea depending greatly on dose and tolerance. It usually manifests roughly 5 hours after the initial dose and generally involves waves of nausea accompanied by excessive sweating and vomiting.
- Increased perspiration
- Motor control loss
- Stomach cramps
- Dizziness
- Dehydration - Dehydration is reported to occur from regular multi-day usage or overdoses.
- Headaches - Moderate to high doses can induce a mild headache many hours after dosing.
- Physical euphoria
- Muscle cramps - Muscle cramps and joint pain are sometimes accompanied at high doses.
- Difficulty urinating - This effect generally only occurs after frequent usage.
- Increased blood pressure
- Temperature regulation loss
- Appetite enhancement
Cognitive effects
- Empathy, love, and sociability enhancement - Unlike alcohol which merely increases sociability through disinhibition, phenibut presents strong entactogenic effects which, although much weaker than that of traditional entactogens such as MDMA, are still prominent and well-defined even at light doses.
- Disinhibition
- Information processing suppression - High doses will usually induce a state of mild stupor and confusion.
- Thought deceleration
- Cognitive euphoria
- Motivation enhancement
- Anxiety suppression
- Depression - A low mood can be experienced as an after-effect of high or frequent dosing.
- Amnesia
- Increased music appreciation
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 diarrhoea 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 drug.
Tolerance and addiction potential
Phenibut is moderately physically and psychologically addictive, although this usually only occurs with heavy abuse of the drug.
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.[3]
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, 2-methyl-2-butanol, alcohol, 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 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.
- Stimulants - It is dangerous to combine phenibut with stimulants due to the risk of excessive intoxication. Stimulants decrease 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.
Legal issues
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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.[12]
- 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".[13]
See also
External links
References
- ↑ 1.0 1.1 1.2 1.3 1.4 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
- ↑ 2.0 2.1 2.2 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
- ↑ 3.0 3.1 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
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ https://www.ncbi.nlm.nih.gov/pubmed/18275958
- ↑ https://www.ncbi.nlm.nih.gov/pubmed/2431377
- ↑ https://www.ncbi.nlm.nih.gov/pubmed/11830761
- ↑ 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
- ↑ 11.0 11.1 11.2 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
- ↑ Phenibut Legal Status by Erowid | https://erowid.org/smarts/phenibut/phenibut_law.shtml
- ↑ Psychoactive Substances Act 2016 (Legislation.gov.uk) | http://www.legislation.gov.uk/ukpga/2016/2/contents/enacted