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Death 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
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.

Threshold 0.25 - 0.5 g
Light 0.5 - 1 g
Common 1 - 2 g
Strong 2 - 3.5 g
Heavy 3.5 g +
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.

β-Phenyl-γ-aminobutyric acid (also known as Fenibut, Phenybut, Noofen, Citrocard, and commonly as Phenibut) is a depressant substance of the gabapentinoid class[2][3] that produces anxiety suppressing, sedating, relaxing, and euphoric effects when administered.

Phenibut is a closely related in structure to gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the brain. The addition of a phenyl ring to the GABA molecule allows it to cross the blood-brain barrier and produce psychoactive effects.[4] It is structurally related to baclofen, pregabalin, and gabapentin.[4]

Phenibut was developed in the Soviet Union in the 1960s, where it has been used 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.

Although it is commonly marketed as a nootropic by retailers, evidence that it enhances cognition is limited. It is generally accepted that phenibut has anxiolytic effects in both animal and in humans.[4] Due to its habit-forming properties, it is highly advised to use harm reduction practices if using this substance.


Phenibut is a derivative of GABA with a phenyl group in the β-position. It has a near identical structure as baclofen, lacking only a chlorine atom in the para-position of the phenyl group[7] and contains phenethylamine in its structure.[8] Pregabalin also has a near identical structure as phenibut, except it has an isobutyl group instead of a phenyl group.

Phenibut is a chiral molecule and thus has two potential configurations, as (R)- and (S)-enantiomers.[9]

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).


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 gains additional activity as a GABAA agonist.[11] 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, which may be due to its structural similarity to phenethylamine which stimulates dopamine release. It is not known how this contributes to its effects. Phenibut has been found to reduce the effects of dextro-amphetamine in mice.[4]

Subjective effects

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

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects

Visual effects

Cognitive effects

After effects
Aftereffects (3).svg

Experience reports

There are currently 0 experience reports which describe the effects of this compound in 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 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.[citation needed]

Due to the extremely long come up period relative to other substances, some users may experience an urge to redose out of the belief that it is weak or not working. This should be avoided to prevent overdose.

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 all GABAgenic depressants, meaning that after its consumption, most depressants will have a reduced effect.

Dangerous interactions

Although many psychoactive substances 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.

Legal status


This legality section is a stub.

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

  • Australia: Phenibut is a schedule 9 substance in Australia as of February 1st 2018, meaning it is illegal to possess, import, supply or manufacture.[citation needed]
  • 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".[14]
  • United States: Phenibut is uncontrolled, meaning it is legal to possess without any sort of license or prescription.[15]

See also

External links


  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. |
  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. |
  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 |
  5. Shulgina, G. I. (1986). "On neurotransmitter mechanisms of reinforcement and internal inhibition". The Pavlovian journal of biological science ( / NCBI) |
  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–. |
  7. Shulgina, G. I. (1986). On neurotransmitter mechanisms of reinforcement and internal inhibition. Integrative Physiological and Behavioral Science, 21(4), 129-140.
  9. 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.
  10. GABAb Receptor Pharmacology: A Tribute to Norman Bowery: A Tribute to Norman Bowery. Academic Press. |
  11. Zyablitseva, E. A.; Pavlova, I. V. (2010). "Effects of the GABA Receptor Agonist Phenibut on Spike Activity and Interactions between Neocortex and Hippocampus Neurons in Emotionally Negative Situations". Neuroscience and Behavioral Physiology. 40 (9): 1003–1011. doi:10.1007/s11055-010-9360-y. ISSN 0097-0549. 
  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 ( / NCBI) |
  13. Koski, A., Ojanperä, I., & Vuori, E. (2002). Alcohol and benzodiazepines in fatal poisonings. Alcoholism: Clinical and Experimental Research, 26(7), 956-959.
  14. Psychoactive Substances Act 2016 ( |
  15. Phenibut Legal Status by Erowid |