|Common names||Phenibut, Fenibut, Phenybut, PhGABA|
|Substitutive name||β-Phenyl-γ-aminobutyric acid|
|Systematic name||(RS)-4-Amino-3-phenyl-butyric acid|
β-phenyl-γ-aminobutyric acid (also known as fenibut, phenybut, noofen, citrocard, and commonly as phenibut) is a depressant substance of the gabapentinoid class.
phenibut acts as a receptor agonist for gaba, the major inhibitory neurotransmitter in the brain.
it is chemically related to baclofen, pregabalin, and gabapentin.
phenibut was developed in the soviet union in the 1960s, where it has been used as a pharmaceutical drug to treat a wide variety of conditions, including post-traumatic stress disorder, anxiety, depression, asthenia, insomnia, alcoholism, stuttering, and vestibular disorders, and others. in the rest of the world, phenibut is not approved for clinical use and is instead sold as a nutritional supplement.
subjective effects include anxiety suppression, sedation, muscle relaxation, enhanced motivation, and euphoria. lower doses (under 1 gram) are typically used as a cognitive and lifestyle supplement while higher doses are used for a recreational high that is reported to be subjectively similar to ghb, alcohol, and certain benzodiazepines.
although phenibut 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. 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. the addition of a phenyl ring to the gaba molecule allows it to cross the blood-brain barrier and produce psychoactive effects. phenibut has a near identical structure as baclofen, lacking only a chlorine atom in the para-position of the phenyl group and contains phenethylamine in its structure. 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.
most commercial phenibut is reported to be 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 has a more complex pharmacological profile than many other depressants.
unlike benzodiazepines, for example, phenibut acts as a full agonist of the gabab receptor, similar to baclofen and high doses of ghb. at higher doses, phenibut loses its selectivity of gabab, and gains additional activity as a gabaa agonist.
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
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.
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.