Phenibut for anxiety
Phenibut for Social Anxiety
The Science of Phenibut

Let's take a look at how Phenibut works on a physiological level to better understand how it may be even more beneficial than a number of prescription medications for stress, anxiety and panic disorder.
Beta-phenyl-gamma-aminobutyric acid, better known as Phenibut, or less commonly called fenibut or phenybut, is a natural derivative of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). Phenibut is available in most countries without a prescription, while in Russia, which is where extensive scientific research has been performed on the compound, Phenibut is available as a neuropsychotropic drug capable of easily crossing the blood-brain barrier. Phenibut has been used in Russia for over 50 years to treat a wide range of neuro-medical complications, including anxiety and insomnia. It has also been used in the therapy of psychological disorders associated with anxiety, depression and post-traumatic stress. Phenibut is also classified as a nootropic (also called smart drugs or smart nutrients) for its ability to improve cognitive function and neurological functions.
The name Phenibut, along with many of the other names for the compound, comes directly from the various chemical names for the compound, beta-phenyl-gamma-aminobutyric acid, 3-phenyl-4-aminobutyric acid, and 4-amino-3-phenyl-butanoic acid. Structurally, phenibut is GABA with a phenyl group in the beta position. GABA is the key inhibitory neurotransmitter in the brain.
Phenibut is one of the most remarkable natural compounds available today and is a true nutraceutical (dietary supplement with therapeutic action). Phenibut exerts its mechanism of action as a very potent GABA agonist (GABA-mimetic), which results in a plethora of GABA-like effects at varying dosages, including as an anxiolytic (anti-anxiety), nootropic (cognition enhancing) and hypnotic (sleep-inducing) agent. Phenibut also stimulates dopamine receptors and antagonizes beta-phenylethylamine (PEA).
To understand how Phenibut exerts its diversity of beneficial effects first requires a basic understanding of GABA action, since Phenibut, primarily as a GABA agonist, significantly potentiates GABA activity at GABA receptors.
There are three types of GABA receptors: GABA-A, GABA-B, and GABA-C with numerous subtypes. Phenibut primarily acts at metabotropic GABA-B and to some extent ionotropic GABA-A receptors. Because Phenibut is a nonselective GABA-A and GABA-B receptor agonist it influences activity throughout GABA-A and GABA-B subtypes, including the six GABA-A alpha subtypes (units), which have a range of actions. For example, stimulation of GABA-A alpha subtype-1 produces a sedative effect. Stimulation of GABA-A alpha subtypes-2 and 3 produces an anxiolytic, muscle-relaxing, and alcohol-potentiating effect. While stimulation of GABA-A alpha subtype-5 produces a cognitive-enhancing (nootropic) effect. Benzodiazepine anxiolytic drugs, such as diazepam (Valium®), which are also often prescribed as hypnotics to promote sleep, act on four of the six alpha subtypes, while drugs, such as zolpidem (Ambien®), target just one GABA-A alpha subtype (alpha-1), which means that this drug is a selective GABA-A agonist. Stimulation of GABA-B receptors produces inhibition of pain signals and plays a role in memory, mood, and other central nervous system functions. Thus, Phenibut’s effects are the result of its interaction of both GABA-A and GABA-B receptors. One might ask why not simply supplement with GABA to enhance GABA receptor activity, since GABA, which is an amino acid, is also classified as a dietary supplement? Unlike Phenibut, which easily crosses the blood-brain barrier, GABA does not. Having developed a basic understanding of the activity of GABA action, a presentation of Phenibut’s effects can be more clearly understood.
Phenibut displays numerous beneficial effects, including:
Nootropic (Cognitive Enhancement)
GABA is the principal inhibitory neurotransmitter in the brain and normally serves as an important regulatory role in reducing the activity of many neurons. GABA is the key neurotransmitter involved in anxiety and in the anxiolytic action of many drugs used to treat the spectrum of anxiety disorders. Benzodiazepines, which are the best-known and most widely used anxiolytics, work by enhancing GABA actions at specific junctions in the brain that results in relief from anxiety. As previously discussed, this benzodiazepine activity occurs from interaction particularly in GABA-A subtype-2 and 3 receptors. Because Phenibut is a nonselective GABA-A (and GABA-B) agonist, it is the essence of this activity that results in Phenibut’s anxiolytic effects.
There are numerous studies that validate the potent anxiolytic action of Phenibut in a wide variety of anxiety states. This anxiolytic effect likely also accounts for Phenibut’s anti-depressant effects, as the pathways and many symptoms related to anxiety and depression are intimately intertwined. This anxiolytic action also probably accounts for, at least in part, the euphoric effects often experienced with Phenibut, which often accompanies the use of benzodiazepines.
One of the desirable anxiolytic properties associated with Phenibut is that a dosage sufficient to exert optimal anxiolytic effects in dealing with stress and anxiety does not produce drowsiness or a hypnotic (sleep-inducing) state, which is often the case with benzodiazepines. Because of this property, Phenibut is required for use by Russian cosmonauts to lower stress levels without adversely affecting work performance. However, higher dosages of Phenibut can be used for its hypnotic effects as discussed hereafter. Phenibut’s unique variance in dose-dependent effects allows for its use both during the day (nootropic, anxiolytic) and at night (hypnotic).
Increased GABA activity filters out most sensory input. Too much sensory input reaches the cerebral cortex and creates a state of hyperarousal that makes it difficult to fall asleep. Thus, enhanced GABA-A and GABA-B activity in dosages higher than that which is sufficient to trigger its anxiolytic and nootropic effects, provides the necessary filter to induce a hypnotic (sleep) state. Herein also lies phenibut’s role as a potent hypnotic agent. Several studies have established the use of phenibut as a hypnotic compound and also for its anti-apnoesic effect (treatment of sleep apnea). In other words, a dose above that required to alleviate stressors and anxiety, Phenibut is also effective at promoting restful sleep.
Phenibut is clearly a nootropic (cognition-enhancing compound) that displays favorable influence on the various aspects of cognitive function, including attention, mood, learning, and memory. It is suggested that this nootropic effect can be attributed to phenibut’s action at GABA-A, GABA-B, and dopamine receptors. Numerous studies and decades of therapeutic use as a nootropic in Russia support the value of phenibut for enhanced cognitive function. In a recent study, it was shown that phenibut increased the transcallosal response amplitude in the brain and thus improves the interhemispheric transmission (communication between the left and right hemispheres of the brain). Researchers in that study concluded that this is objective evidence of phenibut’s nootropic activity and confirms the positive action of phenibut on the learning and memory processes.
There is a wide body of research in which the neuroprotective effects of Phenibut have been studied. This research demonstrates that Phenibut plays a highly protective role in safeguarding brain neurons during stress, including when brain cells are deprived of oxygen from injury (or impaired venous flow) and during times of extreme physical exertion that would otherwise result in overheating and reduced work capacity. It is suggested that under these conditions Phenibut normalizes energy metabolism of brain neurons, increases venous blood flow from the brain (when physical exertion increases blood flow in the brain with a resulting impairment in venous outflow), and increases thermal resistance of brain neurons. Several of these studies have involved using Phenibut to increase work capacity of Russian athletes.
Phenibut has also been demonstrated to help in the treatment of tics and Tourette syndrome, decrease the manifestations of alcohol-induced behavioral disorders and reduce alcohol motivation, and for morphine (opiate) dependence.
Phenibut has been shown to display cardioprotective effects associated with a large number of threats to the myocardium that reduce its functional reserves, including by creating a toxic effect on the functional activity of cardiac mitochondria. These threats include alcohol abuse, chronic renal insufficiency, chronic stress, and other causes of heart rhythm violations.
Scientists have concluded from these studies that Phenibut results in higher cardiac contraction and relaxation rates, higher left-ventricular pressure during functional tests, and increased indexes of oxidative phosphorylation.
That is a brief review of the available science as it pertains to the use of Phenibut for its benefits associated with its anxiolytic, hypnotic, nootropic, neuroprotective, and cardioprotective effects.
If you're interested in further reading on the topics discussed above, may we suggest the following publications, which were used in the compilation of this page:
(1) Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova, 2001;87(9):1217-26
(2) Pavlovian Journal of Biological Science, 1986;21(4):129-40
(3) European Journal of Pharmacology, 2008;583(1):128-34
(4) Eksperimental'naia i klinicheskaia farmakologiia, 2002;65(5):22-6
(5) Eksperimental'naia i klinicheskaia farmakologiia, 2009;72(1):60-3
(6) Stahl's Essential Psychopharmacology, 2008:734
(7) Trends in Pharmacology, 2005;26(1):36-43
(8) Neuropsychopharmacology, 2007;32:1531-9
(9) Trends in Neurosciences, 2004;27(9):569-75
(10) Neuroscience and Behavioral Physiology, 2006;36(7):749-55
(11) Zhurnal Vysshei Nervnoi Deiatelnosti Imeni I. P. Pavlova, 2007;57(4):479-88
(12) Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova, 2009;95(9):907-18
(13) Neuroscience and Behavioral Physiology, 2003;33(3):255-61
(14) Bulletin of Experimental Biology and Medicine, 2009;147(5):606-8
(15) Archivum immunologiae et therapiae experimentalis, 1975;23(6):733-46
(16) Sleep Medicine, 2004;5:S9-S15
(17) CNS Spectrums, 2005;10:21-27
(18) British Journal of Psychiatry, 2005;179:390-6
(19) Eksperimental'naia i klinicheskaia farmakologiia, 2006;69(1):28-32
(20) CNS Drug Reviews, 2001;7(4):471-81
(21) Spanish Journal of Psychology, 2009;12(1):12-20
(22) Eksperimental'naia i klinicheskaia farmakologiia, 2009;72(1):57-9
(23) Vestnik Rossiiskoi Akademii Meditsinskikh Nauk, 2005;(2):35-40
(24) Eksperimental'naia i klinicheskaia farmakologiia, 2006;69(3):19-22
(25) Zhurnal Vysshei Nervnoi Deiatelnosti Imeni I. P. Pavlova, 2006;56(2):236-41
(26) Ukrainskii Biokhimicheskii Zhurnal, 1984;56(6):637-41
(27) Eksperimental'naia i klinicheskaia farmakologiia, 1997;60(1):68-71
(28) Meditsina truda i promyshlennaia ekologiia, 1997;(5):35-8
(29) Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova, 2005;105(9):18-22
(30) Eksperimental'naia i klinicheskaia farmakologiia, 2005;68(3):42-5
(31) Eksperimental'naia i klinicheskaia farmakologiia, 2000;63(1):19-23
(32) Bulletin of Experimental Biology and Medicine, 2007;143(3):341-3
(33) Kardiologiia, 2007;47(6):46-9
(34) Eksperimental'naia i klinicheskaia farmakologiia, 2003;66(4):21-4
(35) Bulletin of Experimental Biology and Medicine, 2007;144(1):21-5
(36) Eksperimental'naia i klinicheskaia farmakologiia, 2002;65(1):77-8

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