Phenibut is a derivative of the inhibitory neurotransmitter GABA. It has been widely used for medical purposes in Russia and former Soviet countries, whereas it is a non-prescription and unapproved (though legal) drug in most other regions.
It has stress-reducing, anxiolytic, and sedative effects. At common doses it is often easier to be alert and functional on it relative to other GABAergic substances like benzodiazepines.
Because it is sold as a “supplement,” many people use the drug under the false assumption that little care is required. This is not the case. It should be treated like other GABAergic substances, recognizing significant impairment and sedation can occur with overdose, as well as that physical dependence is a significant risk with daily or near-daily use. Physical dependence is one of the major downsides of the substance as both tolerance and withdrawal can appear within weeks of beginning daily use, depending on the dose.
Phenibut = Fenibut; Noophen; Phenybut; phenyl-GABA; beta-phenyl-GABA; Phenigama; Anvifen
Molecular formula: C10H13NO2
Molecular weight: 179.219 g/mol
IUPAC: 4-amino-3-phenylbutanoic acid
- Light: 250 – 750 mg
- Common: 750 – 1500 mg
- Strong: 1500 – 2000+ mg
- Common: 500 – 1250 mg
- Total: 10 – 16 hours
- Onset: 01:30 – 03:00
Because it has a slow onset, some people believe it’s not working after waiting an hour or two. Do not redose due to believing it’s not going to work after waiting just a couple hours, it often does take up to three hours or longer to really notice the effects.
Medically it is primarily used in Russia and former Soviet regions, such as Latvia. It is not approved in the EU, US, Canada, or Australia. It is also difficult to see many conditions for which it would be the ideal prescription drug. Some of the Russian literature on the drug has described such a wide array of uses that it practically seems like a wonder drug, but many of its effects have not been sufficiently validated.
Some of the common applications are for psychological/cognitive conditions characterized by hyperactivation, such as anxiety, certain elements of schizophrenia, stuttering/tics, and hyperactivity in children.
It appears to be used in Russia as a treatment for attention-deficit/hyperactivity disorder (ADHD). Studies have shown a decrease in core ADHD symptoms and an improvement in cognition, specifically with memory and attention (Chutko, 2018 ; Zavadenko, 2016). It may normalize altered electrical activity seen in ADHD patients, as shown by EEG data (Zavadenko, 1997).
Anxiety and Panic
Chutko (2014) and Mehilane (1992) report it is effective in anxiety and panic disorders, where it can address core anxious symptoms and improve cognition. This is one of the most common uses of the drug globally.
Like alprazolam and hydroxyzine, it was found to reduce anxiety scores in a study of 42 healthy people (Ikhalaynen, 2005).
A study in people with vascular pathologies showed it was more effective than piracetam for improving cognition when given with ipidacrine, an acetylcholinesterase inhibitor (Khomazyuk, 2018). The presence of ipidacrine is a significant confounding factor that limits how much can be learned from the research.
It’s reportedly a common drug in Latvia for cognitive impairment associated with vascular disorders and it is sold under the name Cognifen, which is a mixture of phenibut 300 mg and ipidacrine 5 mg.
While piracetam and phepyrone improved learning performance in rats when given at low doses, no improvement was seen with phenibut (Kovaleva, 1984).
A couple studies have shown it is effective at treating tension headaches (Esin, 2018 ; Esin, 2016) when used at 250 mg TID. In people who are not already experiencing headaches it may cause headache, as shown by a large number of anecdotal reports.
Phenibut is reportedly protective against neurotoxic and/or cognition impairing insults like electroshock, scopolamine, and hypoxia/ischemia in animals (Brel, 2018 ; Tyurenkov, 2016 ; Vavers, 2015). Baclofen is more effective at reducing convulsions and cognitive impairments caused by electroshock (Tyurenkov, 2016).
It may be effective due to the ability of GABAergics to attenuate the negative effects of excessive glutamate release and calcium influx caused by ischemia. Both GABAB agonism and VDCC antagonism have been demonstrated to offer neuroprotection against ischemia.
It is not as effective for reducing convulsions in animals (Lapin, 1986) and it has not been widely adopted as an anticonvulsant in the regions where it is used medically. Studies have shown diazepam is more effective at protecting against various forms of seizure, though phenibut is protective against kynurenine-induced seizures (Ryzhov, 1981) and some of the effects of quinolinic acid, though possibly not seizures (Lapin, 1986).
Other α2δ antagonists like pregabalin are used for seizures, so it’s possible phenibut simply is not as effective at that target at typical doses.
Perfilova (2017) reported it has a protective effect on cardiomyocytes, specifically via improvements in cellular respiration, following stress in rats. The effect was present with and without inducible nitric oxide synthase (iNOS) blockade, but the effect was greater with blockade.
A study of postmenopausal women with chronic neck pain found phenibut 250 mg BID for 30 days significantly reduced headache and neck pain intensity (Povoroznyuk, 2009).
A small short-term study of 16 patients receiving long-term treatment with antiparkinson drugs found phenibut improved muscle tone, motor activity, rigidity, and tremor in 13 of 16 patients (Gol’dblat, 1986). The effects were negligible in patients not receiving regular antiparkinson drugs.
A study of alcohol dependence in animals found phenibut reduced the motivation to use alcohol and reduced alcohol-induced behavioral disorders (Tiurenkov, 2005), while a separate study of morphine dependence in mice found phenibut reduced naloxone-enhanced withdrawal symptoms, with the same being shown using valproate and baclofen (Belozertseva, 2000).
Phenibut somewhat improved objective measures of sleep during acute alcohol withdrawal, but it did not improve subjective sleep quality (Danilin, 1986).
Gestosis, preeclampsia, and thrombosis
A study of gestosis in animals showed it had anti-thrombotic effects, though the impact of its glutamic acid and nicotinic acid salts was higher (Tyurenkov, 2013). Tyurenkov (2013) found it was comparable to the reference drug sulodexide. Tiurenkov (2014) reported beneficial effects on proteinuria, edema, and blood pressure in pregnant rats with induced pre-eclampsia.
Volkov (1989) reported beneficial effects in pregnant females with gestosis.
This evidence indicates that, at least in gestosis, phenibut may have a positive effect on circulation.
Phenibut HCl and its citrate form were effective in an animal model of chronic stress caused by sleep deprivation. It reduced emotional disruption, cognitive impairemnt, stomach ulceration, and adrenal hypertrophy (Tiurenkov, 2012).
Physical stress tolerance
It improves thermal resistance, work capacity, and blood flow under high-heat conditions (Makarov, 1997 ; Makarov, 1997). It also assists with physical functionality in swimmers, but details of the research aren’t available and exactly how it improves functional status isn’t clear (Likhodeeva, 2010 ; Likhodeeva, 2009).
Asthenia characterized by fatigue/weakness is reduced by phenibut in adolescents (Rodionova, 2016 ; Chutko, 2014). It also reduces anxiety in those patients.
Phenibut can reduce stuttering in children and it also reduces hyperactivity (Surushkina, 2014 ; Dzhanumova, 2010).
Esin (2017) reported it reduced anxiety and improved sleep in people with Meniere’s disease.
It inhibits aggression in mice, but it does not normalize depressive symptoms (Bagmetova, 2015 ; Belozertseva, 1996).
Note: This description is only a generalization. Your experience is not going to perfectly match this description since there are different ways people can respond to a drug.
There are multiple ways to use it, with at least a couple very distinct ones: therapeutic/anxiolytic/stress-reducing (250-1500 mg) or overtly recreational (1500+ mg, sometimes up to a few grams). On the lower end of the range, the drug is definitely capable of being active, but unless it’s addressing stress or anxiety it may be pretty subtle. When people aren’t just looking to make their day a little better, that’s when the dose increases, but the concurrent rise in side effects, after effects, and impairment must be kept in mind.
Phenibut’s activity is dose-dependent, though it’s a bit unpredictable between users and to a lesser extent between uses by the same person. So while it is accurate to say the effects increase the more you take, 750-1000 mg is powerful and adequate for some people, yet others report similar effects at 2-3 grams or more.
It’s common to find the drug works best in a “narrow” dose range, with too little not doing enough and slightly too much greatly increasing the risk of a hangover, headache, nausea, and oversedation. However, the “narrowness” being described here is usually still a range of at least 300 to 500 mg and that only seems like a narrow range when people are viewing phenibut as a drug that can be taken at anywhere from 250 mg to 3000 mg, rather than treating it the way it’s been used in medical settings, where the dose is pretty consistently 250-500 mg up to a few times per day.
Creating an overview of its effects is complicated by the wide range of doses people use and by there simply being different responses to the drug. Some people absolutely love it; it brightens their day, is good for socializing, isn’t very sedating, and it’s either free of after effects or provides an afterglow the next day. For others, it has a mix of positive and negative elements in that it’s effective for sleep and anxiety, but it’s not very euphoric and it may come with a hangover. And yet others mostly don’t respond well to phenibut, reporting it’s ineffective or that any active dose makes them nauseous, hungover, unproductive, and generally unpleasant.
Overall, the majority of users can at least get anxiety and stress reduction, but the rest of its profile is a bit more variable. Impacts on mood, motivation, and how you feel the next day differ a lot.
Like with benzodiazepines, reports of common doses yielding strong mood enhancement and subjectively life-altering effects may be most common among those with preexisting stress and anxiety that would usually hold them back. Going hand in hand with this property, the anti-stress and anxiolytic effects will be most obvious in stressful situations, going as far as to only be good in stressful situations for some people.
There’s also a biphasic aspect to its effects that many users report. Somewhere around 4 to 6 hours after administration the effects change. It appears the first few hours involve a gradual onset of relatively weak and potentially benzodiazepine-like minor sedation and relaxation, but within a few hours later the full effects really come through. Those include a rise in sociability and a stronger uplifted feel, though this is also when many people report it becomes easiest to sleep.
Some common (though unconfirmed) suggestions for enhancing phenibut are to combine it with coffee and/or physical exercise and to take it on an empty stomach. Enough people have reported beneficial effects from these factors that there’s probably some truth to it working well with exercise, perhaps working a bit faster with coffee, and being most noticeable when you’re not eating. With physical activity people often say it speeds up the onset and generally improves the effects, increasing the chance of it being enjoyable rather than producing a bored, drowsy, and disinterested feeling.
It may be less drowsy and more mood enhancing than baclofen. It’s usually said to be weaker at common doses than pregabalin/gabapentin, producing a less “altered” feeling. It’s less cognitively impairing and usually “cleaner” overall with its effects than alcohol. And it’s comparable to benzodiazepines for anxiety reduction, but otherwise it differs by being more energetic, more pro-social, and not having a generalized emotional blunting effect that’s oft reported with benzodiazepines.
The typical response to phenibut is to feel less stressed, more social, and less anxious, perhaps while having a mood brightening effect and a sense of wellbeing. The effects aren’t strong enough at low-common doses to be impairing, so people can usually go about their normal activities without much trouble, although driving should be avoided. At low-to-common doses it’s not very strong with its “altered” effect, so some users describe it as feeling similar to themselves “on a good day” or themselves “but better.” Some level of mood enhancement is typical, though while substantial euphoria might be more common than with benzodiazepines, it’s still not a typical effect at any normal dose, as opposed to simply having a brighter, happier day. Sometimes users will experience short periods of euphoria early in their use from higher doses and proceed to chase that effect in subsequent chronic use, which isn’t a good idea.
It has a general anxiolytic effect and it’s reported to be particularly helpful with social anxiety and other forms of social-related stress, such as performance anxiety. Along with tamping down anxious thoughts and sensations, it may promote more open communication and it doesn’t seem to blunt emotions like benzodiazepines can.
Because of its disinhibitory effect, users can become a bit more animated in conversation and more likely to try new things, especially things they’ve been avoiding due to anxiety. Because it tends to enhance confidence and people’s desire for social interaction while doing so in a cleaner way than higher doses of alcohol, people find it can work well during presentations, interviews, or social events. The disinhibition can become a negative when high doses are taken due to making risky or regrettable decisions, as is the case for most GABAergics.
Lower doses around 0.5-1 g most often have a neutral or stimulating effect on energy. This energetic effect is observed even with higher doses of 1.5 to 2+ g, but it’s less reliable. The impact on energy can contribute to sociability and productivity, though with a variable effect on those two areas of functioning since some users find themselves in a pleasant but unproductive mood, so it’s fair to say pro-social effects are more reliable than pro-work effects.
It’s been somewhat misleadingly labeled a nootropic. While it may support cognition by alleviating stress-induced declines in cognition or by generally assisting with focus and alertness at lower doses, the overall effect of the drug is not that of a pure cognitive enhancer. It appears, however, to at least preserve cognition better than benzodiazepines or alcohol and this contributes to it feeling much more clearheaded. A minority of users experience enough impairment in the form of spaciness and reduced focus/attention at lower doses (<1 g) to make it unsuitable for use during work.
Sleep is usually enhanced, reducing sleep onset latency and increasing sleep efficiency due to its long duration. The long duration can also lead to people sleeping longer than usual if an alarm isn’t used. So long as low-common doses are taken, people usually feel normal or better than normal the subsequent day. The sleep it produces is frequently described as “deep,” but exactly how it affects sleep architecture is unknown. Regardless, it is predominantly positive for people with and without insomnia, but outlier reports do exist, such as people finding it difficult to sleep (more often during the first half of the effect period) or simply noticing no effect. Grogginess or an unproductive mood for the first part of the next day are possible.
Libido often increases, sometimes very substantially, in a dose-dependent way. It’s not a major effect at low doses.
Music enhancement of varying degrees has been reported, allowing music to sound better and for listening to be a more immersive experience than usual.
Nausea and vomiting are common effects and become more likely as the dose increases, causing stomach pain and general GI discomfort. Strong doses can impair your motor skills, leading to less coordinated actions.
Some of the physical effects are pleasurable, such as a body high that can include sensations of warmth and tingling. And it usually has some muscle relaxing properties, yet it can produce paradoxical muscle twitches with higher amounts.
Headache or increased head pressure are common with strong doses, but severe headaches aren’t typical, despite having occurred for some.
Other physical effects include a ringing or buzzing in the ears, slurring of words with high doses, increased urination, cold sweats, and delayed ejaculation (though not coupled with reduced pleasure.)
It has minimal impact on perception at common doses, but it can cause dose-dependent vision impairment with higher amounts. The most noticeable effects include strong+ doses causing some blurriness and lagging, i.e. it taking longer to focus on a new object after you’ve been paying attention to something else.
Like other gabapentinoids it can produce a range of subtle changes in the texture of surfaces, usually at strong+ doses, that may not be very noticeable until you’re paying attention.
There are a few reports of it aggravating visual snow, though it’s not clear if that’s a typical effect given the lack of reports specifically discussing it.
The after effects are highly dependent on dose and timing. Taking a strong+ dose, particularly in the afternoon or evening, can easily lead to effects the next day and those may not be positive. Some people receive an uplifted mood the next morning, essentially continuing a weaker version of the positives from the prior day, but others are groggy and unproductive upon waking up.
Rebound effects usually only kick in after using for at least a few days, so it’s not common to be depressed or anxious from a single use.
It’s pretty common to have a mixture of positives and negatives, such as being relaxed/mellow but not very productive for at least part of the next day.
It is frequently said to improve the effects of stimulants, psychedelics, and perhaps entactogens.
For stimulants, it can reduce jitteriness, uncomfortable physical stimulation, and anxiety, while preserving or enhancing the mood effects. Usually people report this makes the experience feel smoother and the two drugs may also yield a preferable energetic state and greater effects on socialization and libido than either alone. Comedowns, such as sleep trouble and low mood, may be somewhat alleviated.
For psychedelics, it can also make the body load easier to deal with and it can notably reduce the chance of a very stressful, confusing, or anxious experience. Bad trips often begin with a minor negative thought or a bit of confusion spiraling out of control and it seems phenibut can reduce the chance of this happening. So long as the dose is kept relatively low (e.g. 250-750 mg) it may cause little degradation of the visual effects. Like with the stimulant combination, phenibut may make the comedown smoother and sleep easier.
Combining it with alcohol is not a great idea. Although it can be done safely and should not be physically dangerous when a common phenibut dose is combined with 1-3 drinks, it does significantly raise the risk of oversedation, general drunkenness, and hangover. If enough is taken of either drug, the combination can be physically dangerous, coming with risks like severe impairment, respiratory depression, coma, and vomit aspiration. So while they may work together well to improve mood and socialization if taken carefully, the risks associated with the combination make it worth avoiding.
Phenibut is a derivative of γ-aminobutyric acid, commonly known as GABA, that includes a phenyl ring bonded to GABA’s β carbon atom. Structurally it is similar to baclofen, differing only by the absence of a chlorine atom. Despite being similar to baclofen, phenibut is much less potent as a GABAB agonist.
Its R-enantiomer is more active than the S-enantiomer.
Most reports of phenibut’s effects come from people using the HCl salt, but the free amino acid (FAA) version does exist. Some people prefer it due to swallowing the powder or using it sublingually/buccally being much more pleasant because of the lower acidity, although sublingual administration is still fairly impractical due to the large amount of powder. It’s also more potent by weight, so the oral dose is lower. Reports vary as to any other differences. For some, it’s less likely to cause stomach discomfort, but usually the rest of the core psychological and physical effects are essentially the same.
Until the 2010s phenibut was best understood as a GABAB agonist, like baclofen (Ryago, 1983), but more recent studies have shown additional activity as a gabapentin/pregabalin-like antagonist of voltage-dependent calcium channels containing the α2δ subunit (Zvejniece, 2015). Phenibut also has a higher affinity for this site compared to GABAB, so it can be viewed as a major contributor to its effects.
Those two mechanisms, GABAB agonism and α2δ subunit antagonism, cause downstream effects leading primarily to reduced neuronal excitability, which depresses various kinds of activity in the nervous system. A combination of those mechanisms likely yields the core effects of anxiolysis, sedation, and sleep induction/enhancement.
Complete knowledge of its pharmacology is limited by a lack of detailed, accessible, and trustworthy research. It has never been widely studied outside of Russia and a few nearby countries, so the majority of published information about its effects can only be learned about from summaries rather than from the full texts of the studies. However, full studies are available supporting its GABAB and calcium channel blocking effects, so those aspects of the drug can be considered fairly reliable and well-supported.
- Racemate: 177 μM (Dambrova, 2008) [rat]
- R-phenibut: 92 μM (Dambrova, 2008) [rat]
- Baclofen: 6 μM (Dambrova, 2008) [rat]
α2δ of VDCCs
- Racemate: 60 μM (Belozertseva, 2015) [rat]
- R-phenibut: 23 μM (Zvejniece, 2015) [rat]
- S-phenibut: 39 μM (Zvejniece, 2015) [rat]
- Baclofen: 156 μM (Zvejniece, 2015) [rat]
GABAB receptors are G protein-coupled receptors (GPCRs) that exist in presynaptic and postsynaptic regions to modulate neurotransmission. They were originally identified as distinct from GABAA due to being a lower-affinity target of GABA and being insensitive to the activity of the GABAA antagonist bicuculline. Early research showed phenibut interacts with bicuculline-insensitive receptors (Ryago, 1983). The receptors have a core domain of seven transmembrane helices and they are heterodimers, meaning each receptor complex is made of two subunits, GABAB1 and GABAB2. GABAB1’s extracellular domain binds GABA and other ligands, like phenibut, while the GABAB2 subunit couples the receptor with the effector G protein. Functional receptors require both subunits.
This receptor is distributed throughout the central and peripheral nervous systems, with the highest density in the cerebral cortex, thalamus, cerebellum, and amygdala (Benarroch, 2012).
It is primarily coupled to Gαi proteins and via its action on Gαi and the Gβγ complex it causes an inhibitory effect in neurons via the inhibition of presynaptic VDCCs, activation of postsynaptic potassium channels, and inhibition of adenylyl cyclase (the enzyme that causes the transformation of ATP to cAMP, an important second messenger). Presynaptically it mostly inhibits N-type or P/Q-type calcium channels, reducing neurotransmitter release.
Postsynaptically there are interactions with potassium channels, especially inward-rectifying GirK channels, causing hyperpolarization.
Agonism at this site is more often linked with cognitive impairment in animals rather than cognitive enhancement (Bowery, 2006). This even led to the development of a GABAB antagonist, SGS742, that was researched for mild cognitive impairment. Detailed research into phenibut’s cognitive effects in humans does not exist.
When animals lack functional GABAB receptors they are more anxious (Cryan, 2005), though some studies report antidepressant effects when GABAB is absent, despite it often being taken by humans to improve mood and despite phenibut having antidepressant-like effects in animals (Dambrova, 2008) that are blocked by GABAB antagonism.
Clinically, GABAB receptors have been implicated in pain, seizures, and motor disorders. If you knockout functional GABAB receptors in animals, they show spontaneous seizures leading to premature death, decreased pain threshold, and cognitive deficits. Although GABAB activity is protective against some forms of seizure, it seems involved in the generation of absence seizures, so people with that condition could experience an exacerbation from phenibut.
Tentative results linking GABAB abnormalities to autism, bipolar disorder, depression, and schizophrenia also exist (Fatemi, 2011). If any of these connections hold true, they could help explain part of the social and mood benefits associated with phenibut.
The protypical gabapentinoids (pregabalin and gabapentin) block the α2δ subunit of VDCCs and that mechanism is now known to constitute a fair portion of phenibut’s pharmacology. Research in the 2010s demonstrated it competes with gabapentin for its binding site, has a higher affinity for α2δ than for GABAB, and it has some gabapentinoid-like effects on pain (Zvejniece, 2015 ; Belozertseva, 2015). Blocking this site, which reduces the influx of calcium ions, can reduce the release of excitatory neurotransmitters like glutamate.
Phenibut may or may not affect glutamate decarboxylase and/or GABA transaminase, but an increase in the concentration of GABA has been reported. In vitro, phenibut increases calcium-dependent spontaneous release of GABA (up to 116% with 50 μM and 131% with 100 μM) (Rayevsky, 1986). Allikmets (1983) showed an increase in GABA in rat striatum.
Kovalev (1986) reported phenibut and GHB have an inhibitory effect on GABA transaminase. If true and without a cooccurring decline in GABA synthesis, this could contribute to higher GABA levels.
It is frequently claimed to boost dopamine activity, but little evidence exists for that effect. Research has shown it affects dopamine metabolism, though not in a way that produces higher dopamine levels. Rather, it may increase the speed of synthesis and catabolism (Allikmets, 1979). When that effect is combined with its general inhibitory effect on neurons, a reduction in dopaminergic activity could exist, with potential variation between brain regions. Allikmets (1979) reported it antagonized dopaminergic drugs and potentiated the cataleptic effect of the dopamine antagonist haloperidol.
Spontaneous release of dopamine was not altered in the rat nucleus accumbens at 50 μM, but phenibut did reduce potassium-induced release of dopamine at that concentration (Rayevsky, 1986).
Phenibut has received some attention in the bodybuilding/weightlifting communities. In some cases that’s just due to subjective enhancements when working out, but in other cases people are taking it with the belief that it will increase growth hormone (GH) activity.
There is a connection between GABA and growth hormone, though with different effects depending on where the substance is acting. Both inhibition and enhancement of growth hormone have been reported with GABAergic drugs. For example, the benzodiazepine diazepam caused a central inhibitory effect on GH and the same has been seen with muscimol given IV or with γ-acetylenic-GABA injection to increase GABA levels in the brain (Powers, 2013). Yet GABA infusion into the pituitary increases GH release and muscimol has also been shown to raise GH. Some of the studies reporting a positive effect with muscimol failed to show an effect from baclofen, whereas others have shown oral baclofen can stimulate GH secretion.
Research on the effect of phenibut on GH is not available, so extrapolation from baclofen is required. Monteleone (1998) reported oral baclofen administration increased basal GH, but the effect was only significant in males.
Half-life: 5.3 hours
It is not metabolized and is renally excreted (Canino, 2016). 65% of the drug is excreted in the urine (Merchan, 2016).
Phenibut was synthesized in Russia in the 1960s at the Department of Organic Chemistry of the Al Gertsen Leningrad Pedagogical Institute under the supervision of Professor V. V. Perekalin and then researched for use in many conditions, such as weakness, anxiety, depression, PTSD, and insomnia (Masolva, 1965 ; Khaunina, 1976). It was introduced around the 1960s-1970s under the name Citrocard.
Under order No. 1126 on December 18, 1974, phenibut (aka fenibut or fenigam) was added to the State Drug Register by the USSR’s Ministry of Public Health. Research around that time had shown it was similar to sedatives in some respects, but that it was less impairing and less “narcotic”-like in animals. Unlike other typical GABAergics it did not possess anticonvulsive effects in strychnine, corazole, or electrical convulsion seizure models.
Prior to 1976 its efficacy had been studied in over 1000 patients suffering from neurological, psychiatric, and surgical conditions. The typical dose was 300-500 mg three times per day.
Neumyvakin (1978) mentions phenibut was available to Russian cosmonauts during the Soyuz-19 mission in 1975. Exactly how it was used is unclear and how widely it was used in the Russia/Soviet space program is unknown.
Use in Russia has continued ever since its release, but phenibut has minimally expanded in medical settings beyond Russia’s borders. However, since the 2000s to 2010s it’s become a widely used drug globally via the supplement industry.
Legality (as of November 2018)
Australia: Schedule 9 (prohibited substance)
United Kingdom: Not specifically controlled but it may fall under the Psychoactive Substances Act.
United States: Uncontrolled
Common doses appear to be physically safe acutely in otherwise healthy people, but the effects of chronic administration are not well-understood.
Phenibut 50 mg/kg in rats did not have a negative effect on fetal development during pregnancy, though 50 mg/kg diazepam was associated with reduced female body weight gain and disturbed fetal development (Filimonov, 1989).
Overdoses quite reliably trigger dose-dependent cognitive impairment, drowsiness, confusion, bradycardia, hypotension, hypothermia, respiratory depression, and variable levels of coma. If you use too much it’s common to fall asleep at random and to experience drunken-like impairment of motor skills. Phenibut-only overdoses are rarely lethal, but if enough is used to severely impair a person’s mental status and/or if coma is present, they should be monitored in a medical setting since respiratory support is occasionally used and it’s important to prevent vomit aspiration.
Some of the other potential effects of an overdose are mydriasis, agitation, bizarre uncontrolled behavior, hallucinations, and delusions. It’s most often associated with reduced heart rate and blood pressure, but there are reports of hypertension and tachycardia occurring, sometimes leading to treatment with a benzodiazepine. Pinning down the expected effects of an overdose is complicated by the literature containing reports of anywhere from 5 to 10-15+ grams, which may be associated with different effects.
The LD50 was reported to be 1000-1200 mg/kg (IP) in mice and 900-1000 mg/kg (IP) in rats (Khaunina, 1976). Given the ED50 of 50-100 mg/kg for various effects in rodents, it has a relatively good safety ratio.
Typically an overdose, even one capable of producing coma, will significantly resolve itself in under 24 hours, usually faster.
Prolonged phenibut use does cause physical dependence, leading to tolerance and to a progressively worse withdrawal period the longer it is taken or the higher the dose becomes. Rebound effects, which may essentially be withdrawal from early neuroadaptations caused by short-term use, begin within a few days of daily use for some people. This is mostly an issue when taking strong+ doses. Tolerance even to light doses will typically build within a week or two.
Because of the rate of tolerance development, the Russian literature says it is indicated for a few weeks of continuous use at the same dose (e.g. 250 mg 2-3x daily).
Withdrawal can include uncomfortable feelings of physical stimulation/energy, anxiety/fear/panic, depression, social withdrawal, insomnia, muscle twitches, sweating, hot flashes, irritability, and hallucinations (including delirium-type hallucinations of objects or people that don’t exist). Though it is a GABAergic and seizures should be considered a potential risk during withdrawal, it doesn’t seem to be at all common for withdrawal to produce seizures.
It appears gabapentinoids often alleviate a large portion of the withdrawal symptoms. Baclofen and benzodiazepines are also at least partly effective, with the former usually working for countering some of the insomnia and anxiety. Gabapentinoids and baclofen, which more directly replace phenibut, are likely superior.
The timeline of the withdrawal usually involves experiencing relatively minor symptoms during the first 24 hours following the last dose. From there the symptoms increase significantly and peak from Days 2 to 6.
Stimulants will often aggravate the symptoms, so even caffeine is worth avoiding as a general rule.
Risky Combinations (list is not exhaustive)
- Benzodiazepines, opioids, alcohol, barbiturates, and other GABAergics.