We use essential cookies (authentication, your saved goals/stack) by default. With your permission we’ll also enable privacy-respecting analytics (Vercel Web Analytics, anonymous load-time metrics) and error-replay diagnostics (Sentry — DOM snapshots only when an error fires) so we can fix bugs faster. Learn more about cookies
Phenibut (β-phenyl-GABA, β-phenyl-γ-aminobutyric acid) — a Soviet-developed GABA-B receptor agonist prescribed as an anxiolytic/nootropic in Russia (Anvifen/Fenibut/Noofen), with NO Western regulatory approval and a serious dependence/withdrawal liability
A GABA-B receptor agonist — β-phenyl-GABA — developed in the USSR and still prescribed there as an anxiolytic and nootropic (brands Anvifen, Fenibut, Noofen). It is NOT approved in the US, UK or EU, where it is sold online as a 'nootropic' or anxiolytic 'supplement' and used recreationally for anxiety, sleep and sociability. A genuine but mostly Russian, limited clinical literature supports its anxiolytic use; the DOMINANT Western literature, however, is case reports of DEPENDENCE, rapid TOLERANCE, and severe WITHDRAWAL — agitation, insomnia, psychosis, delirium and seizures resembling baclofen or alcohol/benzodiazepine withdrawal — plus OVERDOSE/toxicity with reduced consciousness requiring intensive care. Phenibut is dangerous combined with alcohol or other CNS depressants. Frame: a real GABA-B anxiolytic carrying a serious dependence and withdrawal risk and almost no Western regulatory standing. Informational, harm-reduction entry only — not a recommendation.
Research compound — not a dietary supplement
Phenibut is a research compound, not a regulated dietary supplement. It is sold for research or off-label use. The evidence below is largely preclinical (animal and in-vitro) or early-stage, so no evidence score is assigned. This page is provided for transparency and education — it is not a recommendation to use. Consult a qualified healthcare provider, and be aware that purity, dosing, and legal status vary by jurisdiction.
What the evidence says
Most Phenibut studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from medium-quality randomised trials published 2001–2024.
Based on 15 studies · 3 RCTs
Confidence
Moderate confidenceBy outcome
Phenibut is a GABA-B receptor agonist (with gabapentinoid-like α2δ activity) developed and prescribed in the USSR/Russia as an anxiolytic and nootropic (Anvifen/Fenibut/Noofen), but it has NO US/UK/EU regulatory approval and is sold and used in the West as a grey-market 'nootropic' supplement and recreational anxiolytic. There is a genuine but mostly Russian, older and methodologically limited clinical/pharmacology literature for its anxiolytic use (Lapin 2001), and a plausible mechanism — which is why the score is not at the floor. But there is no robust modern randomised Western evidence, and the DOMINANT peer-reviewed literature is case reports of physiological dependence, rapid tolerance and severe withdrawal (agitation, psychosis, delirium, seizures resembling baclofen/alcohol withdrawal — Ahuja 2018, Brunner 2017, Sethi 2021) plus acute overdose/CNS-depression toxicity requiring supportive care (Sankary 2017, Owen 2016). The dependence/withdrawal liability and absence of Western approval keep the score low.
Phenibut (β-phenyl-γ-aminobutyric acid, 'β-phenyl-GABA') is a GABA analogue in which a phenyl ring has been added to the GABA backbone, allowing the molecule to cross the blood-brain barrier that GABA itself cannot.
It was synthesised in the Soviet Union in the 1960s and has been used clinically in Russia and neighbouring states for decades as an anxiolytic and 'nootropic', sold under the brand names Anvifen, Fenibut and Noofen for anxiety, tension, insomnia and a range of loosely defined indications.
Its principal mechanism is agonism at the GABA-B receptor (the same metabotropic GABA receptor targeted by baclofen), with additional gabapentinoid-like activity at the α2δ subunit of voltage-gated calcium channels and, at higher concentrations, some action at GABA-A receptors and dopaminergic effects.
This GABA-B/α2δ profile is the basis of both its calming, sleep-promoting and pro-social subjective effects and its dependence and withdrawal liability. Phenibut has NEVER been approved as a medicine in the United States, United Kingdom or European Union.
In the West it occupies a grey market: it is sold online as a 'nootropic' or anxiolytic dietary 'supplement' and is widely used recreationally for anxiety relief, sleep, and increased sociability. The honest reading of its evidence base is split.
On one side there is a genuine but mostly Russian, older and methodologically limited clinical literature describing anxiolytic and nootropic use, summarised in the widely cited pharmacology review by Lapin (2001), which characterises phenibut as a tranquiliser and nootropic acting via GABA-B.
On the other side — and dominating the modern, peer-reviewed Western literature — is a steady stream of case reports and case series documenting harm: physiological DEPENDENCE that develops with regular use, rapid TOLERANCE that drives dose escalation, and a severe WITHDRAWAL syndrome on abrupt cessation.
Reported withdrawal features include rebound anxiety and insomnia, agitation, tremor, autonomic instability, hallucinations and frank PSYCHOSIS, delirium, and SEIZURES — a picture clinicians repeatedly liken to baclofen withdrawal and to alcohol/benzodiazepine withdrawal, and which has required management with benzodiazepines, baclofen substitution or phenobarbital tapers (Ahuja 2018; Brunner 2017; Sethi 2021).
Acute OVERDOSE produces dose-dependent CNS depression — somnolence, reduced consciousness, sometimes agitation or delirium — and toxicity reports describe patients requiring intensive supportive care (Sankary 2017); a survey of availability and use characterised the desired effects alongside the acute toxicity profile and the ease of online purchase (Owen 2016).
The combination with alcohol or other CNS depressants is particularly dangerous because the sedative effects are additive.
The score reflects this reality squarely: phenibut is a real GABA-B anxiolytic with a plausible mechanism and some (largely non-Western, limited) efficacy literature, but it has no Western regulatory approval, no robust modern randomised evidence in the populations that actually use it, and a dominant peer-reviewed literature consisting of dependence, tolerance, severe withdrawal and overdose case reports.
It is sold and used as a supplement but is better understood as an unapproved GABAergic drug with a meaningful addiction and withdrawal risk. This is an informational, harm-reduction entry — not a recommendation, and not an endorsement of any dose or protocol.
Phenibut is β-phenyl-GABA — a GABA analogue whose added phenyl ring lets it cross the blood-brain barrier (which GABA itself cannot). Its principal action is agonism at the GABA-B receptor, the same metabotropic GABA receptor targeted by baclofen. This GABA-B activity underlies its anxiolytic, sedative and sleep-promoting subjective effects — and, on regular use, the tolerance and the severe withdrawal syndrome that mirror baclofen withdrawal.
Beyond GABA-B, phenibut binds the α2δ subunit of voltage-gated calcium channels — the gabapentinoid target shared with gabapentin and pregabalin — dampening excitatory neurotransmitter release. This contributes to its calming and analgesic-like effects and is part of why its dependence/withdrawal profile resembles other GABAergic/gabapentinoid drugs rather than a benign supplement.
The same GABA-B/α2δ engagement that produces phenibut's anxiolysis drives neuroadaptation. With regular use, tolerance develops quickly and users escalate the dose; physiological dependence follows, and abrupt cessation precipitates a severe withdrawal syndrome — rebound anxiety/insomnia, agitation, autonomic instability, hallucinations, psychosis, delirium and seizures — clinically managed like baclofen or alcohol/benzodiazepine withdrawal. This is the dominant signal in phenibut's Western literature.
How Phenibut works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Avoid — phenibut has a high dependence liability with rapid tolerance, and cross-dependence with alcohol/GABAergic drugs is likely.
Avoid — additive CNS/respiratory depression is dangerous and a recurring feature of phenibut toxicity.
Do not stop abruptly — withdrawal can include seizures, psychosis and delirium. Seek medical supervision for a taper or substitution.
Avoid entirely — a centrally active GABAergic drug with no human safety data in pregnancy or lactation.
Additive CNS depression. Combining phenibut with alcohol markedly increases sedation and the risk of dangerous respiratory/CNS depression and loss of consciousness, and is a recurring feature of phenibut toxicity presentations.
Additive sedation and CNS depression. Co-use raises the risk of oversedation and respiratory depression; note benzodiazepines are also used clinically to TREAT phenibut withdrawal, which underscores the overlapping GABAergic pharmacology.
Additive CNS and respiratory depression — a potentially fatal combination. Phenibut dependence has been reported alongside opioid treatment, complicating management.
Overlapping GABA-B / α2δ pharmacology means additive sedation and cross-tolerance/cross-dependence; baclofen is sometimes used to substitute during phenibut withdrawal, illustrating how closely related the effects are.
Tip: Regular use leads to tolerance and dose escalation, then physiological dependence. There is no safe self-managed regimen; the only reliable mitigation is not to use regularly, and to seek medical help if dependence has developed.
Tip: Abrupt cessation after regular use precipitates a withdrawal syndrome resembling baclofen/alcohol withdrawal. Do NOT stop abruptly; withdrawal is managed medically with benzodiazepines, baclofen substitution or a phenobarbital taper — seek care rather than self-detoxing.
Tip: Phenibut's long, variable action causes sedation and next-day grogginess and psychomotor impairment. Avoid driving or safety-critical tasks; the effect is amplified by alcohol or other depressants.
Tip: Overdose causes reduced consciousness, sometimes agitation or delirium, and has required intensive supportive care. Risk rises sharply with higher or eyeballed doses and with co-ingested depressants; treat suspected overdose as a medical emergency.
Tip: The anxiolytic and sleep effects rebound on withdrawal, often worse than baseline, reinforcing continued use. A supervised taper rather than abrupt stopping reduces rebound severity.
Tip: Dose-related nausea, dizziness and slowed reactions are reported. Lower exposure reduces these, but no dose is endorsed by this library.
Phenibut has an evidence score of 3.3/10 — emerging evidence based on 10 indexed studies. A GABA-B receptor agonist — β-phenyl-GABA — developed in the USSR and still prescribed there as an anxiolytic and nootropic (brands Anvifen, Fenibut, Noofen). It is NOT approved in the US, UK or EU, where it is sold online as a 'nootropic' or anxiolytic 'supplement' and used recreationally for anxiety, sleep and sociability. A genuine but mostly Russian, limited clinical literature supports its anxiolytic use; the DOMINANT Western literature, however, is case reports of DEPENDENCE, rapid TOLERANCE, and severe WITHDRAWAL — agitation, insomnia, psychosis, delirium and seizures resembling baclofen or alcohol/benzodiazepine withdrawal — plus OVERDOSE/toxicity with reduced consciousness requiring intensive care. Phenibut is dangerous combined with alcohol or other CNS depressants. Frame: a real GABA-B anxiolytic carrying a serious dependence and withdrawal risk and almost no Western regulatory standing. Informational, harm-reduction entry only — not a recommendation. Representative study: PMID 11830761.
The commonly studied dose of Phenibut is There is no Western-approved or endorsed human dose. Phenibut is an unapproved GABA-B agonist with a serious dependence and withdrawal liability; this library does NOT provide a recommended dosing protocol. For context only, where it is prescribed abroad (Russia, as Anvifen/Fenibut/Noofen) typical anxiolytic doses are in the order of 250–500 mg up to a few times daily for short courses, and the pharmacology literature describes that range — but recreational/grey-market use commonly involves higher and escalating doses, and any regular use risks tolerance, dependence and a dangerous withdrawal syndrome. The safest dose is none; if it has been used regularly, do NOT stop abruptly — taper under medical supervision.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
The best time to take Phenibut is in the evening. It can be taken on an empty stomach. Phenibut is sedating, so any use abroad tends to be later in the day; this library endorses no human timing protocol, and the compound is sandboxed from the stack timing optimizer.
Phenibut should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are dependence with rapid tolerance, severe withdrawal (agitation, psychosis, delirium, seizures), sedation, drowsiness & next-day impairment. Use caution if any of these apply to you: Concurrent use of alcohol or other CNS depressants (benzodiazepines, opioids, baclofen, sedating antihistamines, Z-drugs) — additive sedation and dangerous CNS/respiratory depression; History of substance use disorder or dependence — phenibut carries a high dependence liability with rapid tolerance; Abrupt discontinuation after regular use — risks a severe withdrawal syndrome (agitation, psychosis, delirium, seizures); requires a supervised taper.
Melatonin
Likely helpsRegulates the circadian clock to reduce sleep onset time — most effective at low doses (0.3-1mg) for jet lag and rhythm disorders.
Phosphatidylserine
Mostly mechanism / observationalKey brain membrane phospholipid that facilitates neurotransmitter release, memory formation, and post-exercise cortisol reduction.
Tart Cherry
Likely helpsNatural melatonin and anthocyanin source with modest, fairly consistent small-RCT support for post-exercise recovery and sleep quality, plus uric-acid lowering — effects are real but small and not seen in every trial.
Aniracetam
Mostly mechanism / observationalFat-soluble racetam that modulates AMPA receptors; studied for cognition and anxiety, with no RCTs in healthy adults.
Explore: Best supplements for Focus, Memory & MoodBest supplements for Sleep
Reviewed by Dr. Baher Al Hakim · Last reviewed June 2026 · evidence from 15 studies · how we score · editorial policy
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
Tap node to isolate • Pinch to zoom • Tap edge for research