Phenibut (β-phenyl-γ-aminobutyric acid, or β-phenyl-GABA) is a synthetic relative of GABA, the brain’s main calming neurotransmitter, with a phenyl ring added. It was developed in the Soviet Union in the 1960s and is still prescribed in Russia and some other former Soviet countries for anxiety, insomnia and related complaints, under brand names such as Anvifen, Fenibut and Noofen (Lapin, CNS Drug Rev 2001; Gurley & Koturbash, Basic Clin Pharmacol Toxicol 2024).

Outside those countries it has never been approved as a medicine. It is sold online as a “nootropic” or supplement. The most important fact about it is that regular use can cause tolerance, dependence and a withdrawal syndrome that has led to intensive-care admissions, intubation and seizures. US poison centers logged 1,320 phenibut exposures from 2009 to 2019 (Graves et al., MMWR 2020). The FDA’s position is that phenibut is not a lawful dietary ingredient.

This page summarizes what the clinical studies, poison-center data, case series and regulators report. It is for education only and is not medical advice.

Property	Detail
Drug class	GABA analog; GABA-B receptor agonist that also binds the α2-δ subunit targeted by gabapentin and pregabalin
Brands	Anvifen, Fenibut, Noofen (former Soviet Union countries); not approved as a drug elsewhere
Route	Oral (tablets, capsules, powder)
Doses in medical use	250–2,000 mg/day, as reported in reviews of Russian practice
Half-life	≈5.3 h after a single 250 mg oral dose (Soviet human data); 5–6 h in a 2024 review
Elimination	Largely excreted unchanged in urine, although Russian sources disagree on how much is metabolized
US status	Never FDA-approved; FDA says it does not meet the definition of a dietary ingredient
Australia	Schedule 9 (prohibited substance) in the Poisons Standard
WADA status	Not named on the 2026 Prohibited List

What it is

Phenibut’s chemical name is 4-amino-3-phenylbutanoic acid: formula C₁₀H₁₃NO₂, molecular weight 179.22 g/mol (PubChem). It is GABA with a phenyl ring on the β-carbon. Baclofen, a prescription muscle relaxant, is the same molecule with a chlorine atom added to that ring (Lapin, CNS Drug Rev 2001).

According to Gurley and Koturbash, phenibut was first developed for the Soviet military in the 1960s to reduce anxiety and later moved into civilian medicine. Much of the early research was published only in Russian, and some may never have been published (Gurley & Koturbash, 2024).

Mechanism

Phenibut is a racemic mixture (a 50:50 mix of two mirror-image forms). Laboratory work shows two main targets:

Target	What the studies found
GABA-B receptor	Only R-phenibut binds. In rat brain membranes, binding constants were 92 µM for R-phenibut, 177 µM for racemic phenibut and 6.0 µM for baclofen, so phenibut is a much weaker GABA-B agonist than baclofen. S-phenibut was inactive in animal behavioral tests at doses up to 500 mg/kg (Dambrova et al., Eur J Pharmacol 2008).
α2-δ subunit of voltage-gated calcium channels (the gabapentin/pregabalin binding site)	Both forms bind: Ki 23 µM for R-phenibut and 39 µM for S-phenibut, against 0.05 µM for gabapentin. R-phenibut’s pain-relieving effect in rats was not blocked by a GABA-B antagonist, which points to this calcium-channel site (Zvejniece et al., Pharmacol Biochem Behav 2015).

Based on this α2-δ binding, a 2024 German review groups phenibut with the gabapentinoids. It notes that phenibut binds that site far more weakly than gabapentin, the weakest of the clinically used gabapentinoids (Bonnet et al., Dtsch Arztebl Int 2024). Older Russian work also describes effects on dopamine and antagonism of β-phenethylamine, a trace amine (Lapin, 2001). These binding and behavioral data come from animal tissue and animal models, not from people.

How it works in the body

Human pharmacokinetic data are thin and come mostly from older Soviet studies cited by later reviews.

Parameter	Reported value	Source
Half-life after a single 250 mg oral dose (healthy volunteers)	5.3 h	Soviet data cited by Gurley & Koturbash, 2024
Share excreted unchanged in urine (same study)	65%	Same
Time to peak concentration	3–4 h	Bonnet et al., 2024
Elimination half-life	5–6 h	Same

The sources disagree on how phenibut is cleared. Bonnet et al. describe it as almost untouched by liver metabolism. Gurley and Koturbash point out that two current Russian product information sheets instead say that up to 95% is converted in the liver to inactive metabolites. They conclude that the drug’s pharmacology and toxicology remain poorly characterized.

Phenibut is not detected on routine urine drug screens, and no commercial point-of-care test exists. It can be confirmed only by specialized laboratory methods such as liquid chromatography–mass spectrometry (Graves et al., 2020; Bonnet et al., 2024).

Medical use in Russia and Eastern Europe

Lapin’s 2001 review describes phenibut as widely used in Russia for:

tension, anxiety and fear, and poor sleep in “psychosomatic or neurotic” patients;
premedication before surgery and use after surgery;
asthenia (chronic weakness and fatigue) and depression;
post-traumatic stress, stuttering and vestibular (balance) disorders.

Reviews put the doses used in medical practice at 250 mg to 2 g a day (Bonnet et al., 2024; Kupats et al., Pharmacopsychiatry 2020). Two Russian product information sheets list 2,500 mg as the maximum daily dose and advise monitoring liver function during long-term use (Gurley & Koturbash, 2024). In Latvia, phenibut is sold as the prescription drug Noofen (Upmanis et al., Medicina 2024).

Tolerance was noted early. In the original Soviet studies, starting doses often had to be raised by 25–33% after only two weeks of treatment (Gurley & Koturbash, 2024).

What the research shows

Clinical trials are small and mostly uncontrolled

No large placebo-controlled trial of phenibut has been published in an international journal. A 2020 systematic review from Latvian researchers found 11 clinical trials with 583 patients in total (Kupats et al., 2020). Recent trials indexed in PubMed are mostly Russian-language studies that compare phenibut with another drug, with standard care or with a different phenibut regimen, not with placebo:

Study	Design and n	Phenibut regimen	Reported result
Vorob’eva & Rusaya 2016	Randomized vs the anxiolytic adaptol; n = 62 with anxiety and chronic cerebral ischemia	Noofen (dose not given in abstract)	Similar anxiolytic effect in both groups; adaptol better for nonspecific somatic symptoms (p = 0.037)
Vorob’eva & Rusaya 2017	Randomized, add-on vs standard therapy alone; n = 53 with fatigue and cerebrovascular disease	Noofen (dose not given in abstract)	Fatigue fell by 30–50% in about three-quarters of the phenibut group
Esin et al. 2022	21-day vs 60-day course, randomized; n = 120 with anxiety; no placebo	500 mg three times daily	Both improved; only the 60-day group still differed from baseline 30 days after stopping
Esin et al. 2024	Capsule vs powder, randomized; n = 67 aged 60–70 with insomnia; no placebo	250 mg morning and afternoon, 500 mg at night	Sleep scores improved in both groups
Tērauds et al. 2025	Single-arm observational study in Latvian general practice; n = 90 with adjustment disorder	250 mg three times daily for at least 3 weeks	Mean 14.8-point fall on the ADNM-20 symptom scale (p under 0.001)

All of these studies lack a placebo group, so they cannot separate the drug’s effect from natural recovery or expectation. Two of the authors of the 2025 study work for the company that makes Noofen. There are no controlled trials of phenibut as a cognitive enhancer in healthy people, which is how it is usually marketed online.

Safety in trials vs real-world use

In the 11 clinical trials, adverse events were reported in 5.66% of patients, most often somnolence (1.89%). The same review noted that people in published dependence and intoxication case reports had taken 0.5–100 g a day, far above the medical range of 0.25–2 g a day (Kupats et al., 2020). The authors call the gap between the trial data and the case reports a discrepancy. They leave open how much the harms reflect high doses, the quality of online products and the use of alcohol or other drugs.

Side effects and risks

Poison-center data

United States, national. From 2009 to 2019, US poison centers recorded 1,320 phenibut exposures from all 50 states and the District of Columbia (Graves et al., MMWR 2020). Cases rose sharply from 2015, the year “phenibut” became a searchable term in the database.

Finding	Value
Calls from health care facilities	85.0%
Male	75.5%
Aged 18–34	58.4%
Agitation	30.4%
Drowsiness or lethargy	29.0%
Tachycardia (fast heart rate)	21.9%
Confusion	21.3%
Coma	80 cases (6.2%)
Major (life-threatening or disabling) effects	12.6%
Major effects when phenibut was the only substance	10.2%
Deaths	3 (1 with phenibut as the only substance reported)
Other substances also taken (adults)	40.2%

Among children under 10, 93.3% of exposures were unintentional. Exposures were not confirmed by laboratory testing.

Minnesota, regional. The Minnesota Poison Control System received 56 phenibut exposure calls from 2000 through 2018, 48 of them (85.7%) in the last five years (McCabe et al., Am J Emerg Med 2019). More than half of the patients had central nervous system effects, 10.7% had withdrawal concerns, and 11 patients (19.6%) were intubated. Nobody died.

Germany. A regional poison center in northern Germany (GIZ-Nord) logged 17 phenibut cases in 2018–2022, all mild or moderate. Reported overdoses of 2–100 g caused somnolence in 8 people, and no one developed respiratory depression or coma (Bonnet et al., 2024).

Intoxication

Published cases describe a mixed picture: sedation and reduced consciousness, or agitation, delirium and psychosis, often with dilated pupils, low body temperature, seizures, high blood pressure and a fast or slow heart rate (Gurley & Koturbash, 2024). There is no antidote, and treatment is supportive.

A systematic review of 62 published toxicity and withdrawal cases found that 80.7% of patients were male, 86.8% had bought phenibut online, and 63.2% also used other addictive substances, most often benzodiazepines and alcohol (Weleff et al., J Addict Med 2023). 48.7% of the toxicity cases needed intubation. The mean hospital stay was 5.0 days for toxicity and 7.7 days for withdrawal.

Severe poisoning has been reported in adolescents. In Australia, five 15-year-olds needed intubation after taking an estimated 1,250–1,750 mg each over about 3 hours, having taken more capsules because the first dose seemed to have no effect (Isoardi et al., J Paediatr Child Health 2020, as summarized by Gurley & Koturbash, 2024).

Dependence and withdrawal

Withdrawal is the best-documented harm. Three systematic reviews of case reports describe it:

Review	Cases	Key findings
Feldman et al., Clin Toxicol 2023	25 articles	All male; median prior dose 10 g/day (range 1–200 g). Withdrawal seen after as little as one week of use, starting as early as 2 h after the last dose. Symptoms got worse in the first 24 h of care in 64%. Seizures 8%, intubation 24%, ICU admission 44%
Weleff et al., J Addict Med 2023	62 cases (toxicity and withdrawal)	95.7% of withdrawal cases involved daily use; 69.6% needed more than one drug to treat
Stewart et al., Cureus 2024	15 articles	Mean dose 13.6 g/day (range 1.5–28.5 g); 87% male; 73% had a history of alcohol or drug misuse; 60% had anxiety or depression

Reported withdrawal symptoms include anxiety, insomnia, irritability and agitation, tremor, muscle pain, palpitations, psychosis, visual hallucinations, delirium and seizures (Weleff et al., 2023; Gurley & Koturbash, 2024). In one reported case, agitation did not respond to several benzodiazepines, haloperidol or baclofen and took about 4 weeks to resolve (Gurley & Koturbash, 2024). A newborn whose mother had used phenibut throughout pregnancy needed treatment for withdrawal after birth (Pena et al., Pediatr Neonatol 2022).

There is no standard treatment. Published cases were managed in hospital with benzodiazepines (68% in Feldman et al.), baclofen (60%), phenobarbital, antipsychotics and other drugs, usually in combination (Penzak & Bulloch, J Clin Pharmacol 2024). In Feldman et al., one patient on baclofen alone after discharge had a seizure. Every published case of abrupt stopping was managed as an inpatient, and the reviewers recommend involving a toxicologist or addiction specialist.

Interactions with alcohol, opioids and other sedatives

No formal interaction studies exist. Combined use with other drugs is common: 40.2% of adult US poison-center cases involved at least one other substance. Reviewers warn that phenibut is likely to add to the effects of other central nervous system depressants (Gurley & Koturbash, 2024). Bonnet et al. single out opioids as a combination that could raise the risk of coma and respiratory depression.

Deaths

Deaths are rare in the published record and usually involve other substances. A 26-year-old man found dead at home with phenibut containers had phenibut confirmed in blood and urine; routine autopsy and toxicology were otherwise largely unremarkable (Arndt & Gray, J Anal Toxicol 2021). Bonnet et al. found no post-mortem analysis in which phenibut alone was declared the cause of death. In the deaths they found, alcohol, opiates or other drugs were also present.

Liver

Russian product information warns about liver function with long-term use. Two case reports that measured liver enzymes after overdose found no clear liver injury, and the evidence is limited (Gurley & Koturbash, 2024).

Quality of products sold online

Products sold as supplements often do not contain what the label says.

US supplements. Researchers tested four US supplement brands labeled as containing phenibut, before and after FDA’s 2019 warnings. Before the warnings, two contained phenibut (484 and 487 mg per serving). Afterward, all four did, at 21–1,164 mg per serving, and the amount rose in three of the four (Cohen et al., Clin Toxicol 2022).
Online “nootropics.” A Latvian analysis of six phenibut products from three internet sellers found less phenibut than claimed in three, considerably more in one, and undeclared ingredients in all of the capsules (Upmanis et al., 2024).

Regulatory and legal status

United States

Phenibut has never been approved by FDA as a drug (Cohen et al., 2022). FDA’s actions so far:

Date	Action
April 10, 2019	Three warning letters to companies selling products labeled as dietary supplements containing phenibut (Atomixx, Evol Nutrition Associates, NeuroScience). FDA stated that phenibut is not a vitamin, mineral, botanical, amino acid or other dietary substance, so it is not a dietary ingredient, and products listing it as one are misbranded (FDA constituent update; FDA warning letter to Atomixx)
July 20, 2021	Warning letter to the seller of Chill6, a powdered drink marketed for anxiety. FDA said phenibut HCl is neither a dietary ingredient nor generally recognized as safe (GRAS), and is an unsafe food additive (FDA warning letter to Chill6)
June 2, 2023	A federal court in Massachusetts entered a permanent injunction against the Chill6 seller for distributing unapproved and misbranded drugs and adulterated food (FDA ingredient page)

Phenibut was not federally controlled under US drug law as of the 2020 MMWR report (Graves et al., 2020). Researchers report that after the 2019 letters, some products stopped calling themselves dietary supplements, and poison-center calls did not fall (Gurley & Koturbash, 2024).

Other countries

Australia: listed in Schedule 9 (prohibited substance) of the Poisons Standard, including its hydrochloride and hydrobromide salts (Poisons Standard, June 2025).
Germany: not approved as a drug, and controlled under the New Psychoactive Substances Act (NpSG), which bans its production, possession, trade and administration (Bonnet et al., 2024).
Russia and Latvia: registered as a prescription medicine (Bonnet et al., 2024; Upmanis et al., 2024).
Others: Bonnet et al. also list phenibut as illegal in France, the United Kingdom, Italy, Hungary and Lithuania. We have not verified those listings against each country’s own legislation.

Sport

Phenibut is not named on the WADA 2026 Prohibited List.

Phenibut is often grouped with other “nootropics” developed or sold as cognitive enhancers, although its effects and risks are closer to those of sedatives. See piracetam and phenylpiracetam, which have a different structure and mechanism.

Key takeaways

A prescription sedative in Russia, unapproved elsewhere. Phenibut has been used in former Soviet countries since the 1960s for anxiety and sleep, at 250 mg–2 g a day, but has never been approved by FDA or in Australia.
GABA-B and gabapentin-like activity. Its R-form acts on GABA-B receptors and both forms bind the α2-δ site targeted by gabapentin and pregabalin, more weakly than baclofen or gabapentin.
Weak efficacy evidence. The human studies are small, mostly Russian-language and without placebo groups; there is no controlled evidence for cognitive enhancement in healthy people.
Dependence and withdrawal are the main danger. Case series describe withdrawal after as little as a week of daily use, with ICU admission in 44%, intubation in 24% and seizures in 8% of published cases.
Poison-center reports are rising. US centers logged 1,320 exposures from 2009 to 2019, with major effects in 12.6% and 80 cases of coma. Other drugs were often also involved.
Labels are unreliable. FDA says phenibut is not a lawful dietary ingredient, and tested products contained 21–1,164 mg per serving or undeclared ingredients.

Sources

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Phenibut