generation run 2026-04-28
53 min completedmodel pipeline-v5plan not recordedrun/8d6ed613…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
- class_inference
- dose_equivalence_gap
Reproduce
- inputs
- 26 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
- streams
- none — agent transcripts are persisted from 2026-09 onward
24 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | HandWiki | — | 1 | 3 | — |
| 2 | PubMed · absence | F-phenibut fluorophenibut pharmacology | 0 | — | — |
| 3 | WebSearch | F-phenibut 4-fluorophenibut legal status scheduling UK EU US Australia | 10 | 1 | — |
| 4 | PubMed | phenibut alpha-2-delta calcium channel voltage gated gabapentin binding | 1 | — | — |
| 5 | PubChem · absence | fluorophenibut | 0 | — | — |
| 6 | PMC | — | 1 | 2 | — |
| 7 | PubMed | PMID 32735986 full record | 1 | — | — |
| 8 | PubChem | 4-fluorophenibut (CID 103611) | 1 | 1 | — |
| 9 | ClinicalTrials.gov · absence | F-phenibut fluorophenibut | 0 | — | — |
| 10 | WebSearch | F-phenibut CGP-11130 SMILES structure history discovery | 10 | 2 | — |
| 11 | OpenAlex | F-phenibut fluorophenibut GABA-B receptor | 2 | 1 | — |
| 12 | PubMed | phenibut GABA-B receptor agonist pharmacology | 15 | 6 | — |
| 13 | PubMed | baclofen GABA-B agonist abuse dependence withdrawal treatment | 5 | 1 | — |
| 14 | PsychonautWiki | — | 1 | 1 | — |
| 15 | PubMed | Zvejniece R-phenibut pharmacology neuroprotective | 2 | 2 | — |
| 16 | WebSearch | F-phenibut CGP-11130 GABA-B IC50 original paper reference | 10 | 0 | — |
| 17 | WebSearch | phenibut Australia Schedule 4 TGA 2021 scheduling | 10 | 1 | — |
| 18 | WebSearch | F-phenibut Canada legal controlled substance NPS survey | 10 | 1 | — |
| 19 | Multiple | F-phenibut dose/duration cross-reference PsychonautWiki vs brief seed data | 2 | 1 | — |
| 20 | Multiple | Compile all F-phenibut chemical identity data | 1 | 1 | — |
| 21 | PubMed | Zvejniece phenibut GABA-B pharmacology Latvia | 2 | 2 | — |
| 22 | PubMed | PMID 34550038 phenibut dietary supplement FDA warning | 1 | 1 | — |
| 23 | PMC | — | 1 | 2 | — |
| 24 | WebSearch | WHO ECDD phenibut 44th pre-review scheduling recommendation | 10 | 1 | — |
82 claims by section — every cited sentence, checked against its source
safety28 · 19 ok
Claim in safety — inconclusiveinconclusiveworking →
Management is supportive: airway protection, ventilatory support, and hemodynamic monitoring.supported
30-year-old with phenibut intoxication requiring sedation and mechanical ventilation. cureus.23913
The primary acute hazard derives from F-phenibut's approximately 58-fold higher GABA-B potency relative to phenibutsupported
F-phenibut ~58x more potent than phenibut, ~4x less potent than baclofen. j.ejphar.2020.173437
Claim in safety — inconclusiveinconclusiveworking →
More than 80 cases of coma and death have been associated with phenibut consumption and withdrawal in the United States, though most involve polydrug contextssupported
More than 80 cases of coma and death associated. FDA warned phenibut not permitted in supplements. 15563650.2021.1973020
A case of suspected phenibut intoxication presenting with partial brainstem areflexia has been documented, and dissociative features during intoxication have been reported.supported
Unconscious patient with brainstem areflexia after phenibut ingestion; ICU admission. v07250573
A case of suspected phenibut intoxication presenting with partial brainstem areflexia has been documented, and dissociative features during intoxication have been reported.supported
Case report of dissociative intoxication and prolonged withdrawal associated with phenibut. jcp.0000000000000731
Identification requires specialized LC-MS/MS methods not routinely available in emergency departmentssupported
No readily available confirmatory lab tests. cureus.23913
Identification requires specialized LC-MS/MS methods not routinely available in emergency departmentssupported
Routine drug screening limitations highlighted. bkac023
Acute psychological adverse effects at supratherapeutic doses include paradoxical anxiety (anxiogenic rebound), cognitive impairment, amnesia, and dissociative symptomssupported
Case report of dissociative intoxication and prolonged withdrawal associated with phenibut. jcp.0000000000000731
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Withdrawal symptoms can begin within 3–4 hours of the last dose and include severe psychomotor agitation, autonomic instability, neurological signs mimicking serotonin syndrome or neuroleptic malignant syndrome, psychosis, and seizuressupported
Tolerance and significant withdrawal within 3-4 h of last use. bcr-2012-008381
Claim in safety — inconclusiveinconclusiveworking →
Withdrawal symptoms can begin within 3–4 hours of the last dose and include severe psychomotor agitation, autonomic instability, neurological signs mimicking serotonin syndrome or neuroleptic malignant syndrome, psychosis, and seizuressupported
Severe psychomotor agitation prominent. Neurologic and autonomic signs may mimic serotonin or neuroleptic malignant syndrome. bjbms.2018.4008
The higher potency of F-phenibut relative to phenibut suggests potentially more rapid dependence development at lower absolute doses, though this has not been formally studied.supported
F-phenibut ~58x more potent than phenibut, ~4x less potent than baclofen. j.ejphar.2020.173437
Baclofen substitution and taper is the primary documented withdrawal management strategy, at approximately 10 mg baclofen per 1 g phenibut equivalencesupported
Substitution with baclofen (~10 mg baclofen per gram phenibut), then baclofen taper over 9 weeks. bcr-2012-008381
Benzodiazepines and phenobarbital are alternatives; phenobarbital may be preferred when seizure risk is elevatedsupported
Among 29 cases of withdrawal, patients treated with baclofen, benzodiazepines, and phenobarbital. Baclofen tapers successful; phenobarbital preferred if seizure risk. jcph.2414
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — not_supportednot supportedworking →
Polydependence on phenibut and benzodiazepines has been documented, requiring coordinated withdrawal management.supported
Case of comorbid phenibut and benzodiazepine dependence managed by baclofen tapering. jcp.0000000000001104
Alcohol presents a complex interaction: GABA-B agonism reduces the stimulating and rewarding properties of alcohol, but concurrent use produces additive CNS depression with increased risk of respiratory compromise and aspiration.partially supported
GABA-B receptor activation (primarily via baclofen) reduces stimulating/rewarding effects of alcohol, signs of alcohol withdrawal, alcohol drinking, motivational properties of alcohol, and alcohol-seeking. 7854_2020_178
Other GABA-B agonists (baclofen, ghb, gbl) produce additive GABA-B receptor activation with risk of severe CNS depression.supported
GHB and analogs as CNS depressants. GABA-B agonism mechanism of toxicity. 15563650.2012.702218
Phenibut withdrawal has been noted to mimic serotonin syndrome clinically, but this represents a mimicry syndrome rather than a true serotonergic pharmacological interactionsupported
Neurologic and autonomic signs may mimic serotonin or neuroleptic malignant syndrome. bjbms.2018.4008
Given the minimal hepatic metabolism of the phenibut class, CYP-mediated pharmacokinetic drug interactions are not expected but have not been studied.supported
Elimination t1/2 5-6h, bioavailability ~65%, excreted unchanged. arztebl.m2024.0003
Claim in safety — inconclusiveinconclusiveworking →
Renal impairment — Phenibut is excreted largely unchanged in urinesupported
Elimination t1/2 5-6h, bioavailability ~65%, excreted unchanged. arztebl.m2024.0003
pharmacology12 · 12 ok
F-phenibut is a potent agonist at the GABA-B receptor, a class C G-protein coupled receptor forming obligate GB1/GB2 heterodimerssupported
Obligate heterodimers (R1+R2 subunits). pjab.94.026
F-phenibut is a potent agonist at the GABA-B receptor, a class C G-protein coupled receptor forming obligate GB1/GB2 heterodimerssupported
GABA-B class C GPCR heterodimer. VFT and 7TM domains. molecules25133093
Downstream signaling proceeds through Gαi/o proteins, producing inactivation of voltage-gated Ca²⁺ channels, activation of inwardly rectifying K⁺ channels (GIRK/Kir3), and inhibition of adenylate cyclase.supported
GABA-B receptors are GPCRs mediating slow inhibitory action via Gai/o. Activate inwardly rectifying K+ channels, inactivate voltage-gated Ca2+ channels, inhibit adenylate cyclase. pjab.94.026
In mouse cerebellar Purkinje cells, F-phenibut activated K⁺ currents with an EC₅₀ of 23.3 µM, compared with 1362 µM for phenibut and 6.0 µM for baclofen — establishing F-phenibut as approximately 58 times more potent than phenibut and 4 times less potent than baclofen at GABA-Bsupported
EC50 for GABA-B-mediated outward K+ current in Purkinje cells: phenibut 1362 µM, F-phenibut 23.3 µM, baclofen 6.0 µM. F-phenibut ~58x more potent than phenibut, ~4x less potent than baclofen. j.ejphar.2020.173437
F-phenibut suppressed action potential generation in Purkinje cells, consistent with its CNS depressant profile.supported
F-phenibut suppresses action potential generation in Purkinje cells. j.ejphar.2020.173437
R-phenibut binds the α₂-δ subunit with Ki = 23 µM, approximately 4 times higher affinity than its GABA-B binding (Ki = 92 µM), and the anti-nociceptive effects of R-phenibut are mediated via α₂-δ rather than GABA-B, as demonstrated by insensitivity to the GABA-B antagonist CGP35348supported
Binding affinities for α2-δ subunit: R-phenibut Ki=23 µM. R-phenibut α2-δ affinity is 4x higher than GABA-B affinity. Anti-nociceptive effects mediated via α2-δ, not GABA-B. j.pbb.2015.07.014
Phenibut also stimulates dopamine receptors and antagonizes β-phenethylamine (PEA), a putative endogenous anxiogenicsupported
Also stimulates dopamine receptors and antagonizes β-phenethylamine (PEA). pmid:11830761
Phenibut exhibits minor GABA-A activity at very high concentrations, but this is not expected to be clinically significant for F-phenibut at doses producing GABA-B-mediated effects.supported
Phenibut acts as GABA-B agonist and has high affinity at alpha-2-delta subunit calcium channels (gabapentinoid activity), plus minor GABA-A activity. jcp.0000000000001759
Phenibut exhibits oral bioavailability of approximately 65%, with maximal brain concentrations reached within approximately 15 minutes of administration in mice (R-phenibut data)partially supported
Elimination t1/2 5-6h, bioavailability ~65%, excreted unchanged. arztebl.m2024.0003
Phenibut exhibits oral bioavailability of approximately 65%, with maximal brain concentrations reached within approximately 15 minutes of administration in mice (R-phenibut data)supported
R-phenibut reaches brain tissue 15 min after i.p./p.o. CNS penetration data. 9364598
The elimination half-life is approximately 5–6 hourssupported
Elimination t1/2 5-6h, bioavailability ~65%, excreted unchanged. arztebl.m2024.0003
Hepatic metabolism is virtually absent — phenibut is excreted largely unchanged in urine — and CYP enzyme involvement has not been established.supported
Elimination t1/2 5-6h, bioavailability ~65%, excreted unchanged. arztebl.m2024.0003
neuroscience10 · 7 ok
Baclofen reduces the rewarding properties of alcohol and stimulants, yet phenibut-class compounds themselves carry significant dependence liability — suggesting that negative reinforcement (escape from baseline anxiety, relief from inter-dose withdrawal) drives compulsive use more powerfully than positive hedonic reward.supported
GABA-B receptor activation (primarily via baclofen) reduces stimulating/rewarding effects of alcohol, signs of alcohol withdrawal, alcohol drinking, motivational properties of alcohol, and alcohol-seeking. 7854_2020_178
Claim in neuroscience — inconclusiveinconclusiveworking →
Activation of presynaptic GABA-B heteroreceptors inhibits neurotransmitter release (glutamate, monoamines, GABA itself) via inactivation of voltage-gated Ca²⁺ channels, while postsynaptic GABA-B receptors hyperpolarize neurons through activation of K⁺ conductances.supported
Activate inwardly rectifying K+ channels, inactivate voltage-gated Ca2+ channels, inhibit adenylate cyclase. pjab.94.026
In cerebellar Purkinje cells specifically, F-phenibut activates an outward-rectifying K⁺ current rather than the conventional GIRK-mediated inward rectificationsupported
Current is outward-rectifying, insensitive to Ba2+, Cs+, TEA-Cl. j.ejphar.2020.173437
The putative α₂-δ VDCC subunit binding (inferred from phenibut data) would add a gabapentinoid component — reduction of excitatory neurotransmitter release through presynaptic Ca²⁺ channel modulation — that could contribute to anxiolysis, anti-nociception, and the subjective warmth reported by users.supported
R-phenibut binds to the α2-δ subunit of voltage-dependent calcium channels and exerts gabapentin-like anti-nociceptive effects. Anti-nociceptive effects mediated via α2-δ, not GABA-B. j.pbb.2015.07.014
If dopaminergic activity analogous to phenibut's is present, mesolimbic dopamine pathway facilitation could explain the mood elevation and motivation enhancement reported at lower doses, as well as the compulsive redosing potential.supported
Also stimulates dopamine receptors and antagonizes β-phenethylamine (PEA). pmid:11830761
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
Is the outward-rectifying K⁺ current observed in Purkinje cells present in other brain regions, or is it cerebellar-specific? If widespread, it represents a novel GABA-B effector pathway with implications for the entire compound class.supported
Current is outward-rectifying, insensitive to Ba2+, Cs+, TEA-Cl. F-phenibut suppresses action potential generation in Purkinje cells. j.ejphar.2020.173437
Does F-phenibut produce neuroplasticity changes (BDNF upregulation, synaptogenesis) at sub-sedating doses, as suggested by phenibut's nootropic effects in animal models?supported
Aryl GABA analogs (phenibut, baclofen, tolibut) show nootropic activity. Structure-activity comparison of the chemical series. s10517-016-3198-4
summary9 · 7 ok
With an EC₅₀ of 23.3 µM at GABA-B — approximately 58 times more potent than phenibut and 4 times less potent than baclofen — F-phenibut occupies an intermediate position in the halogenated β-phenyl-GABA seriessupported
EC50 for GABA-B-mediated outward K+ current in Purkinje cells: phenibut 1362 µM, F-phenibut 23.3 µM, baclofen 6.0 µM. F-phenibut ~58x more potent than phenibut, ~4x less potent than baclofen. j.ejphar.2020.173437
Claim in summary — inconclusiveinconclusiveworking →
Population-level use has been confirmed through detection in Australian wastewater surveys.supported
4F-phenibut detected across 57 catchments alongside phenibut. Detection frequency ranged 3–100% of sites analyzed. j.scitotenv.2024.170473
F-phenibut activates GABA-B receptors (EC₅₀ = 23.3 µM), triggering downstream Gαi/o-mediated inhibition of voltage-gated Ca²⁺ channels and activation of K⁺ conductancespartially supported
EC50 for GABA-B-mediated outward K+ current in Purkinje cells: F-phenibut 23.3 µM. Current is outward-rectifying, insensitive to Ba2+, Cs+, TEA-Cl. j.ejphar.2020.173437
F-phenibut activates GABA-B receptors (EC₅₀ = 23.3 µM), triggering downstream Gαi/o-mediated inhibition of voltage-gated Ca²⁺ channels and activation of K⁺ conductancessupported
GABA-B receptors are GPCRs mediating slow inhibitory action via Gai/o. Activate inwardly rectifying K+ channels, inactivate voltage-gated Ca2+ channels. pjab.94.026
By structural analogy with phenibut, additional binding at the α₂-δ subunit of voltage-dependent calcium channels is expected but has not been directly measured.supported
Binding affinities for α2-δ subunit: R-phenibut Ki=23 µM, S-phenibut Ki=39 µM, baclofen Ki=156 µM, gabapentin Ki=0.05 µM. j.pbb.2015.07.014
The primary acute hazard is its 58-fold potency increase over phenibut, creating substantial overdose risk when users miscalculate dose conversionssupported
F-phenibut ~58x more potent than phenibut, ~4x less potent than baclofen. j.ejphar.2020.173437
Claim in summary — inconclusiveinconclusiveworking →
Tolerance develops within days of continuous use, and physical dependence with a severe withdrawal syndrome — including psychomotor agitation, autonomic instability, psychosis, and seizures — is documented for the phenibut classsupported
Severe psychomotor agitation prominent. Neurologic and autonomic signs may mimic serotonin or neuroleptic malignant syndrome. bjbms.2018.4008
clinical-evidence7 · 7 ok
Published phenibut clinical data include a systematic literature review of toxicity and withdrawal encompassing multiple case reports, a comprehensive review of acute withdrawal, and individual case reports of dependence, polydependence with benzodiazepines, dissociative intoxication, and suspected brainstem involvement during severe intoxicationsupported
Systematic review of published articles evaluating phenibut toxicity and withdrawal cases to understand clinical presentations and treatments. adm.0000000000001141
Published phenibut clinical data include a systematic literature review of toxicity and withdrawal encompassing multiple case reports, a comprehensive review of acute withdrawal, and individual case reports of dependence, polydependence with benzodiazepines, dissociative intoxication, and suspected brainstem involvement during severe intoxicationsupported
Review of 22 published phenibut withdrawal cases. Severe psychomotor agitation prominent. bjbms.2018.4008
Published phenibut clinical data include a systematic literature review of toxicity and withdrawal encompassing multiple case reports, a comprehensive review of acute withdrawal, and individual case reports of dependence, polydependence with benzodiazepines, dissociative intoxication, and suspected brainstem involvement during severe intoxicationsupported
Case of phenibut dependence for self-medication of anxiety, insomnia, and alcohol cravings. bcr-2012-008381
Published phenibut clinical data include a systematic literature review of toxicity and withdrawal encompassing multiple case reports, a comprehensive review of acute withdrawal, and individual case reports of dependence, polydependence with benzodiazepines, dissociative intoxication, and suspected brainstem involvement during severe intoxicationsupported
Case of comorbid phenibut and benzodiazepine dependence managed by baclofen tapering. jcp.0000000000001104
Published phenibut clinical data include a systematic literature review of toxicity and withdrawal encompassing multiple case reports, a comprehensive review of acute withdrawal, and individual case reports of dependence, polydependence with benzodiazepines, dissociative intoxication, and suspected brainstem involvement during severe intoxicationsupported
Case report of dissociative intoxication and prolonged withdrawal associated with phenibut. jcp.0000000000000731
Published phenibut clinical data include a systematic literature review of toxicity and withdrawal encompassing multiple case reports, a comprehensive review of acute withdrawal, and individual case reports of dependence, polydependence with benzodiazepines, dissociative intoxication, and suspected brainstem involvement during severe intoxicationsupported
Unconscious patient with brainstem areflexia after phenibut ingestion; ICU admission. v07250573
The sole primary pharmacology study — Irie et al. (2020) — was an in vitro electrophysiology investigation in mouse cerebellar Purkinje cells, not a clinical or whole-animal efficacy study.supported
EC50 for GABA-B-mediated outward K+ current in Purkinje cells: phenibut 1362 µM, F-phenibut 23.3 µM, baclofen 6.0 µM. j.ejphar.2020.173437
chemistry5 · 4 ok
The defining structural feature is a fluorine atom at the para position of the phenyl ring, placing F-phenibut in a halogen series between the unsubstituted phenibut and the para-chloro-substituted baclofen (β-(4-chlorophenyl)-GABA)supported
Discusses structure-activity relationship of phenibut and derivatives including baclofen. pmid:11830761
The defining structural feature is a fluorine atom at the para position of the phenyl ring, placing F-phenibut in a halogen series between the unsubstituted phenibut and the para-chloro-substituted baclofen (β-(4-chlorophenyl)-GABA)supported
Aryl GABA analogs (phenibut, baclofen, tolibut) show nootropic activity. Structure-activity comparison of the chemical series. s10517-016-3198-4
The electron-withdrawing fluorine enhances GABA-B receptor binding, consistent with the approximately 58-fold potency increase over unsubstituted phenibut.supported
F-phenibut ~58x more potent than phenibut, ~4x less potent than baclofen. j.ejphar.2020.173437
By analogy with phenibut, where the R-enantiomer carries essentially all GABA-B agonist activity and S-phenibut is inactive at GABA-B, and with baclofen, where R(+)-baclofen is the pharmacologically dominant enantiomer, the R-enantiomer of F-phenibut is expected to carry the majority of GABA-B activitysupported
GABA-B binding affinities: racemic phenibut Ki=177 uM, R-phenibut Ki=92 uM, baclofen Ki=6.0 uM. S-phenibut inactive. R-phenibut 2x more potent than racemic form. j.ejphar.2008.01.015
Claim in chemistry — not_supportednot supportedworking →
comparative-pharmacology4 · 4 ok
All EC₅₀ values derive from the same assay system (mouse cerebellar Purkinje cell K⁺ current).supported
EC50 for GABA-B-mediated outward K+ current in Purkinje cells: phenibut 1362 µM, F-phenibut 23.3 µM, baclofen 6.0 µM. j.ejphar.2020.173437
R-phenibut binds the α₂-δ VDCC subunit with Ki = 23 µM — far weaker than gabapentin (Ki = 0.05 µM) but sufficient to produce gabapentin-like anti-nociceptive effects in animal modelssupported
Binding affinities for α2-δ subunit: R-phenibut Ki=23 µM, gabapentin Ki=0.05 µM. Anti-nociceptive effects mediated via α2-δ, not GABA-B. j.pbb.2015.07.014
Unlike baclofen, which is used clinically as a skeletal muscle relaxant and is under investigation for alcohol use disorder, F-phenibut has no clinical applications and no regulatory pathwaysupported
Strong preclinical evidence for GABA-B as therapeutic target for AUD. 7854_2020_178
Unlike phenibut, which is available as a prescription medication in Russia and as an unregulated supplement in some Western markets, F-phenibut exists exclusively in the research chemical marketsupported
Historical review: phenibut discovered and introduced into clinical practice in Russia in the 1960s. pmid:11830761
history3 · 2 ok
The parent compound, phenibut, was discovered and introduced into clinical practice in the Soviet Union in the 1960s, where it gained widespread use as an anxiolytic and nootropic agentsupported
Historical review: phenibut discovered and introduced into clinical practice in Russia in the 1960s. pmid:11830761
F-phenibut became commercially available from online nootropic and research chemical vendors in the 2010s, marketed under names including "F-phenibut," "fluorophenibut," "fluorobut," and "4F-phenibut." Its presence in the general population was confirmed by a systematic wastewater-based epidemiology survey in Australia spanning February 2022 to February 2023, which detected 4-fluorophenibut alongside other novel psychoactive substances.supported
Wastewater-based epidemiology of NPS in Australia (Feb 2022–Feb 2023). 4F-phenibut detected across 57 catchments alongside phenibut. j.scitotenv.2024.170473
Claim in history — inconclusiveinconclusiveworking →
receptor-pharmacology3 · 2 ok
Irie et al. reported that the K⁺ current activated by F-phenibut, phenibut, and baclofen in cerebellar Purkinje cells is outward-rectifying — pharmacologically distinct from the inwardly rectifying K⁺ current (GIRK/Kir3) conventionally associated with GABA-B receptor activationsupported
Current is outward-rectifying, insensitive to Ba2+, Cs+, TEA-Cl. j.ejphar.2020.173437
By analogy with phenibut, where R-phenibut is approximately 2 times more potent than the racemate and S-phenibut is inactive at GABA-B, and with baclofen, where R(+)-baclofen is the active enantiomer, the pharmacological activity of racemic F-phenibut is expected to reside predominantly in the R-enantiomersupported
GABA-B binding affinities: racemic phenibut Ki=177 uM, R-phenibut Ki=92 uM. S-phenibut inactive. R-phenibut 2x more potent than racemic form. j.ejphar.2008.01.015
Claim in receptor-pharmacology — not_supportednot supportedworking →
pharmacokinetic-detail1 · 1 ok
Given the minimal hepatic metabolism of the phenibut class, CYP-mediated pharmacokinetic interactions with F-phenibut are not expectedsupported
Elimination t1/2 5-6h, bioavailability ~65%, excreted unchanged. arztebl.m2024.0003