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WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.
DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.
F-Phenibut (also known as 4-Fluorophenibut, Fluorophenibut, Fluorobut, Baflofen and CGP-11130) is a central nervous system depressant and closely related structural analog of phenibut. F-Phenibut possesses an effect profile similar to phenibut but with a faster onset, significantly increased potency, and shorter total duration.[citation needed] It has recently become available through online research chemical vendors, although little is known about this substance, particularly its potential toxicity and addiction potential.
The substance can be classified as a gabapentinoid, a class which contains other substances such as gabapentin, pregabalin[1], baclofen, and GABOB.[2][3] It is a derivative of the naturally occurring inhibitory neurotransmitter γ-aminobutyric acid (GABA), with an addition of a phenyl ring that allows it to cross the blood–brain barrier.[2]
As with phenibut, F-Phenibut is a derivative of GABA, except with a fluorine-substituted phenyl group in the β-position of the molecule. It is a chiral molecule and thus has two potential configurations as (R)- and (S)-enantiomers.[4] It has an almost identical chemical structure to baclofen (only replacing a chlorine with a fluorine atom in the para-position of the phenyl group).[5] Additionally, the widely prescribed gabapentinoid pregabalin also possesses a similar structure as phenibut, except that the phenyl group is instead replaced with an isobutyl group in the S configuration. F-Phenibut is water soluble.
Pharmacology
F-phenibut acts as a potent agonist of the GABA-B receptor and in this regard is more similar to baclofen than phenibut.[6]
It is also possible that F-Phenibut binds to the α2δ-1 site of voltage-gated calcium channels in a manner similar to that of other gabapentinoids. By binding to this site, F-Phenibut may reduce the release of several excitatory neurotransmitters, including glutamate, substance P, acetylcholine, and norepinephrine. This, in turn, increases GABAergic activity.[citation needed] As the GABA system is the most prevalent inhibitory receptor set within the brain[citation needed], its modulation may be responsible for the relaxing, sedating, and calming effects of F-Phenibut on the central nervous system.
Subjective effects
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWikicontributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.
In comparison to regular phenibut, this compound has a significantly faster onset, a shorter duration, and slightly less stimulation. Early reports suggest that in comparison to other commonly used GABAgenic depressants such as alcohol or benzodiazepines, this compound produces less inebriation and more euphoria, giving it more recreational potential as well as a correspondingly higher risk of abuse.
Physical effects
Stimulation and Sedation - At lower doses, F-Phenibut has a mild physical and mental stimulation effect, encouraging movement, wakefulness, productivity and socialization. At higher doses, however, it becomes physically sedating, encouraging sleep and lethargy. Sleeping after dosing a small amount may result in a deep, restful sleep which can leave the user feeling refreshed and alert upon waking.
Nausea - F-Phenibut can induce mild to extreme nausea depending greatly on dose and tolerance. It usually manifests roughly 90 minutes after the initial dose and generally involves waves of nausea accompanied by excessive sweating and vomiting.
Dehydration - Dehydration is typically reported to occur from regular multiday usage or excessive doses; however, it can also be present even in average doses of the substance (although perhaps to a lesser degree than phenibut).
Headaches - Moderate to high doses have been reported to induce a mild to strong headache, typically many hours after dosing or during the comedown period.
Muscle cramps - Muscle cramps and joint pain are sometimes accompanied at high doses.
The toxicity and long-term health effects of recreational F-Phenibut use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because F-Phenibut has very little history of human usage. Anecdotal evidence from people who have tried this substance within the community suggests that there do not seem to be any negative health effects attributed to simply trying this substance at low to moderate doses by itself and using it sparingly (but nothing can be completely guaranteed).
F-Phenibut is moderately physically and psychologically addictive, although this usually only occurs with heavy abuse of the substance. This is likely even more so than its predecessor phenibut since its more rapid onset allows more convenient compulsive redosing.
Tolerance will develop to the sedative-hypnotic effects within a couple of days of continuous use. After cessation, the tolerance returns to baseline in 7 - 14 days. Withdrawal symptoms or rebound symptoms may occur after ceasing usage abruptly following a few weeks or longer of steady dosing and may necessitate a gradual dose reduction.
F-Phenibut presents cross-tolerance with [[Cross-tolerance::all GABAgenic depressants]], meaning that after its consumption most depressants will have a reduced effect.
Dangerous interactions
Warning:Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
Dissociatives - This combination can unpredictably potentiate the amnesia, sedation, motor control loss and delusions that can be caused by each other. It may also result in a sudden loss of consciousness accompanied by a dangerous degree of respiratory depression. If nausea or vomiting occurs before consciousness is lost, users should attempt to fall asleep in the recovery position or have a friend move them into it.
Stimulants - Stimulants mask the sedative effect of depressants, which is the main factor most people use to gauge their level of intoxication. Once the stimulant effects wear off, the effects of the depressant will significantly increase, leading to intensified disinhibition, motor control loss, and dangerous black-out states. This combination can also potentially result in severe dehydration if one's fluid intake is not closely monitored. If choosing to combine these substances, one should strictly limit themselves to a pre-set schedule of dosing only a certain amount per hour until a maximum threshold has been reached.
As such, it may contain incomplete or wrong information. You can help by expanding it.
Germany: F-Phenibut is not a controlled substance under the BtMG.[8] It is legal, as long as it is not sold for human consumption, according to §2 AMG.[9]
Switzerland: F-Phenibut is not controlled under Buchstabe A, B, C and D. It could be considered legal.[10]
United Kingdom: It may be illegal to produce, supply, or import this substance under the Psychoactive Substance Act 2016, which blanketly applies the aforementioned restrictions on all "psychoactive substances" with exemptions for alcohol, nicotine and "medicinal products."[11]
↑Wyllie, E., Cascino, G. D., Gidal, B. E., Goodkin, H. P. (17 February 2012). Wyllie’s Treatment of Epilepsy: Principles and Practice. Lippincott Williams & Wilkins. ISBN9781451153484.
↑Benzon, H., Rathmell, J. P., Wu, C. L., Turk, D., Argoff, C. E., Hurley, R. W. (11 September 2013). Practical Management of Pain E-Book. Elsevier Health Sciences. ISBN9780323170802.
↑Dambrova, M., Zvejniece, L., Liepinsh, E., Cirule, H., Zharkova, O., Veinberg, G., Kalvinsh, I. (31 March 2008). "Comparative pharmacological activity of optical isomers of phenibut". European Journal of Pharmacology. 583 (1): 128–134. doi:10.1016/j.ejphar.2008.01.015. ISSN0014-2999.
↑Shulgina, G. I. (December 1986). "On neurotransmitter mechanisms of reinforcement and internal inhibition". The Pavlovian Journal of Biological Science. 21 (4): 129–140. doi:10.1007/BF02734511. ISSN0093-2213.
