Phenylpiracetam

Phenotropil

Phenylpiracetam (Phenotropil) is a cognitive & mood research compound. Phenylated racetam — modulates acetylcholine and NMDA plus a dopaminergic/stimulant edge; also improves physical performance and cold tolerance.

How Phenylpiracetam works

Phenylated racetam — modulates acetylcholine and NMDA plus a dopaminergic/stimulant edge; also improves physical performance and cold tolerance.

Proposed benefits

Researched for focus, memory, neuroprotection, mood and stress resilience.

Where to get Phenylpiracetam

Phenylpiracetam is sold in 2 forms. They are not interchangeable — the dose and the route differ, so pick the one this page describes unless you know why you want another.

The evidence for Phenylpiracetam

Graded by what exists behind each claim.

Human clinical evidence

• The human record is Soviet and post-Soviet clinical work — real patients and real endpoints, published in Russian and rarely replicated to Western standards.

📊 Correlative data

• Registered in Russia as Phenotropil, with domestic trials in stroke recovery, epilepsy and asthenia. Banned by WADA since 2010 after use by athletes including at the Olympics.
• Reported experience is the most stimulant-like of the racetam family, with tolerance building fast — within days to a couple of weeks — which is the most consistent complaint about it.

🧪 Theoretical / extrapolated

• Piracetam with a phenyl group added, which greatly increases lipophilicity and blood-brain-barrier penetration — hence far greater potency at far smaller doses.
• The phenyl group also gives it structural similarity to phenethylamine stimulants, and it appears to act on dopamine and noradrenaline transporters in a way plain piracetam does not. That is the mechanism behind both the stimulant feel and the rapid tolerance.

How to read the Soviet clinical series →

How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →

What Phenylpiracetam actually does

The phenyl ring did two things, and the second one has never made it onto a nootropic page. Phenylpiracetam is N-carbamoylmethyl-4-aryl-2-pyrrolidone, also called carphedon Zvejniece 2011: piracetam with a phenyl group on carbon 4 of the ring. The famous consequence is lipophilicity — a benzene ring bolted onto a small polar amide crosses membranes far better, which is why the dose is 100–200 mg where piracetam's is measured in grams. The unadvertised consequence is that carbon 4 now carries four different groups. It is a stereocentre, and what is sold is a 50:50 mixture of two molecules that do not do the same things.

The separation experiment, in mice, with doses. Open field: R-phenotropil raised locomotor activity at 10 and 50 mg/kg, S-phenotropil only at 50 mg/kg. Forced swim: R at 50 and 100, S at 100. Passive avoidance — the memory task — R significantly enhanced retention at 1 mg/kg, and the S-enantiomer showed no activity at all. Brain concentrations of the two, measured by UPLC/MS/MS, were similar, so this is a pharmacology difference and not a distribution one. The authors' conclusion: memory-improving activity uniquely characterizes R-phenotropil Zvejniece 2011.

Now the transporter, which is where the standard story falls apart. S-phenylpiracetam is characterized as a selective dopamine transporter inhibitor, without effects on norepinephrine or serotonin receptors — and in obese Zucker rats and Western-diet mice dosed perorally every day for 12 and 8 weeks respectively, it did not influence locomotor activity in either model Zvejniece 2017. R-phenylpiracetam is likewise described as a DAT inhibitor by the same group Zvejniece 2020. So both halves of the racemate engage DAT, and the half whose DAT pharmacology is the cleanest is the half with no memory effect and no locomotor effect.

This site's own theoretical tier says the transporter action is ‘the mechanism behind both the stimulant feel and the rapid tolerance’. The enantiomer data say otherwise on both counts. DAT inhibition sits on the enantiomer that does not stimulate; locomotor activation appears at 10–50 mg/kg while the memory effect appears at 1 mg/kg Zvejniece 2011, a ten- to fiftyfold separation between the dose that works and the dose you feel. The honest mechanistic statement is that phenylpiracetam is a dopamine transporter ligand whose subjective stimulation is a high-dose, acute phenomenon rather than a transporter one — and that half of every capsule is an enantiomer with no demonstrated cognitive activity.

Cell, rodent, human — and where it stops

There is no cell rung here either, and the rodent rung is unusually well specified.

Mice, acute, single enantiomers. Open field, forced swim and passive avoidance at 1, 10, 50 and 100 mg/kg, with brain concentrations measured alongside behavior Zvejniece 2011. This is a better-designed rodent package than most compounds on this site get, and it is the source of every number in the section above.

Rodents, chronic, one enantiomer. Western-diet-fed mice for 8 weeks and obese Zucker rats for 12 weeks, S-phenylpiracetam given perorally, daily. Body weight gain and fat mass increase both fell; plasma glucose and leptin fell; hyperglycemia during a glucose tolerance test was reduced in both species; locomotor activity was unchanged Zvejniece 2017. Mice again, R-phenylpiracetam at 50 mg/kg in lipopolysaccharide, carrageenan and formalin models: attenuated the LPS-induced fall in body temperature and reduced TNF-alpha, IL-1beta and iNOS Zvejniece 2020.

Human, and this is where the page has to be blunt. The clinical record for this compound is Soviet and post-Soviet, published in Russian under the trade name Phenotropil. Nothing in it resolved to a PubMed-indexed randomized controlled trial that could be opened and checked while this page was written, and no page should imply otherwise. What is documented in the international literature is its circulation as a cognitive enhancer outside medical supply Napoletano 2020 and its interception by medicines control laboratories as bulk raw material Vanhee 2025. The human tier of this compound is reputation, not published trial data.

The obstacles. (1) Every behavioral number above is a mouse given an acute dose in an anxiety or shock paradigm, or a metabolically diseased rodent dosed for months. Neither is a healthy adult taking 100 mg before a training session. (2) The dose translation, which is extrapolation and is labeled as such. Convert mouse to human by the conventional body-surface-area factor of about 12.3: the 1 mg/kg memory dose becomes roughly 0.08 mg/kg, about 6 mg for a 70 kg person, and the 50 mg/kg locomotor dose becomes about 285 mg. This site's 100–200 mg sits between them and much nearer the stimulant end. That arithmetic is crude — allometric scaling is a rule of thumb, not a measurement — but it is the only bridge that exists between the rodent doses and the capsule, and it points the same way as the tolerance reports. (3) The racemate problem: even if the mouse numbers transferred exactly, a 200 mg capsule delivers 100 mg of the enantiomer with memory activity and 100 mg of the one without Zvejniece 2011.

Phenylpiracetam pharmacokinetics — how much of it actually gets in

Start with the honest gap: there is no human pharmacokinetic study of phenylpiracetam that could be resolved against NCBI for this page. No half-life, no AUC, no Cmax, no urinary excretion profile. The ‘~3–5 hrs’ on this site's card has no primary source this writer could find, and it is repeated across the internet without one. For a compound that is on the WADA Prohibited List and that people are tested for, that absence is not an academic problem — it is the reason nobody can tell an athlete when they are clear.

What has been measured, and it is a brain concentration, which is rare. R-phenylpiracetam at 50 mg/kg reached brain tissue within 15 minutes after both intraperitoneal and peroral dosing, with maximum brain concentrations of 28 micrograms per gram of tissue after injection and 18 micrograms per gram after mouth Zvejniece 2020. Do the division: oral delivers about 64% of the brain exposure that bypassing the gut and liver delivers. That is the oral-barrier number for this molecule, it is unusually good for an orally dosed compound, and it is the quantitative form of the claim that the phenyl ring buys blood-brain-barrier penetration.

What degrades it. The side chain is a primary carboxamide on a lactam nitrogen's neighbor, not an ester, so plasma carboxylesterases have nothing to open — which distinguishes its disposal from the ester nootropics and predicts that gut and blood hydrolysis is not the rate-limiting step. The structural feature that is new relative to piracetam is the aromatic ring, and an unsubstituted phenyl is the classic substrate for cytochrome P450 aromatic hydroxylation followed by conjugation. That is inference from structure, flagged as such: no published human metabolite identification for this compound was resolvable for this page. The consequence, if it is right, is that the between-person variable is hepatic oxidative capacity rather than renal filtration — the opposite of oxiracetam, whose dose leaves unchanged in urine.

The variable nobody has looked at: enantioselective clearance. Brain concentrations of R and S were similar after dosing Zvejniece 2011, which rules out a distribution difference. It does not rule out a clearance difference, and if the two enantiomers are cleared at different rates then the 50:50 ratio in the capsule is not the ratio in your plasma four hours later. Nobody has measured it in any species. Route: oral in the trials and in this site's protocol; a nasal form is also listed and has no pharmacokinetic data of any kind.

What would have to be true, and how you would know it was not

Four predictions. The first has a consequence measured in suspensions rather than in points on a test.

1. An in-competition urine sample will test positive. Phenylpiracetam has been prohibited by WADA since 2010 and the assay looks for carphedon. Prediction: a competing athlete taking this in the week before an event returns an adverse analytical finding. This is the one prediction on this page that does not need a lab of your own to test, and it is the one this compound's reputation as a ‘training aid’ systematically buries.

2. The prediction nobody makes: HbA1c and fasting insulin should fall. S-phenylpiracetam over 8 to 12 weeks of daily oral dosing lowered plasma glucose, lowered leptin, blunted body weight and fat mass gain, and improved glucose tolerance in two rodent species Zvejniece 2017, and half of every racemic capsule is that enantiomer. So: HbA1c and fasting insulin at baseline and at 12 weeks, with body weight logged weekly and diet held as constant as you can manage. A fall would be the first human evidence of a metabolic effect for this compound. No change would locate the rodent result as species-specific or dose-specific, which is also worth knowing.

3. Against, and it is the sharpest test on this page: the ‘buzz’ and the mechanism should come apart. The universal complaint is that the stimulation fades within days to a couple of weeks. If that stimulation were dopamine transporter occupancy, the transporter pharmacology should fade with it. But the cleanest DAT-inhibiting enantiomer produced no locomotor activation at all across 8 to 12 weeks Zvejniece 2017. Prediction: after the subjective stimulation has gone, the metabolic effects in prediction 2 should still be running. Keep dosing, keep weighing, and redraw at 12 weeks. If weight and glucose keep responding after the buzz has stopped, tolerance is to the feeling and not to the drug — which would mean the near-universal advice to cycle hard is aimed at the wrong endpoint.

4. Against the cognitive claim: Trail Making will not move. The memory evidence is passive avoidance in a mouse at 1 mg/kg Zvejniece 2011 — a shock-avoidance latency, not a working-memory score, in an animal, at a dose that scales to single-digit milligrams in a person. Trail Making A and B at baseline and 4 weeks. Prediction: nothing beyond practice, and a strong subjective conviction that something happened, which is exactly the dissociation a stimulant produces.

What nobody has tested yet

Five experiments. Two of them are things an anti-doping laboratory could answer next week.

1. There is no published human washout curve, and athletes need one. This is a banned substance whose detection window has no accessible published estimate. A single-dose excretion study in ten subjects with serial urine collection is the most routine study design in sports pharmacology, and for one of the most-used prohibited nootropics in amateur sport it does not exist in the searchable literature. Until it does, ‘stop two weeks out’ is folklore with a career attached to it.

2. Nobody has asked whether the doping assay sees enantiomers at all. The test detects carphedon. If a single-enantiomer product appeared tomorrow — and both enantiomers have been made and characterized Zvejniece 2011 Zvejniece 2017 — a routine assay would report it identically. That is a live question for both sides of anti-doping and nobody in the nootropic literature has raised it.

3. No human has taken either single enantiomer in a published study. Both exist, both are characterized in rodents, and a crossover of R against S against racemate in healthy adults with a sustained-attention task and an actigraphy sleep endpoint would settle in six weeks which half of the capsule anybody is actually responding to.

4. The metabolic finding has never been taken to a person. Eight to twelve weeks, two species, fat mass, glucose, leptin, glucose tolerance Zvejniece 2017. The human version is a 12-week randomized trial with DEXA body composition and an oral glucose tolerance test. Thousands of people already take this compound daily and not one of them has been measured on the endpoint where the rodent data are strongest.

5. Tolerance has never been measured, only reported. The most consistent thing anyone says about this compound is that it stops working within days to weeks, and there is not one repeated-measures study of it. Daily reaction time and a fixed-time sustained-attention task for 21 days at a constant dose would produce the tolerance curve that the whole cycling protocol is built on and that nobody has ever drawn.

Phenylpiracetam — its own safety story, not its class's

The class block warns about stimulants generally. For this compound the specific hazards are a doping ban with no washout data, a racemate nobody assays, and a tolerance story pointed at the wrong endpoint.

1. It is prohibited in sport, and this is the part of the page an athlete should read twice. Phenylpiracetam has been on the WADA Prohibited List since 2010, banned in competition as a stimulant, after use by athletes including at the Olympics. A capsule taken as a training aid is not a different molecule from a capsule taken on competition day. The Prohibited List is revised annually, so check the current one rather than this paragraph — but the direction of travel for this substance has been one way for fifteen years.

2. The compounding problem is that nobody can tell you when you are clear. Because no human excretion study is published, the interval between a last dose and a clean sample is unknown, and the ‘~3–5 hrs’ half-life circulating online has no primary source. Detection windows routinely run many multiples of a half-life. An athlete calculating a stopping date from an unsourced number is performing arithmetic on a rumor.

3. Half of what you take has no demonstrated cognitive activity. The S-enantiomer had no effect in the memory task at any dose Zvejniece 2011. It is not inert — it is a selective dopamine transporter inhibitor with real metabolic effects Zvejniece 2017 — so the correct statement is not that half the capsule is wasted but that half the capsule is a different drug with a different action, unlabelled and unmeasured. No certificate of analysis reports the enantiomeric ratio, and mass spectrometry cannot distinguish mirror images.

4. The tolerance advice may be aimed at the wrong thing. Cycling hard is sound advice for a stimulant. If prediction 3 above is right and the transporter pharmacology persists while the subjective stimulation does not, then cycling protects the feeling and interrupts the effect. Nobody has tested this, and it is stated here as a consequence of the enantiomer data rather than as a recommendation.

5. Supply. Medicines control laboratories in Europe and Australia intercepted racetam-family compounds including phenylpiracetam as bulk raw material across 159 samples containing 34 distinct unauthorized molecules Vanhee 2025, and the compound is documented circulating in the online cognitive-enhancer market Napoletano 2020. At 100–200 mg the dose is small enough that a quantity error matters and large enough that it will not be obvious.

Sources read for this page

• Zvejniece L, Svalbe B, Veinberg G, Grinberga S, Vorona M, Kalvinsh I, Dambrova M. Investigation into stereoselective pharmacological activity of phenotropil. Basic & Clinical Pharmacology & Toxicology 2011;109(5):407-412 · PMID 21689376
• Zvejniece L, Svalbe B, Vavers E, Makrecka-Kuka M, Makarova E, Liepins V, Kalvinsh I, Liepinsh E, Dambrova M. S-phenylpiracetam, a selective DAT inhibitor, reduces body weight gain without influencing locomotor activity. Pharmacology Biochemistry and Behavior 2017;160:21-29 · PMID 28743458
• Zvejniece L, Zvejniece B, Videja M, Stelfa G, Vavers E, Grinberga S, Svalbe B, Dambrova M. Neuroprotective and anti-inflammatory activity of DAT inhibitor R-phenylpiracetam in experimental models of inflammation in male mice. Inflammopharmacology 2020;28(5):1283-1292 · PMID 32279140
• Vanhee C, Deconinck E, George M, Hansen A, Hackl A, Wollein U, El-Atma O, Beerbaum N, Aureli F, Borioni A, et al. The Occurrence of Illicit Smart Drugs or Nootropics in Europe and Australia and Their Associated Dangers: Results from a Market Surveillance Study by 12 Official Medicines Control Laboratories. Journal of Xenobiotics 2025;15(3):88 · PMID 40558871
• Napoletano F, Schifano F, Corkery JM, Guirguis A, Arillotta D, Zangani C, Vento A. The Psychonauts' World of Cognitive Enhancers. Frontiers in Psychiatry 2020;11:546796 · PMID 33024436

Phenylpiracetam — safety, predicted from mechanism

Phenylpiracetam — interference & stacking

Bloodwork to run alongside Phenylpiracetam

Baseline first, then again at 8–12 weeks.

The Brain Fog & Cognition panel covers these in one order — 12 markers, $233.06 with the discount applied.

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Phenylpiracetam — frequently asked questions

Phenylpiracetam inside a finished plan

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What Phenylpiracetam is used for

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