A reference work, not a recommendation to use: this profile describes mechanism and evidence and does not replace medical advice. The claims come from marketing and forums and are tested here, not endorsed. Manufacture, possession, trade or use may be prohibited; see “Legal status” for details.

Mechanism of action

Evidence map: Phenylpiracetam

Each line stands for a published finding; line style and color show where it comes from. The filter hides weaker evidence levels. Sources: see references.

Phenylpiracetam is a phenyl analogue of piracetam; the first pharmacological description appeared in 1983 in a Soviet journal. In it, it activated operant behavior in animals more strongly than piracetam, abolished the sedative effect of diazepam, and, unlike piracetam, acted as an anticonvulsant; at high doses, however, it was sedating [1]. The substance has one stereocenter and is marketed as a racemate. In mice, both enantiomers increased locomotor activity and acted as antidepressants in the swim test, but only the R form improved memory performance in the passive avoidance test, although both reached the brain to the same extent [2].

The dopamine transporter is regarded as the molecular target: S-phenylpiracetam is described as a selective inhibitor of the dopamine transporter with no influence on noradrenaline and serotonin receptors; in overweight rodents, it reduced weight gain over weeks without increasing locomotor activity [3]. For R-phenylpiracetam, the dopamine transporter was the only significant target in a radioligand screen; in mice, it dampened inflammation-related genes in the brain after endotoxin administration [4]. At AMPA, NMDA, and metabotropic glutamate receptors, phenylpiracetam did not change ligand binding [5]. In mice with poor exploratory behavior, BDNF in the hippocampus rose slightly [6].

A review describes phenylpiracetam as more potent than piracetam and with a broader range of uses [7]. The clinical studies come almost exclusively from Russia and are nonrandomized: in rehabilitation after stroke, treated patients recovered better than a comparison group [8], in an uncontrolled study after brain damage, motor function and memory improved [9], and a Russian meta-analysis summarizes before-and-after comparisons in asthenia [10].

Synaptik serves solely to explain biochemistry and pharmacology and is not medical advice or a recommendation to take anything.

Mechanism of action only. Schematic cross-section of a striatal dopaminergic synapse with a neighbouring noradrenergic terminal, plus an inset with a serotonergic terminal on the left; not to scale. Particle numbers, speeds and the bars of the live readout come from an illustrative model, not from measurements. Only for methylphenidate and modafinil does the share of blocked dopamine transporters (6 and 5 of 10) match a rounded PET occupancy, from two different studies; all other shares are illustrative.

DAT: blocked by phenylpiracetam (share illustrative) · lab and animal data only

DAT
inhibitedscreening, cells and animals
NET
not shown
SERT
not shown
synthesis (TH, AADC)
unchanged
dopamine in the cleft (model)
slightly moreinferred, not measured
Drug
View

dopamine  noradrenaline  serotonin  cAMP  drug  cross = transporter blocked

Phenylpiracetam is a racemate. The S-enantiomer is described as a selective DAT inhibitor without effects on noradrenaline or serotonin receptors [22]; for the R-enantiomer, DAT was the only significant target in a radioligand screen [23]. In the profile's sources, dopamine was measured only for the R-enantiomer (rats) [24]. The direction (“slightly more”) and the share of blocked transporters are inferred here from DAT inhibition and are illustrative.

Tap or focus a labelled part for a short explanation.

Also acting here, not drawn

  • Flmodafinil: DAT inhibition only from unpublished commissioned data (evidence level 0)
  • Saffron: at SERT only a computer simulation (docking), no measured binding or inhibition

What the figure shows, and how sure we are

Mechanism-of-action explainer only. Not medical advice, and no statement about benefit, risk, amount or use; each profile gives the legal status.

What was simplified. One terminal and one cleft stand for a striatal dopamine synapse; sizes, cleft width, numbers of vesicles, transporters and receptors, and all speeds are illustrative. Drugs are drawn on the outside of the transporter, not at their binding sites. The positions of TH, AADC and COMT are schematic. The occupancy values for methylphenidate and modafinil come from two studies with different amounts, brain regions and participants and are not directly comparable; the values for the other drugs come from cells, synaptosomes or animal studies. The numbers in [14] to [28] are in the Synaptik profiles of the drugs, where they were checked against the abstracts; [1] to [13] and [29] were checked on PubMed for this figure (26 Oct 2026), [2] bibliographically only.

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Assigned to the site of action NMDA receptor (GluN1/GluN2B) in the postsynaptic membrane of a dendritic spine; not drawn in its figure: no displacement of ligands at NMDA receptors.

Targets

TargetTypeActionKey dataEvidence
Dopamine transporter (DAT)TransporterInhibitoronly significant target in the radioligand screen (R enantiomer); S enantiomer described as selective Laboratory[3][4]
AMPA, NMDA, and metabotropic glutamate receptorsReceptorBindingno ligand displacement at 10⁻¹⁰–10⁻⁴ M (rat brain) Laboratory[5]

Effect profile

Which signaling systems the compound affects according to current data. ↑ enhanced, ↓ dampened, ≈ modulated, ○ no effect; dots = evidence level.

  • Dopaminemodulated · inhibits the dopamine transporter (binding studies); brain dopamine levels not measured in the sources checked[3][4]
  • Noradrenalineno data
  • Serotoninno data
  • Acetylcholineno data
  • Glutamate · AMPAno data
  • Glutamate · NMDAno data
  • GABAno data
  • Histamineno data
  • Orexinno data
  • Adenosineno data
  • Opioidsno data
  • Melatoninno data
  • Neurotrophins↑ · slight BDNF increase in the hippocampus of mice with poor exploratory behavior[6]
  • Blood flowno data
  • Nitric oxideno data
  • Energy metabolismmodulated · S enantiomer lowered weight gain, glucose, and leptin in overweight rodents[3]
  • Insulin · glucoseno data
  • Inflammation · oxidative↓ · R enantiomer dampened inflammation genes in the brain after endotoxin (mouse)[4]
  • Stress axisno data
  • Testosterone axisno data
  • Endocannabinoidsno data
  • Autophagy · senescenceno data
  • Immune systemno data
  • Lipid metabolismno data
  • Coagulation · fibrinolysisno data
  • Methylationno data

Human studies

  • Rehabilitation after stroke

    controlled, randomization not described · Patients: after ischemic stroke · n = 400 · 1 year, three treatment cycles

    Measured: Barthel Index and further functional scales

    Result: Better recovery of neurological functions and daily activities than in the comparison group.[8]

    Human, non-randomised

  • Consequences of organic brain damage

    open-label, without a control group · Patients: encephalopathy after stroke, brain trauma, or glioma surgery · n = 99 · 1 month

    Measured: motor function, cognitive functions, EEG

    Result: Improvement of paralysis, coordination, memory, and attention reported.[9]

    Human, non-randomised

  • Meta-analysis in asthenia

    meta-analysis of before-and-after comparisons · Patients: asthenia · n = 549 · 1 month

    Measured: fatigue scale MFI-20

    Result: Fatigue score fell by a mean of 16.3 points (95% CI 8.85–23.85); side effects in 5.5%.[10]

    Human, non-randomised

Risks and warnings

  • Sedation at high doses

    In the first animal study, phenylpiracetam had a mentally sedating effect at high doses [1].

    Animal study

  • Side effects in uncontrolled studies

    In the Russian meta-analysis on asthenia, side effects occurred in 5.5%, and they were transient [10]; without a control group, the proportion cannot be put into context.

    Human, non-randomised

  • Uncontrolled products

    Bulk quantities of raw material with nearly 100% purity were seized in Europe; the substance is sold as a dietary supplement or raw powder without quality control [11].

    No data

Fact check: common claims

  • not supported

    “Phenylpiracetam increases concentration and performance in healthy people”

    No controlled study in healthy people; memory effects only in mice and only for the R enantiomer [2].

  • partly supported

    “Phenylpiracetam has a stimulating effect”

    More locomotor activity in mice [2] and inhibition of the dopamine transporter in the laboratory [3][4]; banned in sport as a stimulant [13]. Controlled data in humans are lacking.

  • partly supported

    “Phenylpiracetam is much stronger than piracetam”

    Stronger activation than piracetam in animal experiments [1]; a review calls it more effective [7]. Direct comparison studies in humans were not found.

  • partly supported

    “Phenylpiracetam helps against fatigue”

    Only before-and-after comparisons in asthenia without a placebo group [10]; a placebo effect cannot be ruled out this way.

Pharmacokinetics

Absorption
Not described in humans in the sources checked.
Half-life
Not described in humans in the sources checked.
Metabolism
Not described in the sources checked.
Entry into the brain
Both enantiomers reach the brain in similar amounts in mice [2]; R-phenylpiracetam was detectable in brain tissue 15 minutes after administration [4].

Legal status

Germany
No medicinal product for human use containing the active substance phenylpiracetam (fonturacetam) was found in AMIce, neither among the marketable entries nor among all entries, including lapsed ones (search by substance name “Phenylpiracetam”, “Fonturacetam”, and “Carphedon”, retrieved October 26, 2026; refusals and withdrawals are not included in the public part) [15]; no entry in AMVV Annex 1 [16]. Doping: the 2026 Prohibited List as published in the German Federal Law Gazette names “Fonturacetam [4-Phenylpiracetam (Carphedon)]” under S6.A (non-specified stimulants, prohibited in competition) [18]. Section 2(1) and (2) of the German Anti-Doping Act (AntiDopG) therefore applies: it is prohibited to manufacture doping substances containing this substance for the purpose of doping in sport in humans, to trade in them, to dispense them or otherwise place them on the market, to prescribe them, or to administer them to another person. Fonturacetam is not listed in the annex to the AntiDopG, to which the prohibition of acquisition and possession in non-small quantities is linked (Section 2(3)) [19]. The status under food law has not been verified.
EU
No centrally authorized or assessed medicinal product, no referral, and no orphan designation involving phenylpiracetam in the EMA data exports (timestamp October 25, 2026) [17]; national authorizations in other member states are not captured by the export. In a market surveillance study by official medicines control laboratories from Europe and Australia, phenylpiracetam was found once; the study classifies it as a piracetam homologue that has not been approved for human use by any health authority in the EU or Australia and is prescription-only in Russia (the study's assessment, not a legal source) [11].
USA
Not approved for human use [14].
Other countries
Russia: prescription-only medicinal product [11]. Sport: banned in 1998 as the first nootropic [12]; the 2026 Prohibited List as published in the German Federal Law Gazette names “Fonturacetam [4-Phenylpiracetam (Carphedon)]” under S6.A (non-specified stimulants) [13][18].

Related compounds

R-PhenylpiracetamR-enantiomer (German only)PiracetamanalogOxiracetamsame class (German only)Pramiracetamsame class (German only)Aniracetamsame class (German only)

Open questions

  • How strongly do the enantiomers inhibit the dopamine transporter in humans, and does this raise dopamine in the brain?
  • How does phenylpiracetam perform in a randomized, placebo-controlled study in healthy people?
  • How high is the abuse and dependence potential of a dopamine transporter inhibitor of this kind?

References

  1. Bobkov IuG, Morozov IS, Glozman OM, Nerobkova LN, Zhmurenko LA. [Pharmacological characteristics of a new phenyl analog of piracetam – 4-phenylpiracetam]. Biull Eksp Biol Med. 1983;95(4):50–3. PubMed
  2. Zvejniece L, Svalbe B, Veinberg G, Grinberga S, Vorona M, Kalvinsh I, et al. Investigation into stereoselective pharmacological activity of phenotropil. Basic Clin Pharmacol Toxicol. 2011;109(5):407–12. doi:10.1111/j.1742-7843.2011.00742.x · PubMed
  3. Zvejniece L, Svalbe B, Vavers E, Makrecka-Kuka M, Makarova E, Liepins V, et al. S-phenylpiracetam, a selective DAT inhibitor, reduces body weight gain without influencing locomotor activity. Pharmacol Biochem Behav. 2017;160:21–9. doi:10.1016/j.pbb.2017.07.009 · PubMed
  4. Zvejniece L, Zvejniece B, Videja M, Stelfa G, Vavers E, Grinberga S, et al. Neuroprotective and anti-inflammatory activity of DAT inhibitor R-phenylpiracetam in experimental models of inflammation in male mice. Inflammopharmacology. 2020;28(5):1283–92. doi:10.1007/s10787-020-00705-7 · PubMed
  5. Firstova IuIu, Vasil'eva EV, Kovalev GI. [Studying specific effects of nootropic drugs on glutamate receptors in the rat brain]. Eksp Klin Farmakol. 2011;74(1):6–10. PubMed
  6. Firstova IuIu, Dolotov OV, Kondrakhin EA, Dubynina EV, Grivennikov IA, Kovalev GI. [Effects of nootropic drugs on hippocampal and cortical BDNF levels in mice with different exploratory behavior efficacy]. Eksp Klin Farmakol. 2009;72(6):3–6. PubMed
  7. Malykh AG, Sadaie MR. Piracetam and piracetam-like drugs: from basic science to novel clinical applications to CNS disorders. Drugs. 2010;70(3):287–312. doi:10.2165/11319230-000000000-00000 · PubMed
  8. Koval'chuk VV, Skoromets AA, Koval'chuk IV, Stoianova EG, Vysotskaia ML, Melikhova EV, et al. [Efficacy of phenotropil in the rehabilitation of stroke patients]. Zh Nevrol Psikhiatr Im S S Korsakova. 2010;110(12 Pt 2):38–40. PubMed
  9. Savchenko AIu, Zakharova NS, Stepanov IN. [The phenotropil treatment of the consequences of brain organic lesions]. Zh Nevrol Psikhiatr Im S S Korsakova. 2005;105(12):22–6. PubMed
  10. Devlikamova FI, Safina DR. [Efficacy and safety of fonturacetam in asthenia: a systematic review and meta-analysis]. Zh Nevrol Psikhiatr Im S S Korsakova. 2025;125(2):69–79. doi:10.17116/jnevro202512502169 · PubMed
  11. Vanhee C, Deconinck E, George M, Hansen A, Hackl A, Wollein U, 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. J Xenobiot. 2025;15(3):88. doi:10.3390/jox15030088 · PubMed
  12. Jędrejko K, Catlin O, Stewart T, Anderson A, Muszyńska B, Catlin DH. Unauthorized ingredients in “nootropic” dietary supplements: a review of the history, pharmacology, prevalence, international regulations, and potential as doping agents. Drug Test Anal. 2023;15(8):803–39. doi:10.1002/dta.3529 · PubMed
  13. Pokrywka A, Surała O, Grabowska K, Przybyła M, Granda D, Małecki A, et al. “Brain doping” substances: prohibited or not in sports? Biol Sport. 2025;42(4):189–201. doi:10.5114/biolsport.2025.150047 · PubMed
  14. Cohen PA, Avula B, Wang YH, Zakharevich I, Khan I. Five unapproved drugs found in cognitive enhancement supplements. Neurol Clin Pract. 2021;11(3):e303–7. doi:10.1212/CPJ.0000000000000960 · PubMed
  15. Bundesinstitut für Arzneimittel und Medizinprodukte. AMIce – Arzneimittel-Informationssystem, öffentlicher Teil [Datenbank]. Suche Stoffname „Phenylpiracetam“, „Fonturacetam“ bzw. „Carphedon“, Humanarzneimittel, nur verkehrsfähige sowie ohne Einschränkung (alle Einträge, auch erloschene), jeweils ohne Treffer [zitiert 26.10.2026]. Verfügbar unter: https://portal.bfarm.de/amguifree/
  16. Verordnung über die Verschreibungspflicht von Arzneimitteln (Arzneimittelverschreibungsverordnung – AMVV), Anlage 1 (zu § 1 Nr. 1 und § 5). Stand: zuletzt geändert durch Art. 1 V v. 19.5.2026 (BGBl. 2026 I Nr. 149). Bundesministerium der Justiz [Internet]. Abgerufen am 26.10.2026. Verfügbar unter: https://www.gesetze-im-internet.de/amvv/anlage_1.html (kein Eintrag zu „Phenylpiracetam“, „Fonturacetam“ bzw. „Carphedon“).
  17. European Medicines Agency. Datenexporte (JSON) Medicines, Referrals und Orphan designations, Zeitstempel 25.10.2026. Amsterdam: EMA; abgerufen am 26.10.2026. Verfügbar unter: https://www.ema.europa.eu/en/documents/report/medicines-output-medicines_json-report_en.json, https://www.ema.europa.eu/en/documents/report/referrals-output-json-report_en.json und https://www.ema.europa.eu/en/documents/report/medicines-output-orphan_designations-json-report_en.json (Suche nach „phenylpiracetam“, „fonturacetam“, „carphedon“ und „phenotropil“ ohne Treffer).
  18. Bekanntmachung der Neufassung der Anlage I zu dem Internationalen Übereinkommen vom 19. Oktober 2005 gegen Doping im Sport/des Anhangs zu dem Übereinkommen vom 16. November 1989 gegen Doping vom 18. Dezember 2025 (Verbotsliste 2026, gültig ab 1. Januar 2026, mit amtlicher deutscher Übersetzung), Abschnitt S6 „Stimulanzien“. BGBl. 2025 II Nr. 312, ausgegeben am 23.12.2025. Abgerufen am 26.10.2026. Verfügbar unter: https://www.recht.bund.de/bgbl/2/2025/312/regelungstext.pdf
  19. Gesetz gegen Doping im Sport (Anti-Doping-Gesetz – AntiDopG), § 2 und Anlage (zu § 2 Absatz 3). Stand: zuletzt geändert durch Art. 1 V v. 10.3.2023 (BGBl. 2023 I Nr. 67). Bundesministerium der Justiz [Internet]. Abgerufen am 26.10.2026. Verfügbar unter: https://www.gesetze-im-internet.de/antidopg/__2.html und https://www.gesetze-im-internet.de/antidopg/anlage.html (kein Eintrag „Fonturacetam“ in der Anlage).
How this profile was checked

Last reviewed: 2026-10-26. All sources with a DOI or PMID were resolved automatically via Crossref or doi.org and PubMed.

Translated from the German profile (version of 2026-10-26); translation checked on 2026-10-26.

Checked

  • October 26, 2026 (decision n017, audit report E-20 question 12, first step, primary source WADA list): `kategorie` changed from Nootropikum to “Nicht zugelassener Wirkstoff”, promises, levels, and results unchanged. F1 (no medicinal product in DE/EU): AMIce, substance name “Phenylpiracetam”, “Fonturacetam”, and “Carphedon”, medicinal products for human use, only marketable and without restriction, 0 hits each (retrieved October 26, 2026 in the browser; control “Modafinil” 21 and 32 hits, respectively) [15]; AMVV Annex 1 in full text without an entry (status Art. 1 of the Ordinance of May 19, 2026, BGBl. 2026 I No. 149) [16]; EMA exports Medicines, Referrals, and Orphan designations (timestamp October 25, 2026) without hits for “phenylpiracetam”, “fonturacetam”, “carphedon”, “phenotropil” [17]. F2 (food): no food-law evidence, remains “not verified”. F3 (circulation): 2026 Prohibited List in the German publication BGBl. 2025 II No. 312 read in the PDF, S6.A names “Fonturacetam [4-Phenylpiracetam (Carphedon)]” [18]; Section 2 AntiDopG and its annex read, fonturacetam not in the annex [19]. Market surveillance study by the official control laboratories in full text, Table A1: one finding [11]; detection in US dietary supplements [14]. Basis: audit report docs/pruefberichte/rechtsstatus-e20.md, blocks C and F; all queries repeated by myself on October 26, 2026.
  • October 26, 2026 (cross-check n017): AMIce wording in `status.deutschland` rephrased. The AMIce filter “without restriction” on marketability includes all entries, including lapsed ones (control “Modafinil”: 21 hits under “only marketable”, 32 without restriction); the earlier wording “without restriction of marketability” could be misread as “unrestrictedly marketable”. Now as in the audit report (block A, armodafinil): neither among the marketable entries nor among all entries, including lapsed ones.
  • All 8 DOIs resolved via Crossref and all 14 PMIDs via PubMed (checking script); six Russian papers without a DOI.
  • Key figures checked against abstracts: more potent than piracetam, anticonvulsant, sedating at high doses [1]; R vs. S enantiomer, same brain concentration [2]; selective DAT inhibitor, 8 and 12 weeks [3]; DAT only target, brain tissue after 15 min [4]; no binding at 10⁻¹⁰–10⁻⁴ M [5]; n = 400 [8]; n = 99 [9]; 11 studies, n = 549, −16.3 points, 5.5% side effects [10]; banned in 1998 as the first nootropic [12].
  • In the full text: classification as prescription-only in Russia and not authorized in the EU, bulk quantities with almost 100% purity [11]; WADA category S6.A [13].
  • ClinicalTrials.gov: 0 entries for fonturacetam, 1 for phenylpiracetam (study on the reliability of IQ tests; October 23, 2026).

Not verified

  • Inhibition constants (Ki/IC50) at the dopamine transporter: not in the abstracts; the original paper on DAT binding was not found in PubMed.
  • Pharmacokinetics in humans.
  • Russian studies [1][5][6][8][9][10] read as abstracts only; whether [8] was randomized is unclear.
  • Whether the racemate or individual enantiomers are marketed under the name fonturacetam.

No dosages, no sources of supply. This information does not replace medical advice.

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