Noopept

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

Noopept was constructed as a dipeptide analogue of piracetam; in a cell model of Alzheimer's disease, it protected PC12 cells from amyloid-β and reduced oxidative stress, calcium overload, and tau phosphorylation ^[1]. In rats, noopept was undetectable in the brain one hour after injection, while the concentration of cyclo-prolylglycine rose 2.5-fold; the authors therefore interpret noopept as a prodrug of this cyclic peptide, which is also endogenous ^[2].

In transfected cells, noopept at 10 µM selectively increased the DNA binding of the transcription factor HIF-1, but not that of CREB, NF-κB, p53, or other factors tested; piracetam had no effect, and docking calculations predict binding to HIF prolyl hydroxylase 2 ^[3]. In neuronal cells, a reporter assay pointed to inhibition of this prolyl hydroxylase ^[4]. In rats, the mRNA of the growth factors NGF and BDNF rose in the hippocampus after administration ^[5]. In hippocampal slices, noopept increased the activity of inhibitory interneurons; α7 nicotinic acetylcholine receptor antagonists abolished this ^[6]. At AMPA receptors, it displaced a ligand only at high concentrations (IC50 80 µM) ^[7].

The studies in humans are small and not placebo-controlled: in 60 people after stroke, cognitive tests improved more than in a control group in an open-label study ^[8], and in mild cognitive impairment, the EEG changed in a way typical of nootropics ^[9]. In healthy people, only adaptation to climatic stress ^[10] and the working capacity of older teachers in combination with self-massage ^[11] were studied. Almost all of the work comes from Russian institutes, many of it from the group that developed noopept.

Assigned to the site of action Nutrient switches AMPK and mTORC1 at the lysosome, autophagy and senescent cells; not drawn in its figure: acts at HIF/PHD2, a different site of action.

Targets

Effect profile

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

• ·Dopamineno data
• ·Noradrenalineno data
• ·Serotoninno data
• ≈Acetylcholinemodulated · effect on interneurons via α7 nicotinic receptors (rat brain slice)^[6]
• ?Glutamate · AMPAunclear · ligand displacement only at high concentration^[7]
• ·Glutamate · NMDAno data
• ↑GABA↑ · more inhibitory interneuron activity in the hippocampus (rat brain slice)^[6]
• ·Histamineno data
• ·Orexinno data
• ·Adenosineno data
• ·Opioidsno data
• ·Melatoninno data
• ↑Neurotrophins↑ · more NGF and BDNF mRNA in the rat hippocampus^[5]
• ·Blood flowno data
• ·Nitric oxideno data
• ≈Energy metabolismmodulated · activates the hypoxia transcription factor HIF-1 in cell culture^[3][4]
• ·Insulin · glucoseno data
• ↓Inflammation · oxidative↓ · fewer reactive oxygen species in the amyloid cell model^[1]
• ·Stress axisno data
• ·Testosterone axisno data
• ·Endocannabinoidsno data
• ·Autophagy · senescenceno data
• ·Immune systemno data
• ·Lipid metabolismno data
• ·Coagulation · fibrinolysisno data
• ·Methylationno data

Human studies

• Mild cognitive impairment after stroke

  open-label, prospective, with a control group · Patients: after stroke · n = 60 · 2 months of treatment, 12 months of follow-up

  Measured: MMSE, verbal fluency

  Result: Greater improvement than in the control group after 2 months.^[8]

  Human, non-randomised

• EEG in mild cognitive impairment

  open-label, without placebo · Patients: cognitive impairment after trauma or vascular disease · not stated in the abstract

  Measured: EEG rhythms

  Result: More alpha and beta power, less delta; interpreted by the authors as activation.^[9]

  Human, non-randomised

• Adaptation to climatic stress

  controlled, randomization and placebo not described in the abstract · healthy · not stated in the abstract

  Measured: psychological and physiological functional state

  Result: Psychological functional state better under cold and heat; physical performance increased in heat.^[10]

  Human, non-randomised

• Working capacity of older teachers

  comparison of noopept plus self-massage vs. noopept alone, without placebo · healthy (older teachers) · 2 weeks

  Measured: functional state, occupational performance

  Result: Combination better than noopept alone; effect faded after three months.^[11]

  Human, non-randomised

Risks and warnings

• Lack of safety data

  No systematic safety data according to Western authorization standards in the sources checked; the open-label study after stroke reports high safety without a placebo comparison ^[8].

  No data

• Uncontrolled products

  In dietary supplements up to four times usual pharmacological amounts, in part undeclared ^[13]; seized in Europe as raw powder with up to 100% purity ^[12].

  No data

• Heat stroke during endurance sport (case report)

  A case report describes heat stroke with acute liver failure in an amateur marathon runner who had taken modafinil and noopept; a causal relationship has not been shown ^[14].

  Human, non-randomised

Interactions

• Modafinil: Only one case report of co-ingestion with a severe course ^[14]; no interaction study.

Fact check: common claims

• not supported

  “Noopept is a thousand times stronger than piracetam”

  No study in the sources checked compares the potency of the two substances in humans. In a cell assay, only noopept activated HIF-1, not piracetam; that is not a clinical efficacy comparison ^[3].

• partly supported

  “Noopept increases BDNF and NGF”

  mRNA increase in the hippocampus of rats ^[5]; not measured in humans.

• not supported

  “Noopept improves memory and concentration in healthy people”

  Only studies of functional state without a described placebo control ^[10][11].

• partly supported

  “Noopept acts via the acetylcholine system”

  In rat brain slices, the effect on interneurons is abolished by α7 antagonists ^[6]; the developers, by contrast, see HIF-1 as the main mechanism ^[3].

Pharmacokinetics

Absorption

Not described in humans in the sources checked.

Half-life

Not described in humans in the sources checked.

Metabolism

Rapidly converted in rats; in the brain, cyclo-prolylglycine rises 2.5-fold, and the parent compound is undetectable after one hour ^[2].

Entry into the brain

Parent compound not detectable in the rat brain one hour after injection; the metabolite cyclo-prolylglycine probably is ^[2].

Legal status

Germany

No medicinal product for human use containing the active substance noopept (omberacetam) was found in AMIce, neither among the marketable entries nor among all entries, including lapsed ones (search by substance name “Noopept” and “Omberacetam”, retrieved October 26, 2026; refusals and withdrawals are not included in the public part) ^[15]; no entry in AMVV Annex 1 ^[16]. The status under food law has not been verified.

EU

No centrally authorized or assessed medicinal product, no referral, and no orphan designation involving noopept 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, noopept was found nine times in four laboratories; the study classifies it as an active substance that has not been approved for human use by a health authority in any of the countries where it was found (the study's assessment, not a legal source) ^[12].

USA

Not approved for human use; detected in dietary supplements ^[13].

Other countries

Russia: prescription-only medicinal product, among other uses in traumatic brain injury, affective disorders, and cerebrovascular disorders ^[12]. Sport: not named in the 2026 Prohibited List as published in the German Federal Law Gazette; section S6 is worded openly (“All stimulants … are prohibited”; S6.B ends with “and other substances with a similar chemical structure or similar biological effect(s)”); whether the substance falls under it is a matter of interpretation ^[18]. A review considers coverage by the WADA criteria likely because of the similarity to phenylpiracetam ^[14].

Related compounds

Open questions

• Is the effect in humans due to noopept itself or to cyclo-prolylglycine?
• Does the HIF-1 mechanism withstand scrutiny by independent groups?
• How does noopept perform in a randomized, placebo-controlled study with cognition tests?