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Noopept

N-phenylacetyl-L-prolylglycine ethyl ester

Noopept (N-phenylacetyl-L-prolylglycine ethyl ester; developmental code GVS-111; also marketed as omberacetam) is a synthetic proline-containing dipeptide "nootropic" developed at the Zakusov Institute of Pharmacology in Russia, where it is a prescription drug for cognitive and asthenic disorders. It is not approved by the FDA, EMA, or any Western regulator; outside Russia it circulates only as an unregulated research chemical/"supplement" of uncertain identity and purity. Almost the entire human evidence base is small, short (weeks to a few months), largely open-label or single-comparator, and comes from the same institution that developed the drug, mostly published in Russian. Transient blood-pressure elevation has been observed in patients with pre-existing hypertension; insomnia, irritability, and anxiety can occur; and there are essentially no long-term human safety data and no data on hepatic, renal, reproductive, or hematologic effects in humans. This monograph is educational harm-reduction information, not medical advice or an endorsement of use.

Clinical readoutPED-adjacent · nootropic
Hepatic strainNone
CardiovascularModerate
HPTA suppressionNone
Half-life
1 h
Route
Oral
Evidence
C
Active
Not well defined in hum…
1 h2 h3 h4 h5 h
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Poorly characterized in humans. In rodents the parent compound is very short-lived in plasma (on the order of tens of minutes) and is largely undetectable in brain within about 1 hour after dosing, having been converted to metabolites; the active metabolite cycloprolylglycine peaks in brain roughly 1 hour post-dose. No robust published human half-life exists.
Pharmacology

Mechanism of action

Noopept is a prodrug: after oral administration it is rapidly hydrolyzed, and its principal active metabolite is cycloprolylglycine (cyclo-L-prolylglycine), a cyclic dipeptide that is also an endogenous neuropeptide, which is proposed to mediate much of the nootropic activity (demonstrated in rat brain). Proposed mechanisms, characterized almost entirely in rodent and cell-culture models, include: increased hippocampal expression of the neurotrophins NGF and BDNF; selective enhancement of hypoxia-inducible factor 1 (HIF-1) DNA-binding activity (proposed as a primary molecular target via inhibition of HIF-prolyl hydroxylase 2), supporting an adaptive/neuroprotective response to hypoxia; antioxidant and anti-inflammatory effects; and modulation of cholinergic and glutamatergic (AMPA/NMDA) neurotransmission. Human mechanistic confirmation is lacking; EEG studies in patients show a nonspecific activating and mild anxiolytic pattern (increased alpha/beta, reduced delta power).
Kinetics

Pharmacokinetics

Half-life

Poorly characterized in humans. In rodents the parent compound is very short-lived in plasma (on the order of tens of minutes) and is largely undetectable in brain within about 1 hour after dosing, having been converted to metabolites; the active metabolite cycloprolylglycine peaks in brain roughly 1 hour post-dose. No robust published human half-life exists.

Active duration

Not well defined in humans. Clinical dosing regimens use 2-3 divided doses per day, implying a short pharmacodynamic window; EEG/behavioral effects in rats persisted for several hours after a single dose. This information is for washout/monitoring context, not for evading drug testing.

Route

Oral (tablets in Russian clinical use, typically taken after meals); sublingual use is also described. Parenteral routes used only in preclinical work.

Metabolism & clearance

Acts as a prodrug: hydrolyzed by plasma and brain enzymes to phenylacetic acid, prolylglycine, and cycloprolylglycine (the latter the putative active moiety). Human metabolic and clearance data are sparse; the metabolism-to-cycloprolylglycine pathway is established in rats. Assume renal/hepatic elimination of small-peptide metabolites but note this is not well quantified in humans.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • In patients with mild cognitive impairment of vascular or post-traumatic origin, small clinical studies reported modest improvement in attention, memory, and global cognitive measures over 4-8 weeks, broadly comparable to piracetam.
  • In an open, uncontrolled 12-month study of 60 stroke patients, 20 mg/day for 2 months was associated with improved MMSE and verbal-association scores versus controls, with the authors describing a high safety level (low-quality, non-randomized evidence).
  • EEG studies in patients with post-traumatic and vascular cognitive/asthenic disturbances showed a nootropic activation pattern (increased alpha and beta power, decreased delta) and a mild anxiolytic effect.
  • Reported as having an anxiolytic/mood-stabilizing quality in asthenic and emotionally labile states (Russian clinical use).
  • In healthy volunteers under environmental stress (heat/cold/hypobaric hypoxia), described as improving the psychological component of functional state ('meteoadaptogenic'); this is weak, non-clinical evidence.
  • Popularly used off-label as a self-administered cognitive enhancer, but there are no rigorous human data supporting cognitive benefit in healthy young adults.
Safety

Adverse effects by system

Cardiovascular

Transient increases in blood pressure were observed in some patients with pre-existing arterial hypertension in the comparative Noopept/piracetam trial; no dedicated cardiovascular safety study exists. Treat BP effects as a real signal in hypertensive individuals and monitor.

Hepatic

No adequate human data. Hepatotoxicity has not been systematically studied in humans; no clear hepatotoxic signal has been reported in the short trials, but the absence of liver-panel surveillance means hepatic safety is effectively unknown.

Endocrine / HPTA

No adequate human data. Noopept is a neuropeptide-type nootropic with no known androgenic, estrogenic, or gonadotropic activity and no described mechanism for suppressing the hypothalamic-pituitary-testicular/gonadal axis; however, endocrine endpoints have not been formally evaluated in humans.

Reproductive

No adequate human data. Effects on fertility, pregnancy, or lactation have not been established; use is not recommended in pregnancy/breastfeeding due to lack of data.

Neuropsychiatric

Insomnia/sleep disturbance, irritability, and anxiety/restlessness can occur (consistent with its activating profile), particularly with later-in-day dosing; conversely mild anxiolytic effects are also described. Reported adverse events in the short trials were generally mild and transient. Long-term neuropsychiatric effects are unknown.

Renal

No adequate human data. Renal effects have not been characterized; no nephrotoxic signal reported, but renal safety is essentially unstudied.

Hematologic

No adequate human data. Hematologic parameters have not been systematically reported; hematologic safety is unknown.

Dermatologic

No adequate human data. Hypersensitivity/allergic skin reactions are listed as a theoretical precaution in Russian prescribing information but are not well documented in the literature.

Recovery

HPTA suppression & recovery

Suppression: No expected HPTA suppression; not a hormonal agent (no adequate human endocrine data)

Noopept is not an anabolic-androgenic steroid, SERM, or aromatase inhibitor and has no described mechanism for suppressing the hypothalamic-pituitary-gonadal axis, so HPTA suppression and post-cycle recovery concerns are not applicable in the way they are for those drug classes. It should not be used as, or combined with, any SERM-based recovery protocol; single-SERM or any SERM use is a separate clinical decision. Formal endocrine endpoints have not been studied in humans, so anyone with hormonal concerns, or considering combining substances, should consult an endocrinologist rather than self-managing.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Baseline and periodic blood pressure and heart rate (especially in anyone with hypertension or cardiovascular risk)Baseline liver function panel (AST, ALT, bilirubin) and renal function (creatinine, eGFR) as general safety surveillance, since human organ-safety data are absentComplete blood count as baseline general monitoring

Cadence: If used at all, obtain baseline measurements before starting, recheck blood pressure within the first 1-2 weeks, and repeat basic labs/BP periodically (e.g., every few months) or sooner if symptoms arise; clinical trials generally limited exposure to about 4-8 weeks and long-term data do not exist.

Warning signs — seek care
  • Sustained or symptomatic rise in blood pressure (headache, chest pressure, visual changes)
  • New or worsening insomnia, irritability, agitation, or anxiety
  • Signs of allergic/hypersensitivity reaction (rash, itching, swelling, difficulty breathing)
  • Signs of possible liver injury (jaundice, dark urine, right-upper-quadrant pain, marked fatigue)
  • Any unexplained new neurological or psychiatric symptoms — stop and seek medical evaluation
Do not use if

Contraindications

  • Not approved outside Russia; unregulated 'research chemical' products carry unverified identity, dosage accuracy, and contamination risk.
  • Pregnancy and breastfeeding (no safety data).
  • Children/adolescents (insufficient data).
  • Pre-existing poorly controlled hypertension or significant cardiovascular disease, given the reported transient blood-pressure elevation in hypertensive patients.
  • Known hypersensitivity to the compound.
  • Severe hepatic or renal impairment (metabolism/clearance not characterized in humans; use cannot be assumed safe).
  • Concurrent use with other stimulant/activating agents or in individuals with insomnia or anxiety disorders, given its activating psychiatric profile.
  • Self-treatment of serious cognitive or neurological symptoms in place of proper medical evaluation.
Combinations

Interaction profile

  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • This is not medical advice and not an endorsement. Noopept is unapproved outside Russia; there is no rigorous evidence of benefit in healthy people and no long-term human safety data.
  • Because Western products are unregulated, actual content and purity are unverifiable; this alone is a major risk independent of the molecule itself.
  • Lead with monitoring: check blood pressure at baseline and early in use, especially if you have any history of hypertension or cardiovascular disease, since transient BP elevation was seen in hypertensive patients.
  • Avoid dosing late in the day to reduce insomnia; be alert for irritability, anxiety, or agitation.
  • Do not combine with other stimulants/activating agents, and do not use it as part of any hormonal 'recovery' or SERM protocol — it has no role there.
  • Avoid entirely in pregnancy, breastfeeding, and in children/adolescents, and if you have significant liver or kidney disease, given the absence of safety data.
  • Clinical studies limited exposure to roughly 4-8 weeks (up to a few months); there is no basis for indefinite use.
  • Stop and seek medical care for sustained/symptomatic high blood pressure, allergic reactions, signs of liver injury (jaundice, dark urine), or any new neurological or psychiatric symptoms.
  • Do not self-treat serious cognitive or neurological symptoms with Noopept in place of a proper medical evaluation — see a clinician, and involve an endocrinologist for any hormonal questions.
Evidence

Citations (10)

Every clinical claim above is tied to a primary source. Overall evidence grade C — graded to the best available evidence for its core claims.

  1. 01

    Noopept (N-phenylacetyl-L-prolylglycine ethyl ester, GVS-111) is a prodrug metabolized to cycloprolylglycine, an endogenous cyclic dipeptide proposed to mediate its nootropic activity (rat).

    PreclinicalPMID 9358206 ↗

  2. 02

    Noopept increases hippocampal expression of the neurotrophic factors NGF and BDNF after acute and chronic administration (rat), without tolerance.

    PreclinicalPMID 19240853 ↗

  3. 03

    Noopept selectively increases HIF-1 DNA-binding activity and can bind HIF-prolyl hydroxylase 2, proposed as a primary molecular mechanism underlying its neuroprotective effects (cell culture / molecular docking).

    PreclinicalPMID 27099787 ↗

  4. 04

    Noopept does not stimulate cell proliferation (no mitogenic effect on Ki-67 or cell-cycle distribution in HEK293 and SH-SY5Y lines).

    PreclinicalPMID 30788746 ↗

  5. 05

    In patients with mild cognitive disorders of vascular and traumatic origin, Noopept produced cognitive improvement broadly comparable to piracetam, and transient blood-pressure increases were observed in some patients with pre-existing hypertension (primary human safety/efficacy signal).

    CohortDOI 10.1007/s11055-009-9128-4 ↗

  6. 06

    In an open, non-randomized 12-month study of 60 stroke patients, Noopept 20 mg/day for 2 months improved MMSE and verbal-association scores versus controls with a reported high safety level.

    CohortPMID 22500312 ↗

  7. 07

    In patients with post-traumatic and vascular cognitive/asthenic disturbances, Noopept produced an EEG nootropic-activation pattern (increased alpha/beta, decreased delta) and a nonspecific activating and mild anxiolytic effect.

    CohortPMID 19008801 ↗

  8. 08

    In healthy volunteers under environmental stress, Noopept was described as improving the psychological component of functional state ('meteoadaptogenic').

    CohortPMID 18318195 ↗

  9. 09

    Noopept and its metabolite improve interhemispheric (transcallosal) signal transfer in rat brain, a proposed neurophysiological basis of its behavioral effects.

    PreclinicalPMID 12109288 ↗

  10. 10

    Noopept reduces cortical infarct size in a rat middle-cerebral-artery-occlusion model, supporting preclinical neuroprotective activity.

    PreclinicalPMID 16995431 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice