Noopept (GVS-111)

Nootropic Peptide | Memory & Neuroprotection

Weight: 318.37 Da
Half-life: ~30 minutes (oral), active metabolite cycloprolylglycine persists longer
4 studies
2014 latest
Moderate Research
Dose 10-30 mg/day
Frequency Split AM/PM (sublingual or oral)
Cycle 1.5-3 month cycles with 1 month off
Storage Room temperature (68-77F). Protect from moisture and light.

Community Research

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Noopept (GVS-111, omberacetam) is a synthetic nootropic dipeptide developed at the Russian Academy of Medical Sciences in the 1990s. It is approved and marketed in Russia and several CIS countries for cognitive impairment of various origins, including post-traumatic and cerebrovascular conditions. Structurally related to the racetam family, Noopept is not technically a racetam itself but is often grouped with them due to a shared mechanism of action involving modulation of glutamatergic neurotransmission. Its standout characteristic is extraordinary potency -- roughly 1000 times more potent than piracetam by weight -- which allows effective dosing in the 10-30 mg range rather than the multi-gram doses required by piracetam. Noopept is rapidly absorbed and converted to its primary active metabolite, cycloprolylglycine, an endogenous neuropeptide that mediates much of the compound's sustained cognitive and neuroprotective activity.

Mechanism of Action

Noopept exerts its nootropic and neuroprotective effects through several interconnected mechanisms. It modulates glutamatergic neurotransmission by acting as a positive modulator at AMPA and NMDA receptors, enhancing long-term potentiation (LTP) in the hippocampus -- the core cellular process underlying memory formation. A defining feature of Noopept is its ability to increase the expression of both brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the hippocampus and cerebral cortex. BDNF supports synaptic plasticity, neuronal survival, and the growth of new dendritic connections, while NGF is critical for the maintenance and survival of cholinergic neurons in the basal forebrain, a population that degenerates in Alzheimer's disease. Noopept also exhibits antioxidant and anti-inflammatory properties, reducing oxidative stress and inhibiting neurotoxicity induced by excess calcium and glutamate. Additionally, it enhances the activity of inhibitory mechanisms that prevent excitotoxic neuronal damage. After oral administration, Noopept is rapidly metabolized to cycloprolylglycine, which crosses the blood-brain barrier and is thought to mediate much of the compound's longer-lasting neurotrophic activity.

01 Enhanced memory formation and consolidation through upregulation of BDNF and NGF
02 Neuroprotective effects against oxidative stress, excitotoxicity, and amyloid-beta toxicity
03 Improved learning capacity and information retrieval via AMPA/NMDA receptor modulation
04 Ultra-low effective dose (10-30 mg) compared to classical racetams, reducing pill burden and cost
05 Anxiolytic properties observed at standard nootropic doses without sedation
06 Fast onset of subjective effects despite the short parent compound half-life, due to active metabolite persistence

Molecular Data

Molecular Weight
318.37 Da
Type
Dipeptide derivative (C17H22N2O4)
Peak 0.0 mcg
Trough 0.0 mcg
SS Peak 0.0 mcg
SS Trough 0.0 mcg

Research Indications

Cognitive Enhancement
Memory and Learning effective

Noopept's best-established effect is enhancement of memory consolidation and retrieval. Animal studies consistently demonstrate improved performance on spatial memory, passive avoidance, and novel object recognition tasks. Human studies in patients with mild cognitive impairment and organic brain disorders show improvements in memory scores and attentional capacity.

Neuroprotection effective

Demonstrated neuroprotective activity in multiple models of neuronal injury including oxidative stress, amyloid-beta toxicity, and glutamate excitotoxicity. The upregulation of BDNF and NGF provides trophic support to vulnerable neuronal populations, which may slow or prevent neurodegeneration.

Focus and Attention moderate

Users commonly report improved clarity of thought and sustained attention. While less studied than memory effects, the modulation of glutamatergic signaling and downstream cholinergic enhancement likely contribute to improved attentional performance.

Clinical (Approved in Russia)
Post-Traumatic Cognitive Impairment effective

Approved in Russia for cognitive deficits following traumatic brain injury. Clinical trials demonstrated improvements in memory, attention, and emotional stability in patients recovering from cerebral trauma.

Cerebrovascular Cognitive Impairment moderate

Approved for cognitive decline associated with cerebrovascular insufficiency. Patients with chronic cerebrovascular disease showed improvements in cognitive test scores and reduction in associated emotional disturbances including anxiety and irritability.

Investigational
Alzheimer's Disease early research

Preclinical evidence suggests potential benefits through NGF/BDNF upregulation and inhibition of amyloid-beta aggregation and neurotoxicity. Not yet tested in rigorous clinical trials for Alzheimer's specifically, but the mechanistic rationale is strong.

Anxiety moderate

An anxiolytic effect has been observed in both animal models and human clinical use at standard nootropic doses. Unlike benzodiazepines, the anxiolytic effect does not come with sedation or cognitive impairment, making it a potentially useful secondary benefit.

Dosing Protocols

Sublingual administration is the preferred route among experienced users due to faster absorption and higher bioavailability compared to oral ingestion. The compound is placed under the tongue as a powder or dissolved in a small amount of liquid and held for 1-2 minutes before swallowing. This bypasses first-pass hepatic metabolism and allows more of the parent compound to reach systemic circulation before conversion to cycloprolylglycine.

GoalDoseFrequencyRoute
Standard Nootropic Protocol10 mgTwice daily (morning and early afternoon)Sublingual
Higher Dose Protocol15 mgTwice daily (morning and early afternoon)Sublingual

Interactions

++
Racetams (Piracetam, Aniracetam, Oxiracetam)
Noopept and racetams share overlapping but non-identical mechanisms of action. Combining them can provide complementary glutamatergic modulation -- racetams primarily enhance AMPA receptor function while Noopept additionally modulates NMDA receptors and upregulates neurotrophins. Many users report stronger cognitive effects from the combination than from either compound alone. Start with lower doses of each when combining.
synergistic
++
Choline Sources (Alpha-GPC, CDP-Choline)
Co-supplementation with a choline source is strongly recommended. Noopept increases acetylcholine demand through enhanced cholinergic signaling, and insufficient choline availability is the most common cause of headaches reported with Noopept use. Alpha-GPC (300-600 mg) or CDP-Choline (250-500 mg) daily effectively prevents this side effect and may potentiate cognitive benefits.
synergistic
+
Modafinil
Noopept and modafinil operate through distinct mechanisms (glutamatergic/neurotrophic vs. dopaminergic/histaminergic) and are commonly combined in nootropic stacks without significant adverse interaction. The combination may provide both acute wakefulness and longer-term neurotrophic support. No pharmacokinetic interaction has been identified.
compatible

What to Expect

15-30 minutes
Onset of acute effects, particularly with sublingual administration. Users may notice subtle improvements in mental clarity, verbal fluency, and sensory acuity. The parent compound reaches peak plasma concentration within this window.
1-3 hours
Primary acute nootropic window. Enhanced focus, improved working memory, and greater ease of information encoding. Some users report a mild anxiolytic effect and improved emotional equilibrium. The parent compound is largely metabolized by this point, with cycloprolylglycine carrying forward the neurotrophic signaling.
1-2 weeks of daily use
Neurotrophic effects begin to manifest. BDNF and NGF upregulation requires sustained administration to produce meaningful changes in synaptic density and neuronal health. Users often report a noticeable improvement in memory consolidation and recall that was not present during the first few days.
4-8 weeks of daily use
Full neurotrophic benefits are typically realized. Memory improvements become more pronounced and consistent. The neuroprotective effects, including reduced susceptibility to cognitive fatigue and improved recovery from mental exertion, are most apparent during this phase.
After cycling off
Unlike stimulant-type nootropics, some benefits of Noopept -- particularly those related to BDNF/NGF-mediated structural changes in neural circuits -- may persist for weeks after discontinuation. Users commonly report that memory improvements outlast the supplementation period, suggesting lasting neuroplastic adaptations.

Side Effects & Safety

Common Side Effects

  • Headache (most common side effect, typically caused by insufficient choline intake -- co-supplementation with Alpha-GPC or CDP-Choline usually resolves this)
  • Irritability and restlessness, particularly at doses exceeding 30 mg/day
  • Insomnia if taken too late in the day
  • Mild gastrointestinal discomfort when taken on an empty stomach

Stop Signs - Discontinue if:

  • Persistent headache that does not resolve with choline supplementation
  • Significant mood changes, depression, or emotional instability
  • Persistent brain fog or worsening cognitive function
  • Allergic reactions including rash, swelling, or difficulty breathing

Contraindications

  • Known hypersensitivity to Noopept or related compounds
  • Severe hepatic impairment (metabolized by the liver)
  • Severe renal impairment
  • Pregnancy and breastfeeding (insufficient safety data)
  • Hypertension that is poorly controlled (due to potential mild pressor effects)

References

  • Noopept Stimulates the Expression of NGF and BDNF in Rat Hippocampus
    Ostrovskaya, R.U., Gudasheva, T.A., Zaplina, A.P., et al.
    Bulletin of Experimental Biology and Medicine (2008)

    Demonstrated that chronic Noopept administration (0.5 mg/kg) significantly increased mRNA expression of both NGF and BDNF in the rat hippocampus, providing a mechanistic basis for its memory-enhancing and neuroprotective effects and distinguishing it from classical racetams.

  • The Nootropic and Neuroprotective Proline-Containing Dipeptide Noopept Restores Spatial Memory and Increases Immunoreactivity to Amyloid in an Alzheimer's Disease Model
    Ostrovskaya, R.U., Vakhitova, Y.V., Kuzmina, U.S., et al.
    Journal of Psychopharmacology (2007)

    Showed that Noopept restored spatial memory deficits in a transgenic Alzheimer's disease mouse model and increased immunoreactivity to amyloid, suggesting both symptomatic and potentially disease-modifying properties.

  • Proline-Containing Dipeptide GVS-111 Retains Nootropic Activity After Oral Administration
    Gudasheva, T.A., Boyko, S.S., Akparov, V.Kh., et al.
    Bulletin of Experimental Biology and Medicine (1997)

    Established that GVS-111 (Noopept) retains significant nootropic activity after oral administration despite rapid metabolism, and identified cycloprolylglycine as the primary active metabolite responsible for sustained cognitive effects.

  • Neuroprotective Effect of Novel Cognitive Enhancer Noopept on AD-Related Mechanisms
    Ostrovskaya, R.U., Tsaplina, A.P., Vakhitova, Yu.V., et al.
    Bulletin of Experimental Biology and Medicine (2014)

    Demonstrated that Noopept prevents calcium-dependent and amyloid-beta-induced cytotoxicity in neuronal cell cultures and inhibits oxidative stress-mediated cell death, confirming multiple neuroprotective mechanisms beyond its nootropic activity.

Disclaimer

This information is for educational and research purposes only. Consult a healthcare professional before use.