Noopept
Tier 2 · PreclinicalThe strongest evidence present is Tier 1: an information site (src-8) states Noopept completed Russian Phase III clinical trials and received Russian regulatory approval (~2006), and several human observational/open-label Russian studies are reported (src-2, src-3, src-5, src-7). However, sources heavily qualify this: only two small open-label Russian-language clinical reports are described, no randomized double-blind placebo-controlled trial exists, no study has been done in healthy people, and zero trials were registered on ClinicalTrials.gov as of 3 August 2026 (src-7). The ADDF review states little clinical evidence supports use as a cognitive-enhancing supplement (src-3). Almost all preclinical data come from the originating Zakusov Institute (src-7). Antidiabetic and antithrombotic findings are animal/in vitro only.
- Half-life
- ~0.27 h
- Routes
- Oral (studied and standard community route) · Intraperitoneal (animal studies) · Parenteral/injection (animal studies)
- Goals
- Cognitive enhancement / nootropic · Memory support · Anxiety / mood · Neuroprotection
- Cost / mg
- Not recorded
How it works
According to Examine and an information site, Noopept is a synthetic dipeptide built as an analog of piracetam and based on the natural brain peptide cycloprolylglycine. Sources report that Noopept itself is broken down very quickly and is barely detectable in the body, and that it works largely as a prodrug — it is converted into cycloprolylglycine, which is thought to be responsible for its longer-lasting nootropic effects. Animal and cell studies attribute its cognitive and neuroprotective actions to raising the neurotrophic factors BDNF and NGF, boosting acetylcholine signaling, reducing oxidative stress and glutamate excitotoxicity, and increasing HIF-1 activity. Human observational and open-label Russian studies report improvements in memory, attention, and mood along with an anxiolytic effect in people with mild cognitive impairment, though sources stress the human evidence is thin.
Overview
Overview
Noopept (also known as omberacetam, GVS-111, and chemically N-phenylacetyl-L-prolylglycine ethyl ester) is described by Examine as a synthetic molecule commonly grouped with the racetam class, although Examine notes this is technically untrue because Noopept lacks a 2-oxo-pyrrolidine nucleus (src-1, src-11, src-21). Examine reports it was synthesized in 1996, based on the endogenous neuropeptide cycloprolylglycine (src-1, src-11). The ADDF review and vendor/information sources state it was developed at the V.V. Zakusov Research Institute of Pharmacology of the Russian Academy of Medical Sciences in Moscow in the mid-1990s, designed as a dipeptide analog of piracetam on the hypothesis that piracetam's pyrrolidine ring mimics a proline residue and its N-acetamide moiety mimics glycine (src-3, src-7, src-8, src-49). Sources give its molecular formula as C17H22N2O4, molecular weight ~318.4 g/mol, and CAS 157115-85-0 (src-3, src-8, src-33, src-54).
Reported uses and effects
Examine and vendor sources say Noopept is claimed to be anxiolytic and mildly psychostimulatory while promoting cognitive health and memory (src-1, src-11). An information site states Noopept has a broader spectrum of cognitive effects than piracetam — memory acquisition, consolidation and retrieval — plus a selective anxiolytic action absent from piracetam (src-8, src-51). A comparative human study describes it as enhancing brain BDNF and NGF and reports more pronounced anxiolytic and neuroprotective properties than piracetam, decreasing cognitive impairment and showing anxiolytic and vegetostabilizing activity in patients with mild cognitive impairment of cerebrovascular and post-traumatic origin (src-2, src-4, src-23). A 28-day trial in 40 patients reported improvements in memory, attention and short visual memory, with the most marked improvement in attention (src-5, src-36), and reported relief of cerebroasthenic, hyperesthetic and sleep disturbances (src-37). An open-label study reported that 56-day treatment with 10 mg twice daily improved mood and cognition, with MMSE rising from 26 to 29 (src-3, src-29). Study authors suggest it holds promise for preventing Alzheimer's disease development in mild cognitive impairment (src-6, src-43).
Pharmacokinetics and the prodrug model
Multiple sources converge on a prodrug model. Examine reports Noopept itself is not detectable in serum even after high injected concentrations but increases cycloprolylglycine, functioning as a cycloprolylglycine prodrug (src-1, src-6, src-11). Rat studies report an oral 50 mg/kg dose (human equivalent 8 mg/kg) crosses the GI tract with a Tmax of ~7 minutes and a serum Cmax of 0.82 mcg/mL, a brain Cmax of 1.289 mcg/mL at ~7 minutes, and — because serum and neural concentrations differ little — that Noopept easily crosses the blood-brain barrier (src-1, src-8, src-9, src-11). Examine reports oral bioavailability roughly 10% and rapid metabolism within 25 minutes of oral ingestion, with the major metabolite structurally similar to cycloprolylglycine (src-1, src-11, src-12, src-13, src-40, src-54). A study found the parent GVS-111 below detection in rat brain one hour after 5 mg/kg i.p., while cyclo-prolylglycine rose ~2.5-fold, concluding conversion to cyclo-prolylglycine (identical to the endogenous cyclopeptide) produces the nootropic activity (src-15, src-46, src-71, src-72). Examine notes cycloprolylglycine itself has nootropic potential when injected, though less than Noopept (src-1, src-11).
Mechanistic findings
In vitro studies report Noopept at 10 μM increases HIF-1 DNA-binding activity in HEK293 cells without affecting several other transcription factors, and propose HIF-1 prolyl hydroxylase inhibition and HIF1α stabilization as a primary mechanism (src-2, src-10, src-19, src-25). Animal studies report increased NGF and BDNF expression in hippocampus, reduced oxidative stress and repression of stress-induced kinases (src-2, src-24, src-41), with chronic 28-day treatment reported not to produce tolerance but to potentiate the neurotrophic effect (src-6, src-42). The ADDF review lists proposed mechanisms including increased acetylcholine signaling, increased BDNF/NGF, protection from glutamate toxicity, and increased inhibitory neurotransmission (src-3). Additional animal/in vitro reports describe antioxidant, anti-inflammatory, antihyperglycemic (via GLP-1/insulin, not DPP-IV inhibition), and antithrombotic/anticoagulant effects (src-16, src-17, src-26, src-28, src-62); sources note these non-cognitive findings are animal/in vitro only.
Regulatory status and evidence caveats
An information site states Noopept was patented in 1996, completed Russian Phase III clinical trials, and received Russian regulatory approval (~2006) for cognitive disorders of cerebrovascular and post-traumatic origin (src-8, src-52). It is available by prescription in Russia but is not approved by the FDA, EMA or other Western agencies; a vendor site states the FDA treats it as an unapproved new drug and has stated in warning letters that it is not generally recognized as safe and effective, and it is not sold over the counter in the United States (src-3, src-7, src-8, src-33, src-47, src-55). Sources emphasize the human evidence is thin: a vendor site notes the large preclinical literature is almost entirely from the originating Zakusov Institute, that only two small open-label Russian-language clinical reports exist, that no randomized double-blind placebo-controlled trial has been conducted, no study has been done in healthy people, and zero trials were registered on ClinicalTrials.gov as of 3 August 2026 (src-7, src-48). The ADDF review states little clinical evidence supports use as a cognitive-enhancing supplement (src-3, src-32).
What the research shows
247 findings extracted from the 29 sources cited below, strongest evidence first within each group. Every one links to the source it came from.
What human studies found
Based on 1 human trial finding, 10 human study findings, 14 animal findings, 1 in vitro finding and 4 expert opinion findings.
human trialNoopept was patented in 1996, completed Russian Phase III clinical trials, and received regulatory approval in Russia for the treatment of cognitive disorders of cerebrovascular and post-traumatic origin28
human studyEEG effects of noopept depended on the character of brain pathology and were more typical for those of nootropic drugs in vascular pathology than in posttraumatic disorders1
human studyNoopept showed improvement of memory, attention, minimization of mistakes with interference, improvement of short memory1
human studyThe most marked improvement was in attention (distribution, stability and volume), increase of complex sensomotor reactions, volume of short visual memory1
human studyNoopept relieved cerebro asthenic, hyperesthetic and sleep disturbances, vegetative dysfunctions as well as cognitive and dismnestic problems1
human studyNoopept has more pronounced anxiolytic and neuroprotective properties compared to Piracetam4
human studyIn patients with mild cognitive impairment of cerebrovascular and post-traumatic origin, Noopept decreased cognitive impairment, showed an anxiolytic effect, and vegetostabilizing activity4
human studyNoopept appears to have bioactivity following oral ingestion in humans8
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human studyIn an open-label study of patients with mild cognitive disorders, 56-day treatment with noopept (10mg twice per day) improved several aspects of mood and cognition (MMSE increased from 26 to 29)24
human studyNoopept has published human data from Russian trials, mostly open-label or piracetam-comparator, in impaired populations25
human studyNoopept has a broader spectrum of cognitive effects encompassing memory acquisition, consolidation, and retrieval, as well as a selective anxiolytic action absent from piracetam28
animalNoopept positively influences memory consolidation and retrieval steps, in contrast to pyracetam which facilitates only early stages of memory6
animalNoopept abolished the amnesic effect of cholinoceptor antagonists (scopolamine and mecamylamine) and improved spatial preference in rats6
animalNoopept is protective against DM end organ complications in streptozotocin induced diabetic pubertal rats10
animalThe D + I, D + N and D + I + N groups exhibited fewer DM induced pathological changes than the DC group10
animalDelayed puberty was normalized by noopept in prepubertal diabetic rats15
animalBlood glucose levels were lower in noopept-administered diabetic groups15
animalNoopept decreased HOMA-IR in insulin administered diabetic group15
animalNo difference in kisspeptin, serum LH, FSH, hippocampal NGF-BDNF levels and spatial learning assessment among groups15
animalNoopept demonstrated cognition restoring effect in several animal models of Alzheimer disease17
animalNoopept shows antihyperglycemic activity that is more pronounced under conditions of oral application than after intraperitoneal injection in adult Wistar rats with streptozotocin-induced diabetes18
animalNoopept positively influences memory consolidation and retrieval steps, while pyracetam facilitates only early stages of memory process22
animalNoopept demonstrates neuroprotective effect in vivo in cases of various forms of brain ischemia22
animalIn a rodent model of Alzheimer's disease, 7-day treatment with noopept improved fear memory24
animalNoopept improved memory in olfactory bulbectomy model of Alzheimer's disease after 21 days of treatment24
in vitroNoopept demonstrates neuroprotective effect in vitro on various neuronal models22
expert opinionLittle clinical evidence supports noopept's use as a cognitive-enhancing supplement24
expert opinionEffects on brain wave function have been noted for over 70 minutes following injections26
expert opinionNo randomised, double-blind, placebo-controlled trial exists, and no study has been done in healthy people27
expert opinionNoopept is a synthetic enhancer that shows promise in improving cognitive functions29
How it works
Based on 3 human study findings, 42 animal findings, 51 in vitro findings, 13 expert opinion findings and 13 theoretical findings.
human studyNoopept caused EEG changes typical for those induced by nootropic drugs which were more pronounced in the right hemisphere1
human studyNoopept is a synthetic di-peptide that can enhance the levels of neurotrophic factors (BDNF and NGF) in the brain2
human studyNoopept functions as a prodrug of the endogenous neuropeptide cycloprolylglycine (cyclo-Pro-Gly, cPG)28
animalNoopept has been characterized as a nootropic agent capable of increasing cognitive function in cell culture and in vivo models of brain-degenerative diseases by clearing out protein aggregates from brain tissue2
animalNoopept increases the expression of NGF and BDNF in the hippocampus4
animalNoopept reduces oxidative stress and enhances the activity of antioxidant systems4
animalNoopept represses kinases pSAPK/JNK and pERK1 induced by stress4
animalNoopept demonstrates neuroprotective effect in vivo in various forms of brain ischemia6
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animalNoopept mechanism of action is based on antioxidant effect, anti-inflammatory action, inhibition of neurotoxicity of excess calcium and glutamate, and improvement of blood rheology6
animalNoopept and its metabolite cyclo-L-prolylglycine increased transcallosal evoked potential amplitude in rat brain and retained this level over entire observation time above 3.5 hours6
animalCycloprolylglycine itself has nootropic potential when injected, although to a lesser degree than Noopept8
animalNoopept is a cognitive enhancer that exhibits antidiabetic properties10
animalRenal tubule diameter and corneal and retinal thickness were increased significantly in DC groups compared to the control group10
animalNoopept has anti-diabetic properties15
animalNumber of degenerated cells in hippocampus and testis were higher in diabetes control group compared with noopept-treated groups15
animalGnRH immunoreactivity in Diabetes + Noopept group was increased when compared to insulin + noopept group15
animalNoopept prevents ionic disbalance, excitotoxicity, free radicals and pro-inflammatory cytokines accumulation, and neurotrophine deficit17
animalStreptozotocin decreases the concentrations of incretin GLP-1 and insulin in the blood18
animalNoopept has a normalizing effect on GLP-1 and insulin parameters in streptozotocin-induced diabetic rats18
animalNoopept's influence on incretin parameters is not related to the inhibition of dipeptidyl peptidase IV18
animalGLP-1 increases NGF expression in the insular system18
animalThe increase in incretin activity contributes to the antiapoptotic effect of Noopept on pancreatic β cells18
animalNoopept stimulates the expression of NGF and BDNF mRNA in rat hippocampus19
animalExpression of NGF and BDNF mRNA in the cerebral cortex was below control after single administration of Noopept19
animalChronic administration of Noopept caused a slight increase in BDNF expression in cerebral cortex19
animalExpression of mRNA for both neurotrophins increased in hippocampus after acute administration of Noopept19
animalChronic treatment with Noopept was not followed by the development of tolerance, but even potentiated the neurotrophic effect19
animalNootropic drug increases expression of neurotrophic factors in the hippocampus19
animalNeurotrophin synthesis in the hippocampus determines cognitive function, particularly in consolidation and delayed memory retrieval19
animalGVS-111 produces an antithrombotic effect, influencing various stages of the blood coagulation process21
animalGVS-111 exhibits anticoagulant and fibrinolytic properties21
animalGVS-111 enhances fibrin destabilization by reducing the XIIIa factor activity21
animalNoopept drug action is based on antioxidant effect22
animalNoopept drug action is based on antiinflammatory action22
animalNoopept inhibits neurotoxicity of excess calcium and glutamate22
animalNoopept improves blood rheology22
animalGVS-111 is prodrug which converts in the body to cyclo-prolylglycine, and which is identical to the endogenous cyclopeptide that produces the nootropic activity23
animalOne of noopept's metabolites, cycloprolyglycine (cPG) is increased in the brain one hour after noopept administration, and it is thought to be responsible for noopept's longer-term nootropic activities24
animalProposed mechanisms of action based on preclinical studies include increasing acetylcholine signaling, increasing the expression of BDNF and NGF, protecting from glutamate toxicity, and increasing inhibitory neurotransmission24
animalNoopept prevented the amnestic effects of cholinergic neurotransmission inhibitors suggesting mechanism to boost cholinergic neurotransmission24
animalThe major metabolite of administered Noopept appears to be structurally similar to the endogenous neurodipeptide cycloprolylglycine26
animalCycloprolylglycine itself has nootropic potential when injected, although to a lesser degree than Noopept26
animalCycloprolylglycine increased 2.4-fold in neural tissue following 5mg/kg injections, from 2.8nmol/g to 6.7nmol/g wet brain weight26
animalOstrovskaya et al. (2008) demonstrated that noopept stimulates expression of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) mRNA in the rat hippocampus28
animalAcute noopept administration increased both NGF and BDNF neurotrophins, while chronic 28-day treatment potentiated rather than diminished the effect, demonstrating absence of tolerance28
in vitroNoopept (ethyl ester of N-phenylacetyl-L-prolylglycine, GVS-111) at 10 μM increases the DNA-binding activity of HIF-1 in HEK293 cells4
in vitroNoopept at 10 μM lacks the ability to affect DNA-binding activity of CREB, NFAT, NF-κB, p53, STAT1, GAS, VDR, and HSF14
in vitroNoopept provoked an additional increase in the DNA-binding activity of HIF-1 when applied in conditions of CoCl2-induced HIF-1 stabilization4
in vitroThe HIF-positive effect of Noopept is concentration-dependent4
in vitroPiracetam at 1 mM failed to affect significantly any of the transcription factors under study4
in vitroNoopept (10 μM) was shown to increase the DNA-binding activity of HIF-1 only, while lacking the ability to affect that of CREB, NFAT, NF-κB, p53, STAT1, GAS, VDR, and HSF15
in vitroNoopept provoked an additional increase in the DNA-binding activity of HIF-1 when applied in conditions of CoCl2-induced HIF-1 stabilization5
in vitroThe degree of this HIF-positive effect of Noopept was shown to be concentration-dependent5
in vitroPiracetam (1 mM) failed to affect significantly any of the TF under study5
in vitroNoopept demonstrates neuroprotective effect in vitro on various neuronal models6
in vitroNoopept increased the frequency of spontaneous calcium transients in neurons of CA1 radial layer in cultured rat hippocampal slices6
in vitroNoopept exerted no significant effect on intracellular calcium concentration and dynamics in neurons of hippocampal CA1 pyramidal layer6
in vitroThe conversion of Noopept to cycloprolylglycine increased 2.4-fold in neural tissue following 5mg/kg injections, from 2.8nmol/g to 6.7nmol/g wet brain weight8
in vitroOmberacetam (500 μM) increased the content of OATP1B1 and OATP1B3 in HepG2 cells11
in vitroFabomotizole did not affect the level of OATP1B1 and OATP1B3 transporters in HepG2 cells11
in vitroEMHPS (500 μM) increased the content of OATP1B1 compared to control and did not affect the level of OATP1B3 in HepG2 cells11
in vitroOmberacetam (100-500 μM), fabomotizole (500 μM), and EMHPS (10-500 μM) reduced the OATP1B1/OATP1B3 ratio as evidenced by decreased atorvastatin penetration into HepG2 cells11
in vitroNoopept increases both the basal DNA-binding activity of HIF-1 and the activity induced by various hypoxia mimetics13
in vitroThe mechanism of stabilization of the oxygen-sensitive HIF1α subunit by noopept involves the inhibition of HIF-1 prolyl hydroxylase13
in vitroNoopept has a positive effect on the level of the HIF1α protein13
in vitroThe effect of noopept is accompanied by changes in gene expression which belong to different metabolic pathways and are controlled by the transcription factor HIF-113
in vitroNoopept enhances neurotrophin NGF and BDNF expression14
in vitroNoopept increases HIF-1 activity14
in vitroNoopept did not affect cell distribution over G1, S, G2 cell cycle phases in HEK293 and SH-SY5Y cell lines14
in vitroNoopept did not affect the relative level of proliferation marker Ki-67 in HEK293 and SH-SY5Y cell lines14
in vitroNoopept does not stimulate cell growth14
in vitroNoopept (10 μM) increased the DNA-binding activity of HIF-1 in HEK293 cells16
in vitroNoopept lacked the ability to affect DNA-binding activity of CREB, NFAT, NF-κB, p53, STAT1, GAS, VDR, and HSF1 in HEK293 cells16
in vitroNoopept provoked an additional increase in HIF-1 DNA-binding activity under CoCl2-induced HIF-1 stabilization conditions16
in vitroThe HIF-positive effect of Noopept was shown to be concentration-dependent16
in vitroPiracetam (1 mM) failed to affect significantly any of the transcriptional factors under study16
in vitroNoopept L-isomer and its metabolite L-isomer of N-phenylacetylprolyl are able to bind to the active site of prolyl hydroxylase 216
in vitroNoopept D-isomer is pharmacologically ineffective and unable to bind to prolyl hydroxylase 2 active site16
in vitroNoopept at 10 μM concentration pretreatment improved PC12 cells viability against Aβ 25-35 induced injury17
in vitroNoopept reduced the number of early and late apoptotic cells in PC12 cells exposed to Aβ 25-3517
in vitroNoopept reduced levels of intracellular reactive oxygen species in PC12 cells exposed to Aβ 25-3517
in vitroNoopept reduced intracellular calcium levels in PC12 cells exposed to Aβ 25-3517
in vitroNoopept enhanced mitochondrial membrane potential in PC12 cells exposed to Aβ 25-3517
in vitroNoopept pretreatment significantly attenuated tau hyperphosphorylation at Ser396 in PC12 cells17
in vitroNoopept ameliorated alterations of neurite outgrowth evoked by Aβ 25-35 in PC12 cells17
in vitroGVS-111 significantly increased neuronal survival after H2O2-treatment displaying dose-dependent neuroprotective activity from 10nM to 100 microM20
in vitroGVS-111 inhibited the accumulation of intracellular free radicals and lipid peroxidation damage in neurons treated with H2O2 or FeSO420
in vitroGVS-111 exhibited significantly higher neuroprotection compared to Piracetam, Vitamin E, propyl gallate and s-PBN20
in vitroIn Down's syndrome cortical cultures, chronic treatment with GVS-111 significantly reduced the appearance of degenerative changes and enhanced neuronal survival20
in vitroGVS-111 metabolite cyclo-L-prolylglycine exhibits anticoagulant properties in vitro21
in vitroGVS-111 metabolite cyclo-L-prolylglycine exhibits fibrinolytic properties in vitro21
in vitrocyclo-L-prolylglycine metabolite exhibits antifibrin-stabilizing properties21
in vitrocyclo-L-prolylglycine metabolite exhibited an antiaggregant effect21
in vitroCyclo-prolylglycine formation from GVS-111 in the presence of plasma and brain enzymes was shown in vitro23
in vitroCycloprolylglycine is a positive modulator of AMPA receptors and exerts neuroprotective effects through AMPA- and TrkB-receptor activation28
in vitroNoopept at micromolar concentrations reduces both spontaneous and potassium-stimulated glutamate release from cortical slices, suggesting a protective mechanism against glutamate excitotoxicity28
expert opinionNoopept is commonly said to be 1000-fold as potent as piracetam (derived from the abstract of a German review) although elsewhere it has been claimed to be more variable, at somewhere between 200 and 50,000 when comparing the two molecules on a dose-per-dose basis8
expert opinionNoopept is included in the group of racetams, although its chemical structure is quite different than other compounds from this group9
expert opinionThe 1000x more potent than piracetam claim refers to potency by dose — Noopept is active at tens of milligrams where piracetam is dosed in grams25
expert opinionNoopept is a synthetic molecule commonly said to be in the racetam class (although this is technically not true, due to Noopept not having a 2-oxo-pyrollidine nucleus)26
expert opinionNoopept was synthesized in 1996 and was based off of the endogenous neuropeptide cycloprolylglycine26
expert opinionNoopept is commonly said to be 1000-fold as potent as piracetam26
expert opinionPotency compared to piracetam has been claimed to be somewhere between 200 and 50,000 when comparing on a dose-per-dose basis26
expert opinionOn a structural basis, Noopept is a dipeptide conjugate of Piracetam26
expert opinionNoopept is a water-soluble proline containing dipeptide structure, and is a Cycloprolylglycine pro-drug26
expert opinionNoopept acts as a pro-drug for cycloprolylglycine26
expert opinionNoopept is N-phenylacetyl-L-prolylglycine ethyl ester (omberacetam, GVS-111), a proline-glycine dipeptide derivative with a phenylacetyl group and ethyl ester on glycine27
expert opinionNoopept was designed as a dipeptide analog of piracetam at the Zakusov Institute of Pharmacology in Moscow27
expert opinionNoopept was designed as a dipeptide analog of piracetam based on the hypothesis that piracetam's pyrrolidine ring mimics a proline residue and its N-acetamide moiety mimics glycine28
theoreticalDipeptides are orally active owing to higher stability and ability to penetrate biological barriers due to the presence of specific ATP–dependent transporters in enterocytes and blood-brain barrier3
theoreticalAn active site of regulatory peptides represents a peptide chain β turn with four residues involved, two of which (i + 2, i + 3) are in the middle and play a major role in recognition of whole peptide by receptor3
theoreticalNoopept (L-isomer) and its metabolite L-isomer of N-phenylacetylprolyl are able to bind to the active site of prolyl hydroxylase 2, unlike the pharmacologically ineffective D-isomer4
theoreticalNoopept (L-isomer), as well as its metabolite, L-isomer of N-phenylacetylprolyl, unlike its pharmacologically ineffective D-isomer, is able to bind to the active site of prolyl hydroxylase 25
theoreticalThe ability of Noopept to provoke a selective increase in the DNA-binding activity of HIF-1 explain the wide spectrum of neurochemical and pharmacological effects of Noopept5
theoreticalThe HIF-positive effect is proposed as the primary mechanism of the activity of this Pro-Gly-containing dipeptide5
theoreticalN-phenylacetyl-L-prolylglycine ethyl ester is commonly referred to as 'Noopept', and is a synthetic molecule commonly said to be in the racetam class (although this is technically not true, due to Noopept not having a 2-oxo-pyrollidine nucleus)8
theoreticalOn a structural basis, Noopept is a dipeptide conjugate of Piracetam8
theoreticalThe mechanism of action of Noopept is multifaceted and involves modulation of various neurotransmitter systems within the brain9
theoreticalHIF-positive effect is proposed as the primary mechanism of activity of Noopept16
theoreticalNoopept (N-phenyl-acetyl-L-prolylglycine ethyl ester) was constructed as a dipeptide analog of piracetam17
theoreticalNoopept (N-phenylacetyl-L-polyglycine ethyl ester) structure was designed using dipeptide nootropes based on imitation of pyracetam22
theoreticalNoopept is the ethyl ester of N-phenylacetyl-L-prolylglycine, a dipeptide-derived compound that is orally active25
Dosing
Based on 7 human study findings, 4 animal findings and 2 anecdotal findings.
human studyEqual therapeutic response was observed in patients of young and medium age with the course of 30mg daily1
human studyYounger patients with psychoorganic syndrome of posttraumatic origin showed better results with 15 mg daily1
human studyNoopept is pharmacologically active at doses 1,000 times lower than those for Piracetam4
human studyConsumers could be exposed to up to four-fold greater than pharmaceutical dosages when using individual cognitive enhancement supplement products12
human study10 mg twice daily regimen used in Russian clinical trials of patients with mild cognitive impairment25
human studyThe published clinical dosing amount is 20 mg per day, conventionally split 10 mg twice daily, taken for two months in an open study of 60 stroke patients27
human studyNoopept demonstrated nootropic effects at doses approximately 1000-fold lower than piracetam (effective at 10-30 mg/day versus 1200-4800 mg/day)28
animalNoopept (N-phenylacetyl-L-polyglycine ethyl ester) has an effective dose 1000 times lower than pyracetam6
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animalGVS-111 shows antithrombotic effects upon intraperitoneal administration21
animalGVS-111 shows antithrombotic effects upon peroral administration21
animalNoopept is 1000 times lower effective dose than pyracetam22
anecdotalPeople take 10-30 mg/day, but Russian trials used 20 mg25
anecdotalCommunity sources commonly describe cycling several weeks on followed by a break, but this is not trial-defined25
How the body handles it
Based on 5 human study findings, 24 animal findings, 2 in vitro findings, 3 expert opinion findings and 2 theoretical findings.
human studyThe specific nootropic effect of noopept developed after a latent period, starting from the 3-4th week of therapy1
human studyNoopept is able to penetrate the blood-brain barrier (BBB) when administered orally2
human studyNoopept is orally active, and the oral route is both the studied route and the standard community one25
human studyCycloprolylglycine was identified as the major brain metabolite in 199728
human studyOral bioavailability of noopept is approximately 10% for the parent compound with high CNS penetration confirmed28
animalNoopept was determined in rat blood plasma independently of the route of administration for 25 min1
animalNoopept was more resistant to the action of metabolizing enzyme systems as compared to naturally occurring neuropeptides1
animalNoopept was subjected to an intense biotransformation thus demonstrating rather low bioavailability1
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animalNoopept retains activity upon parenteral introduction and peroral administration6
animalNoopept can cross the gastrointestinal tract in rats following an oral dose of 50mg/kg, where it possesses a Tmax of 0.116 hours (7 minutes) and reaches a Cmax of 0.82mcg/mL in serum8
animalThe Cmax of 50mg/kg in rats after oral ingestion (human equivalent of 8mg/kg) reaches 1.289mcg/mL at a Tmax of 0.115 hours (7 minutes); due to the lack of difference between serum and neural concentrations it is said Noopept can easily cross the blood brain barrier8
animalThe half-life of Noopept is around 16 minutes in rats8
animalThere appear to be interspecies differences with rats having more rapid metabolism of Noopept in serum relative to humans8
animalAn oral dose is about the equivalent of one tenth an injected dose (10% bioavailability)8
animalNoopept per se is not reliably detectable in serum as it is rapidly metabolized within 25 minutes of oral ingestion8
animalNoopept activity is retained upon parenteral introduction and peroral administration22
animalGVS-111 itself was not found in rat brain 1 h after 5 mg/kg i.p. administration up to limit of detection (LOD) under high performance liquid chromatography (HPLC) conditions23
animalThree substances corresponding to the three possible GVS-111 metabolites, namely phenylacetic acid, prolylglycine and cyclo-prolylglycine, were found in experimental rat brain samples23
animalOnly cyclo-prolylglycine concentration increased (2.5-fold) 1 h after GVS-111 administration23
animalNoopept has a short half-life (~5-10 minutes in rodents) and is not present in the brain one hour after administration24
animalNoopept crosses the blood brain barrier in rodents24
animalNoopept can cross the gastrointestinal tract in rats following an oral dose of 50mg/kg with a Tmax of 0.116 hours (7 minutes) and Cmax of 0.82mcg/mL in serum26
animalCmax of 50mg/kg oral Noopept in rats in brain reaches 1.289mcg/mL at Tmax of 0.115 hours (7 minutes)26
animalNoopept can easily cross the blood brain barrier26
animalThe half-life of Noopept is around 16 minutes in rats26
animalNoopept is not detectable in serum 25 minutes following oral ingestion26
animalThere appear to be interspecies differences with rats having more rapid metabolism of Noopept in serum relative to humans26
animalNoopept is a prodrug; the parent molecule was undetectable in rat brain after dosing, and its metabolite cyclo-prolylglycine is what rises27
animalThe parent compound was below the limit of detection in rat brain one hour after dosing, while its metabolite cyclo-prolylglycine rose 2.5-fold27
in vitroNoopept is a water-soluble proline containing dipeptide structure, and while it per se is not detectable in serum even after high injected concentrations it increases concentrations of Cycloprolylglycine and, as such, is a Cycloprolylglycine pro-drug8
in vitroThe major metabolite of administered Noopept appears to be structurally similar to the endogeous neurodipeptide known as Cycloprolylglycine (Proline and Glycine in a cyclic configuration)8
expert opinionMost nootropics do not have an immediate effect after a single dose, and therefore long-term use is necessary to achieve the desired results7
expert opinionNoopept appears to have bioactivity following oral ingestion in humans26
expert opinionAn oral dose appears to be about one tenth an injected dose (approximately 10% bioavailability)26
theoreticalDipeptides have oral bioavailability due to ability to penetrate biological barriers and absence of targets bounds for exopeptidases3
theoreticalNoopept is an orally available active pharmaceutical ingredient9
Safety and side effects
Based on 4 human study findings, 3 animal findings, 1 in vitro finding, 5 expert opinion findings, 1 anecdotal finding and 1 theoretical finding.
human studyThe stimulatory effect differed from that of psychostimulators: it was not accompanied by anxiety, aggressiveness, sleep and vegetative disturbances1
human study75% of declared drug quantities on supplement labels were inaccurate12
human studyMultiple unapproved drugs were detected in cognitive enhancement supplements, with some not declared on labels and some declared drugs not detected12
human studyPossible side effects of noopept in clinical trial included sleep disturbances (5/31 patients), irritability (3/31), and increased blood pressure (7/31)24
animalNoopept (0.5 mg/kg, i.p.) does not possess anticonvulsant properties when given as single or repeated administration6
animalGVS-111 has low toxicity21
animalGVS-111 has absence of complications21
in vitroThe effect of tested substances on OATP1B1/OATP1B3 is clinically insignificant according to FDA approach C/I ratio calculation11
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expert opinionNootropics tend to be well tolerated in patients with cognitive impairments; the incidence of side effects is low, and those that do occur are usually mild7
expert opinionThe long-term effects of nootropics on healthy individuals are still unknown7
expert opinionHealth effects of consuming untested combinations of unapproved drugs at unpredictable dosages without clinician oversight in supplements are unknown12
expert opinionThe FDA treats Noopept as an unapproved new drug, not a dietary ingredient, and has stated in warning letters that it is not generally recognised as safe and effective27
expert opinionNoopept is not approved by the FDA, EMA, or other Western regulatory agencies28
anecdotalCommunity sources frequently describe pairing Noopept with a choline source to manage anecdotal headache25
theoreticalPeptide drugs have high activity, low toxicity since they consist of endogenous amino acids, absence of severe side effects due to regulatory action, and lower probability of tolerance or dependence3
What people use it for
Based on 6 human study findings, 3 animal findings, 5 expert opinion findings and 7 theoretical findings.
human studyNoopept is effective for the treatment of psychoorganic disorders with cerebroasthenic and cognitive disturbances1
human studyNoopept is a safe, nootropic compound that is commercially available to humans to enhance cognitive activity2
human studyNoopept is currently used in Europe to treat mild cognitive decline2
human studyNoopept tablets (5 and 10 mg) are under clinical assessment for treating cognitive deficiency of cerebrovascular and post-traumatic origin6
human studyOver-the-counter dietary supplements marketed for memory and cognitive function may contain unapproved pharmaceutical drugs including omberacetam, aniracetam, phenibut, vinpocetine, and picamilon12
human studyNoopept tablets (5 and 10 mg) are under clinical assessment for treating cognitive deficiency of cerebrovascular and post-traumatic origin22
animalNoopept produces selective anxiolytic action6
animalProlonged five-week preliminary administration of noopept enhanced the anticonvulsant activity of valproate in mice6
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animalNoopept produces selective anxiolytic action22
expert opinionNoopept is a nontoxic, orally available, highly effective dipeptide nootropic drug designed as a dipeptide analog of piracetam3
expert opinionNoopept is said to be anxiolytic and mildly psychostimulatory while promoting cognitive health and memory8
expert opinionTherapeutic effectiveness of Noopept should be evaluated at the initial stage of Alzheimer's disease19
expert opinionNoopept is not sold over the counter in the United States and is available with prescription in Russia24
expert opinionNoopept is said to be anxiolytic and mildly psychostimulatory while promoting cognitive health and memory26
theoreticalNootropics improve human thinking, learning, and memory, especially in cases where these functions are impaired7
theoreticalNoopept has neuroprotective properties9
theoreticalNoopept has ability to enhance cognitive function9
theoreticalNoopept holds much promise to prevent the development of Alzheimer's disease in patients with mild cognitive impairment19
theoreticalThe neuroprotective effect of GVS-111 against oxidative damage and its potential nootropic activity may present a valuable therapeutic combination for treatment of mental retardation and chronic neurodegenerative disorders20
theoreticalGVS-111 has neuroprotector properties21
theoreticalGVS-111 is a promising antistroke drug21
Other findings
Based on 1 in vitro finding, 7 expert opinion findings, 1 anecdotal finding and 1 theoretical finding.
in vitroGVS-111 (Noopept) is a novel N-acylprolyl-containing dipeptide analog of Piracetam20
expert opinionDipeptides are more technically available in comparison to poly- and oligopeptides3
expert opinionNoopept belongs to nootropic family of drugs9
expert opinionVery little is known about Noopept's structural and physicochemical properties9
expert opinionNoopept is a nootropic developed at the Zakusov Institute of Pharmacology (Russian Academy of Medical Sciences)24
expert opinionNoopept is a prescription nootropic in Russia27
expert opinionLarge preclinical literature exists, almost all from the originating institute; two small Russian-language clinical reports, both open-label; zero registered trials on ClinicalTrials.gov as of 3 August 202627
expert opinionNoopept (N-phenylacetyl-L-prolylglycine ethyl ester) is a synthetic dipeptide nootropic developed at the V.V. Zakusov Research Institute of Pharmacology of the Russian Academy of Medical Sciences in Moscow in the mid-1990s28
Points of contention
Where the evidence is unsettled, thin, or says less than the popular claim — worth knowing before you draw conclusions.
Limited evidence
Human clinical evidence is thin, exclusively Russian, and open-label
Sources note only two small open-label Russian-language clinical reports exist, no randomized double-blind placebo-controlled trial has been conducted, no study has been done in healthy people, zero trials were registered on ClinicalTrials.gov as of 3 August 2026, and the ADDF review states little clinical evidence supports use as a cognitive-enhancing supplement.
Single source
Almost all preclinical data come from the originating institute
The vendor summary notes the large preclinical literature is almost entirely from the Zakusov Institute of Pharmacology, the originating institution, which limits independent replication.
Contested
Potency relative to piracetam is quoted very differently across sources
Some sources cite a fixed '1000-fold' potency versus piracetam (from a German review abstract), while others report a much wider range of 200 to 50,000 on a dose-per-dose basis; community guides clarify this refers to potency by dose (tens of mg vs grams).
Contested
Reported half-life in rodents varies between sources
Examine reports a rat half-life of ~16 minutes, while the ADDF review cites ~5-10 minutes (and ~6.5 minutes per Boiko et al 2000); all agree the parent compound is rapidly cleared and undetectable in brain by one hour.
Other
Regulatory status differs sharply between Russia and the West
Noopept is an approved prescription nootropic in Russia (approved ~2006 for cerebrovascular/post-traumatic cognitive disorders) but is not approved by the FDA, EMA or other Western agencies; the FDA treats it as an unapproved new drug and has issued warning letters stating it is not generally recognized as safe and effective.
Limited evidence
Supplement products labeled as containing omberacetam are frequently mislabeled
A study of cognitive-enhancement supplements found 75% (9/12) of declared drug quantities inaccurate, detected 40.6 mg omberacetam versus a typical 10 mg dose (up to four-fold pharmaceutical dosages), with some drugs undeclared and some declared drugs absent; health effects of these combinations are unknown.
Limited evidence
Antidiabetic and antithrombotic findings are animal/in vitro only
Reports of Noopept's antidiabetic, antihyperglycemic, and antithrombotic/anticoagulant effects come from rat studies (e.g., 60 rats, 0.5 mg/kg, 14 days) and in vitro assays, not from human trials.
- Tier 2Effects of noopept on ocular, pancreatic and renal histopathology in streptozotocin induced prepubertal diabetic rats.
- Tier 2Effects of noopept on cognitive functions and pubertal process in rats with diabetes.
- Tier 2[Multicomponent antithrombotic effect of the neuroprotective prolyl dipeptide GVS-111 and its major metabolite cyclo-L-prolylglycine].
- Tier 2Noopept normalizes parameters of the incretin system in rats with experimental diabetes.
Single source
Claims that Noopept passed Russian Phase III trials are not backed by any publicly documented randomized controlled trial.
One information website states Noopept completed Russian Phase III clinical trials and received Russian regulatory approval around 2006. However, the traceable human record consists only of two small, open-label Russian-language studies in cognitively impaired patients; no randomized, double-blind, placebo-controlled trial has been published, no study has been done in healthy people, and no trial for Noopept or omberacetam is registered on ClinicalTrials.gov. The 'Phase III' description therefore rests on a single unverified source rather than a documented controlled trial.
Using it with other compounds
- SelankComplementary
May be complementary
Selank and Noopept both engage BDNF signaling and both report anxiolytic plus nootropic effects, but through distinct mechanisms — Selank via GABAergic/serotonergic modulation and enkephalinase inhibition, Noopept via AMPA/TrkB neurotrophic pathways. Their overlapping calming-plus-cognitive profiles are complementary and this combination is a well-known real-world nootropic pairing.
Tier 4Theoretical — not establishedWhat the research doesn't fully establish
The mechanism descriptions clearly establish both shared dimensions: (1) BDNF_signaling is explicitly listed in approved tags for both peptides, and both pathways sections reference BDNF/NGF neurotrophin signaling; (2) anti_inflammatory is explicitly approved for both. The explanation correctly identifies distinct mechanistic routes—Selank via GABAergic/serotonergic/enkephalinase pathways versus Noopept via AMPA/TrkB/HIF-1 pathways—that converge on overlapping anxiolytic and nootropic effects. This constitutes a valid complementary relationship: shared functional outcomes (anxiety reduction, cognitive support) achieved through non-overlapping molecular mechanisms, with both engaging the claimed shared dimensions. The distinction between mechanisms supports rather than undermines complementarity.Shares anti inflammatory · BDNF signaling
- SemaxComplementary
May be complementary
Both are cognitive-enhancing peptides that raise BDNF/NGF and act through the TrkB neurotrophin pathway, but by different upstream routes — Noopept via its cycloprolylglycine metabolite modulating AMPA/TrkB, and Semax via ACTH-fragment neurotrophin signaling. They converge on the same goals (memory, attention, neuroprotection, anxiolysis) and are commonly used together in nootropic practice, making the pairing potentially additive rather than redundant.
Tier 4Theoretical — not establishedWhat the research doesn't fully establish
The mechanism descriptions clearly establish both shared dimensions: (1) anti_inflammatory — both peptides have documented anti-inflammatory effects (Noopept: 'Antioxidant and anti-inflammatory action'; Semax: 'Anti-inflammatory / immune modulation'); (2) BDNF_signaling — both explicitly target BDNF/NGF neurotrophin pathways via TrkB receptor activation (Noopept: 'BDNF / NGF neurotrophin signaling' and 'TrkB receptor (neuroprotection via activation)'; Semax: 'BDNF/NGF-TrkB neurotrophin signaling' and 'TrkB receptor'). The explanation correctly identifies convergent endpoints (memory, attention, neuroprotection, anxiolysis) achieved through distinct upstream mechanisms (Noopept via AMPA/cycloprolylglycine; Semax via ACTH-fragment/enkephalinase inhibition), which justifies the 'complementary' relationship type as additive rather than redundant. The mechanisms support this characterization.Shares anti inflammatory · BDNF signaling
- SS-31Complementary
No documented conflict
SS-31 protects neurons by stabilizing mitochondria and cutting oxidative stress, while Noopept provides neurotrophic (BDNF) and anti-excitotoxic support. Both share mitochondrial, anti-inflammatory and BDNF-related tags but act through different targets, so they can converge on neuroprotection from complementary angles.
Tier 4Theoretical — not establishedWhat the research doesn't fully establish
Both peptides' mechanisms explicitly support the three claimed shared dimensions. Noopept lists approved tags: mitochondrial_function, anti_inflammatory, BDNF_signaling. SS-31 lists identical approved tags: mitochondrial_function, anti_inflammatory, BDNF_signaling. The mechanisms confirm distinct targets and pathways: SS-31 acts directly on cardiolipin, mPTP, and ETC complexes to stabilize mitochondria and reduce ROS; Noopept acts via AMPA/TrkB receptors, HIF-1 stabilization, and cholinergic signaling to provide neuroprotection and BDNF signaling. Both demonstrate anti-inflammatory effects through different mechanisms (SS-31 via ferroptosis/pyroptosis suppression; Noopept via stress kinase repression and antioxidant action). The explanation accurately characterizes them as converging on neuroprotection through complementary but distinct mechanistic pathways, which is justified by the provided material.Shares mitochondrial function · anti inflammatory · BDNF signaling
- P21Same downstream effect
May be complementary
Both peptides ultimately drive the BDNF/TrkB neurotrophin cascade and promote synaptic plasticity and memory — P21 as a CNTF-derived fragment that upregulates BDNF, Noopept via its metabolite acting on TrkB and AMPA. They reach the same downstream output (enhanced BDNF signaling and neuroprotection) from different upstream starting points, which is generally synergistic but worth noting as overlapping rather than independent.
Tier 4Theoretical — not establishedWhat the research doesn't fully establish
Both peptides' mechanisms clearly establish BDNF/TrkB pathway engagement as a shared downstream output. Noopept's mechanism explicitly lists 'BDNF / NGF neurotrophin signaling' as a pathway and 'BDNF_signaling' as an approved tag, with TrkB receptor activation documented. P21's mechanism explicitly states 'Upregulation of BDNF expression and secretion' and 'BDNF/TrkB' as a primary pathway with 'BDNF_signaling' as an approved tag. Both mechanisms converge on enhanced synaptic plasticity and neuroprotection through this shared cascade, despite different upstream mechanisms (Noopept via metabolite/TrkB/AMPA; P21 via CNTF-derived BDNF upregulation). The 'same_downstream' relationship type and BDNF_signaling shared dimension are directly supported by the provided mechanism material.Shares BDNF signaling
- CerebrolysinComplementary
May be complementary
Noopept raises BDNF/NGF, activates TrkB, and provides antioxidant/anti-inflammatory neuroprotection, echoing Cerebrolysin's neurotrophic and mitochondrial-support actions through a distinct dipeptide mechanism. The two can reinforce cognitive and neuroprotective signaling; combination evidence is anecdotal.
Tier 4Theoretical — not establishedWhat the research doesn't fully establish
The mechanism descriptions clearly establish the three claimed shared dimensions: (1) mitochondrial_function—both peptides are tagged with this and show antioxidant/anti-inflammatory actions supporting mitochondrial health; (2) anti_inflammatory—both explicitly target anti-inflammatory pathways (Cerebrolysin via TNF-α downregulation and microglia modulation; Noopept via antioxidant and anti-inflammatory action); (3) BDNF_signaling—both are tagged with this and their mechanisms confirm it (Cerebrolysin upregulates BDNF; Noopept activates BDNF/NGF signaling via TrkB). The explanation correctly identifies distinct mechanisms (Cerebrolysin's multi-target neurotrophic approach vs. Noopept's HIF-1/TrkB pathway) that converge on overlapping neuroprotective and cognitive outcomes, which justifies the 'complementary' relationship type. The claim that they can reinforce each other through these shared dimensions is supported by the parallel but mechanistically distinct pathways described.Shares mitochondrial function · anti inflammatory · BDNF signaling
- DavunetideComplementary
No documented conflict
Both offer neuroprotection and cognitive support via different routes — davunetide through microtubule/tau stabilization, noopept through TrkB/BDNF activation and protection against glutamate excitotoxicity. The mechanisms are distinct and potentially additive for neuronal resilience.
Tier 4Theoretical — not establishedWhat the research doesn't fully establish
Both peptides' mechanisms explicitly include anti-inflammatory activity as an approved tag and effect. Davunetide shows 'Anti-inflammatory activity' in its effects list with approved tag 'anti_inflammatory'. Noopept shows 'Antioxidant and anti-inflammatory action' in its effects with approved tag 'anti_inflammatory'. The proposed relationship correctly identifies that both peptides operate through distinct mechanistic pathways (davunetide via microtubule/tau stabilization; noopept via TrkB/BDNF, HIF-1, and glutamate excitotoxicity protection) while sharing anti-inflammatory effects, making them mechanistically complementary for neuroprotection. The explanation accurately reflects the provided mechanism material.Shares anti inflammatory
- CortexinComplementary
May be complementary
Cortexin modulates AMPA/glutamate signaling and protects neurons from excitotoxicity, while Noopept positively modulates AMPA receptors and raises BDNF/NGF via its cycloprolylglycine metabolite. They act on overlapping glutamatergic/neurotrophic machinery through distinct entry points, making them a plausible complementary nootropic pairing.
Tier 4Theoretical — not establishedWhat the research doesn't fully establish
Both peptides' mechanisms clearly establish the two shared dimensions claimed: (1) Anti-inflammatory: Cortexin explicitly lists 'Anti-inflammatory (central and systemic)' with neuroinflammatory pathway involvement; Noopept lists 'Antioxidant and anti-inflammatory action (animal/in vitro)' with anti_inflammatory tag. (2) BDNF_signaling: Cortexin explicitly includes 'BDNF-like / NGF-like neurotrophic signaling' and BDNF_signaling tag; Noopept lists 'BDNF / NGF neurotrophin signaling' and BDNF_signaling tag. The explanation's claim of complementary action through distinct entry points on overlapping glutamatergic/neurotrophic machinery is also supported: Cortexin targets AMPA/kainate/mGluR receptors directly; Noopept positively modulates AMPA receptors via cycloprolylglycine metabolite and activates TrkB (neurotrophin receptor). Both converge on neuroprotection against excitotoxicity and neurotrophic support through mechanistically distinct pathways, justifying the 'complementary' relationship type.Shares anti inflammatory · BDNF signaling
Safety and side effects
Safety and side effects
Reported side effects (human). A clinical trial reported possible side effects including sleep disturbances (5 of 31 patients), irritability (3 of 31) and increased blood pressure (7 of 31) (src-3, src-30). A separate trial reported that the stimulatory effect of Noopept differed from psychostimulators in not being accompanied by anxiety, aggressiveness, sleep or vegetative disturbances, and that the specific nootropic effect developed after a latent period beginning in the 3rd-4th week of therapy (src-5, src-39).
General tolerability claims. A review states peptide drugs tend to have high activity and low toxicity because they consist of endogenous amino acids, with an absence of severe side effects and a lower probability of tolerance or dependence (src-13, src-69). A nootropics review states nootropics tend to be well tolerated with low, mild side effects in cognitively impaired patients, but that their long-term effects in healthy individuals remain unknown (src-14, src-70). An animal study reported that chronic 28-day treatment did not produce tolerance (src-6, src-42). These are general or animal-based characterizations rather than controlled human safety data.
Community-reported management. A community dosing guide reports users frequently pair Noopept with a choline source to manage anecdotal headache, and commonly cycle several weeks on followed by a break, though this cycling is not trial-defined (src-9, src-59).
Regulatory safety position. A vendor site states the FDA treats Noopept as an unapproved new drug rather than a dietary ingredient and has stated in warning letters that it is not generally recognized as safe and effective; an information site states it is not approved by the FDA, EMA or other Western regulatory agencies (src-7, src-8, src-47, src-55).
Product-quality risk. A study reports that over-the-counter cognitive-enhancement supplements may contain unapproved drugs including omberacetam, and that across products tested 75% (9/12) of declared drug quantities were inaccurate (src-20, src-78). The same study reports detecting 40.6 mg omberacetam versus a typical 10 mg pharmacologic dose — up to four-fold greater than pharmaceutical dosages — with some drugs undeclared and some declared drugs not detected, and states the health effects of these untested combinations at unpredictable dosages without clinician oversight are unknown (src-20, src-79).
Evidence limits. Sources stress that human clinical evidence is thin, exclusively Russian, and open-label, with no randomized double-blind placebo-controlled trial and no study in healthy people (src-7, src-48). Antidiabetic and antithrombotic/anticoagulant findings — which bear on bleeding and glucose-related safety — come only from animal and in vitro work (src-16, src-17, src-26, src-28).
Reconstitution and handling
Dosing
No dose has been established for this compound by any Western regulatory agency. Noopept is not approved by the FDA, EMA or other Western agencies (which treat it as an unapproved new drug); it is an approved prescription nootropic only in Russia (src-7, src-8, src-47, src-55). The figures below are what sources report — from Russian clinical studies, vendor pages and community guides — not guidance.
- A vendor site states the published clinical dosing is 20 mg per day, conventionally split as 10 mg twice daily, taken for two months, in an open study of stroke patients (src-7, src-45).
- An open-label study used 10 mg twice per day for 56 days in patients with mild cognitive disorders (src-3, src-29).
- A clinical trial reported an equal therapeutic response in young and medium-age patients on 30 mg daily, while younger patients with post-traumatic psychoorganic syndrome did better on 15 mg daily; test doses were 5 and 10 mg (src-5, src-38).
- An information site reports nootropic effects at approximately 10-30 mg/day, roughly 1000-fold lower than piracetam (which it dose as 1200-4800 mg/day) (src-8, src-50).
- A community dosing guide reports people take 10-30 mg/day, that Russian trials used 20 mg/day (10 mg twice daily) for about 56 days, and that the oral route is both the studied and the standard community route (src-9, src-57, src-58).
- A database summary notes tablets of 5 and 10 mg were under clinical assessment, with activity retained via both parenteral and peroral administration (src-12, src-63).
Potency framing
The frequently quoted "1000× more potent than piracetam" claim is described by Examine as derived from a German review abstract, with other sources reporting a much wider range of 200 to 50,000 on a dose-per-dose basis (src-1, src-11). A community guide clarifies this refers to potency by dose — Noopept being active at tens of milligrams where piracetam is dosed in grams (src-9, src-58).
Preparation and purity
Sources describe Noopept as an orally available compound taken in tablet/oral form; oral bioavailability of the parent compound is reported at approximately 10% with high CNS penetration (src-8, src-54, src-68). A community dosing guide notes vendors commonly claim roughly 98%+ purity by HPLC (src-9, src-60). Because a study found that supplement products labeled as containing omberacetam were frequently mislabeled — 75% of declared drug quantities inaccurate, and one product containing ~40.6 mg versus a typical 10 mg dose — the actual content of a given product may differ substantially from its label (src-20, src-78, src-79).
Sources
Ordered by evidence quality — the strongest first.
- PII: S0924-977X(05)80441-9(opens in a new tab)Tier 1Web · pillbuys.com
- Comparative studies of Noopept and piracetam in the ...(opens in a new tab)Tier 1Web · researchgate.net · 2024
- Current Pharmaceutical Design(opens in a new tab)Tier 2Web · pdfs.semanticscholar.org
- Molecular Mechanism Underlying the Action of Substituted ...(opens in a new tab)Tier 2Web · pmc.ncbi.nlm.nih.gov
- Molecular Mechanism Underlying the Action of Substituted Pro-Gly Dipeptide Noopept(opens in a new tab)Tier 2Web · pmc.ncbi.nlm.nih.gov
- nootropic drug noopept: Topics by Science.gov(opens in a new tab)Tier 2Web · science.gov
- Nootropics as Cognitive Enhancers: Types, Dosage and Side ...(opens in a new tab)Tier 2Web · pmc.ncbi.nlm.nih.gov
- N-Phenylacetyl-L-prolylglycine ethyl ester(opens in a new tab)Tier 2Web · examine.com · 2025
- Physicochemical and structural analysis of N-phenylacetyl-L-prolylglycine ethyl ester (Noopept) - An active pharmaceutical ingredient with nootropic activity.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2025
- Effects of noopept on ocular, pancreatic and renal histopathology in streptozotocin induced prepubertal diabetic rats.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2023
- The Effect of Original Russian Neurotropic Drugs on Organic Anion Transporting Polypeptides OATP1B1 and OATP1B3.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2023
- Five Unapproved Drugs Found in Cognitive Enhancement Supplements.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2021
- Cognitive Enhancer Noopept Activates Transcription Factor HIF-1.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2020
- Drug with Neuroprotective Properties Noopept Does Not Stimulate Cell Proliferation.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2019
- Effects of noopept on cognitive functions and pubertal process in rats with diabetes.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2019
- Molecular Mechanism Underlying the Action of Substituted Pro-Gly Dipeptide Noopept.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2016
- Neuroprotective effect of novel cognitive enhancer noopept on AD-related cellular model involves the attenuation of apoptosis and tau hyperphosphorylation.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2014
- Noopept normalizes parameters of the incretin system in rats with experimental diabetes.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2014
- GVS-111 prevents oxidative damage and apoptosis in normal and Down's syndrome human cortical neurons.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2003
- [Multicomponent antithrombotic effect of the neuroprotective prolyl dipeptide GVS-111 and its major metabolite cyclo-L-prolylglycine].(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2002
- [The original novel nootropic and neuroprotective agent noopept].(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2002
- The major metabolite of dipeptide piracetam analogue GVS-111 in rat brain and its similarity to endogenous neuropeptide cyclo-L-prolylglycine.(opens in a new tab)Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 1997
- Noopept(opens in a new tab)Tier 3Web · alzdiscovery.org
- Noopept Dosage: What the Data Shows (2026)(opens in a new tab)Tier 3Web · thepeptidecatalog.com
- Noopept Dosage Chart - Dosage Peptide(opens in a new tab)Tier 3Web · dosagepeptide.com · 2026
- Noopept (Omberacetam): Research Evidence & Safety Profile | PeptideInsight(opens in a new tab)Tier 3Web · peptideinsight.com · 2026
- A Mini-review on Unlocking Cognitive Enhancement: An Innovative Strategy for Optimal Brain Functions.(opens in a new tab)Tier 3PubMed · pubmed.ncbi.nlm.nih.gov · 2026