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Noopept

Tier 3 · Reported use
Also known as Omberacetam · GVS-111 · N-phenylacetyl-L-prolylglycine ethyl ester

The strongest evidence present is Tier 1: an information site states Noopept completed Russian Phase III clinical trials and received Russian regulatory approval (~2006), and several human observational/open-label Russian studies are reported3,21. 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. The ADDF review states little clinical evidence supports use as a cognitive-enhancing supplement21. Almost all preclinical data come from the originating Zakusov Institute. 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(vendor claim). 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 nucleus6,7. Examine reports it was synthesized in 1996, based on the endogenous neuropeptide cycloprolylglycine6. The ADDF review and vendor/information sources state it was developed at the V.V(vendor claim). 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 glycine21. Sources give its molecular formula as C17H22N2O4, molecular weight ~318.4 g/mol, and CAS 157115-85-021.

Reported uses and effects

Examine and vendor sources say Noopept is claimed to be anxiolytic and mildly psychostimulatory while promoting cognitive health and memory6. 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(vendor claim). 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 origin1,3,12. A 28-day trial in 40 patients reported improvements in memory, attention and short visual memory, with the most marked improvement in attention, and reported relief of cerebroasthenic, hyperesthetic and sleep disturbances. An open-label study reported that 56-day treatment with 10 mg twice daily improved mood and cognition, with MMSE rising from 26 to 2914,21. Study authors suggest it holds promise for preventing Alzheimer's disease development in mild cognitive impairment16.

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 prodrug6,16. 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 barrier6. Examine reports oral bioavailability roughly 10% and rapid metabolism within 25 minutes of oral ingestion, with the major metabolite structurally similar to cycloprolylglycine2,4,6. 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 activity20. Examine notes cycloprolylglycine itself has nootropic potential when injected, though less than Noopept6.

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 mechanism3,11. Animal studies report increased NGF and BDNF expression in hippocampus, reduced oxidative stress and repression of stress-induced kinases3,9, with chronic 28-day treatment reported not to produce tolerance but to potentiate the neurotrophic effect16. The ADDF review lists proposed mechanisms including increased acetylcholine signaling, increased BDNF/NGF, protection from glutamate toxicity, and increased inhibitory neurotransmission21. Additional animal/in vitro reports describe antioxidant, anti-inflammatory, antihyperglycemic (via GLP-1/insulin, not DPP-IV inhibition), and antithrombotic/anticoagulant effects8,13,15,18; 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(vendor claim). 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 States21. 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(vendor claim). The ADDF review states little clinical evidence supports use as a cognitive-enhancing supplement21.

What the research shows

203 findings extracted from the 22 sources cited below, strongest evidence first within each group. Every one links to the source it came from.

What human studies found

Based on 4 human study findings, 14 animal findings, 1 in vitro finding and 3 expert opinion findings.

  • human studyNoopept has more pronounced anxiolytic and neuroprotective properties compared to Piracetam3

  • human studyIn patients with mild cognitive impairment of cerebrovascular and post-traumatic origin, Noopept decreased cognitive impairment, showed an anxiolytic effect, and vegetostabilizing activity3

  • human studyNoopept appears to have bioactivity following oral ingestion in humans6

  • 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)21

  • animalNoopept positively influences memory consolidation and retrieval steps, in contrast to pyracetam which facilitates only early stages of memory4

  • animalNoopept abolished the amnesic effect of cholinoceptor antagonists (scopolamine and mecamylamine) and improved spatial preference in rats4

  • animalNoopept is protective against DM end organ complications in streptozotocin induced diabetic pubertal rats8

  • animalThe D + I, D + N and D + I + N groups exhibited fewer DM induced pathological changes than the DC group8

Show 14 more findings

  • animalDelayed puberty was normalized by noopept in prepubertal diabetic rats13

  • animalBlood glucose levels were lower in noopept-administered diabetic groups13

  • animalNoopept decreased HOMA-IR in insulin administered diabetic group13

  • animalNo difference in kisspeptin, serum LH, FSH, hippocampal NGF-BDNF levels and spatial learning assessment among groups13

  • animalNoopept demonstrated cognition restoring effect in several animal models of Alzheimer disease14

  • animalNoopept shows antihyperglycemic activity that is more pronounced under conditions of oral application than after intraperitoneal injection in adult Wistar rats with streptozotocin-induced diabetes15

  • animalNoopept positively influences memory consolidation and retrieval steps, while pyracetam facilitates only early stages of memory process19

  • animalNoopept demonstrates neuroprotective effect in vivo in cases of various forms of brain ischemia19

  • animalIn a rodent model of Alzheimer's disease, 7-day treatment with noopept improved fear memory21

  • animalNoopept improved memory in olfactory bulbectomy model of Alzheimer's disease after 21 days of treatment21

  • in vitroNoopept demonstrates neuroprotective effect in vitro on various neuronal models19

  • expert opinionEffects on brain wave function have been noted for over 70 minutes following injections6

  • expert opinionLittle clinical evidence supports noopept's use as a cognitive-enhancing supplement21

  • expert opinionNoopept is a synthetic enhancer that shows promise in improving cognitive functions22

How it works

Based on 1 human study finding, 40 animal findings, 49 in vitro findings, 9 expert opinion findings and 12 theoretical findings.

  • human studyNoopept is a synthetic di-peptide that can enhance the levels of neurotrophic factors (BDNF and NGF) in the brain1

  • 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 tissue1

  • animalNoopept increases the expression of NGF and BDNF in the hippocampus3

  • animalNoopept reduces oxidative stress and enhances the activity of antioxidant systems3

  • animalNoopept represses kinases pSAPK/JNK and pERK1 induced by stress3

  • animalNoopept demonstrates neuroprotective effect in vivo in various forms of brain ischemia4

  • animalNoopept mechanism of action is based on antioxidant effect, anti-inflammatory action, inhibition of neurotoxicity of excess calcium and glutamate, and improvement of blood rheology4

  • 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 hours4

Show 103 more findings

  • animalCycloprolylglycine itself has nootropic potential when injected, although to a lesser degree than Noopept6

  • animalThe major metabolite of administered Noopept appears to be structurally similar to the endogenous neurodipeptide cycloprolylglycine6

  • animalCycloprolylglycine itself has nootropic potential when injected, although to a lesser degree than Noopept6

  • animalCycloprolylglycine increased 2.4-fold in neural tissue following 5mg/kg injections, from 2.8nmol/g to 6.7nmol/g wet brain weight6

  • animalNoopept is a cognitive enhancer that exhibits antidiabetic properties8

  • animalRenal tubule diameter and corneal and retinal thickness were increased significantly in DC groups compared to the control group8

  • animalNoopept has anti-diabetic properties13

  • animalNumber of degenerated cells in hippocampus and testis were higher in diabetes control group compared with noopept-treated groups13

  • animalGnRH immunoreactivity in Diabetes + Noopept group was increased when compared to insulin + noopept group13

  • animalNoopept prevents ionic disbalance, excitotoxicity, free radicals and pro-inflammatory cytokines accumulation, and neurotrophine deficit14

  • animalStreptozotocin decreases the concentrations of incretin GLP-1 and insulin in the blood15

  • animalNoopept has a normalizing effect on GLP-1 and insulin parameters in streptozotocin-induced diabetic rats15

  • animalNoopept's influence on incretin parameters is not related to the inhibition of dipeptidyl peptidase IV15

  • animalGLP-1 increases NGF expression in the insular system15

  • animalThe increase in incretin activity contributes to the antiapoptotic effect of Noopept on pancreatic β cells15

  • animalNoopept stimulates the expression of NGF and BDNF mRNA in rat hippocampus16

  • animalExpression of NGF and BDNF mRNA in the cerebral cortex was below control after single administration of Noopept16

  • animalChronic administration of Noopept caused a slight increase in BDNF expression in cerebral cortex16

  • animalExpression of mRNA for both neurotrophins increased in hippocampus after acute administration of Noopept16

  • animalChronic treatment with Noopept was not followed by the development of tolerance, but even potentiated the neurotrophic effect16

  • animalNootropic drug increases expression of neurotrophic factors in the hippocampus16

  • animalNeurotrophin synthesis in the hippocampus determines cognitive function, particularly in consolidation and delayed memory retrieval16

  • animalGVS-111 produces an antithrombotic effect, influencing various stages of the blood coagulation process18

  • animalGVS-111 exhibits anticoagulant and fibrinolytic properties18

  • animalGVS-111 enhances fibrin destabilization by reducing the XIIIa factor activity18

  • animalNoopept drug action is based on antioxidant effect19

  • animalNoopept drug action is based on antiinflammatory action19

  • animalNoopept inhibits neurotoxicity of excess calcium and glutamate19

  • animalNoopept improves blood rheology19

  • animalGVS-111 is prodrug which converts in the body to cyclo-prolylglycine, and which is identical to the endogenous cyclopeptide that produces the nootropic activity20

  • 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 activities21

  • 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 neurotransmission21

  • animalNoopept prevented the amnestic effects of cholinergic neurotransmission inhibitors suggesting mechanism to boost cholinergic neurotransmission21

  • in vitroNoopept (ethyl ester of N-phenylacetyl-L-prolylglycine, GVS-111) at 10 μM increases the DNA-binding activity of HIF-1 in HEK293 cells3

  • in vitroNoopept at 10 μM lacks the ability to affect DNA-binding activity of CREB, NFAT, NF-κB, p53, STAT1, GAS, VDR, and HSF13

  • in vitroNoopept provoked an additional increase in the DNA-binding activity of HIF-1 when applied in conditions of CoCl2-induced HIF-1 stabilization3

  • in vitroThe HIF-positive effect of Noopept is concentration-dependent3

  • in vitroPiracetam at 1 mM failed to affect significantly any of the transcription factors under study3

  • 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 HSF13

  • in vitroNoopept provoked an additional increase in the DNA-binding activity of HIF-1 when applied in conditions of CoCl2-induced HIF-1 stabilization3

  • in vitroThe degree of this HIF-positive effect of Noopept was shown to be concentration-dependent3

  • in vitroPiracetam (1 mM) failed to affect significantly any of the TF under study3

  • in vitroNoopept (10 μM) increased the DNA-binding activity of HIF-1 in HEK293 cells3

  • in vitroNoopept lacked the ability to affect DNA-binding activity of CREB, NFAT, NF-κB, p53, STAT1, GAS, VDR, and HSF1 in HEK293 cells3

  • in vitroNoopept provoked an additional increase in HIF-1 DNA-binding activity under CoCl2-induced HIF-1 stabilization conditions3

  • in vitroThe HIF-positive effect of Noopept was shown to be concentration-dependent3

  • in vitroPiracetam (1 mM) failed to affect significantly any of the transcriptional factors under study3

  • in vitroNoopept L-isomer and its metabolite L-isomer of N-phenylacetylprolyl are able to bind to the active site of prolyl hydroxylase 23

  • in vitroNoopept D-isomer is pharmacologically ineffective and unable to bind to prolyl hydroxylase 2 active site3

  • in vitroNoopept demonstrates neuroprotective effect in vitro on various neuronal models4

  • in vitroNoopept increased the frequency of spontaneous calcium transients in neurons of CA1 radial layer in cultured rat hippocampal slices4

  • in vitroNoopept exerted no significant effect on intracellular calcium concentration and dynamics in neurons of hippocampal CA1 pyramidal layer4

  • 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 weight6

  • in vitroOmberacetam (500 μM) increased the content of OATP1B1 and OATP1B3 in HepG2 cells9

  • in vitroFabomotizole did not affect the level of OATP1B1 and OATP1B3 transporters in HepG2 cells9

  • in vitroEMHPS (500 μM) increased the content of OATP1B1 compared to control and did not affect the level of OATP1B3 in HepG2 cells9

  • 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 cells9

  • in vitroNoopept increases both the basal DNA-binding activity of HIF-1 and the activity induced by various hypoxia mimetics11

  • in vitroThe mechanism of stabilization of the oxygen-sensitive HIF1α subunit by noopept involves the inhibition of HIF-1 prolyl hydroxylase11

  • in vitroNoopept has a positive effect on the level of the HIF1α protein11

  • 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-111

  • in vitroNoopept enhances neurotrophin NGF and BDNF expression12

  • in vitroNoopept increases HIF-1 activity12

  • in vitroNoopept did not affect cell distribution over G1, S, G2 cell cycle phases in HEK293 and SH-SY5Y cell lines12

  • in vitroNoopept did not affect the relative level of proliferation marker Ki-67 in HEK293 and SH-SY5Y cell lines12

  • in vitroNoopept does not stimulate cell growth12

  • in vitroNoopept at 10 μM concentration pretreatment improved PC12 cells viability against Aβ 25-35 induced injury14

  • in vitroNoopept reduced the number of early and late apoptotic cells in PC12 cells exposed to Aβ 25-3514

  • in vitroNoopept reduced levels of intracellular reactive oxygen species in PC12 cells exposed to Aβ 25-3514

  • in vitroNoopept reduced intracellular calcium levels in PC12 cells exposed to Aβ 25-3514

  • in vitroNoopept enhanced mitochondrial membrane potential in PC12 cells exposed to Aβ 25-3514

  • in vitroNoopept pretreatment significantly attenuated tau hyperphosphorylation at Ser396 in PC12 cells14

  • in vitroNoopept ameliorated alterations of neurite outgrowth evoked by Aβ 25-35 in PC12 cells14

  • in vitroGVS-111 significantly increased neuronal survival after H2O2-treatment displaying dose-dependent neuroprotective activity from 10nM to 100 microM17

  • in vitroGVS-111 inhibited the accumulation of intracellular free radicals and lipid peroxidation damage in neurons treated with H2O2 or FeSO417

  • in vitroGVS-111 exhibited significantly higher neuroprotection compared to Piracetam, Vitamin E, propyl gallate and s-PBN17

  • in vitroIn Down's syndrome cortical cultures, chronic treatment with GVS-111 significantly reduced the appearance of degenerative changes and enhanced neuronal survival17

  • in vitroGVS-111 metabolite cyclo-L-prolylglycine exhibits anticoagulant properties in vitro18

  • in vitroGVS-111 metabolite cyclo-L-prolylglycine exhibits fibrinolytic properties in vitro18

  • in vitrocyclo-L-prolylglycine metabolite exhibits antifibrin-stabilizing properties18

  • in vitrocyclo-L-prolylglycine metabolite exhibited an antiaggregant effect18

  • in vitroCyclo-prolylglycine formation from GVS-111 in the presence of plasma and brain enzymes was shown in vitro20

  • 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 basis6

  • 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)6

  • expert opinionNoopept was synthesized in 1996 and was based off of the endogenous neuropeptide cycloprolylglycine6

  • expert opinionNoopept is commonly said to be 1000-fold as potent as piracetam6

  • expert opinionPotency compared to piracetam has been claimed to be somewhere between 200 and 50,000 when comparing on a dose-per-dose basis6

  • expert opinionOn a structural basis, Noopept is a dipeptide conjugate of Piracetam6

  • expert opinionNoopept is a water-soluble proline containing dipeptide structure, and is a Cycloprolylglycine pro-drug6

  • expert opinionNoopept acts as a pro-drug for cycloprolylglycine6

  • expert opinionNoopept is included in the group of racetams, although its chemical structure is quite different than other compounds from this group7

  • 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 barrier2

  • 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 receptor2

  • 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-isomer3

  • 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 23

  • 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 Noopept3

  • theoreticalThe HIF-positive effect is proposed as the primary mechanism of the activity of this Pro-Gly-containing dipeptide3

  • theoreticalHIF-positive effect is proposed as the primary mechanism of activity of Noopept3

  • 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)6

  • theoreticalOn a structural basis, Noopept is a dipeptide conjugate of Piracetam6

  • theoreticalThe mechanism of action of Noopept is multifaceted and involves modulation of various neurotransmitter systems within the brain7

  • theoreticalNoopept (N-phenyl-acetyl-L-prolylglycine ethyl ester) was constructed as a dipeptide analog of piracetam14

  • theoreticalNoopept (N-phenylacetyl-L-polyglycine ethyl ester) structure was designed using dipeptide nootropes based on imitation of pyracetam19

Dosing

Based on 2 human study findings and 4 animal findings.

  • human studyNoopept is pharmacologically active at doses 1,000 times lower than those for Piracetam3

  • human studyConsumers could be exposed to up to four-fold greater than pharmaceutical dosages when using individual cognitive enhancement supplement products10

  • animalNoopept (N-phenylacetyl-L-polyglycine ethyl ester) has an effective dose 1000 times lower than pyracetam4

  • animalGVS-111 shows antithrombotic effects upon intraperitoneal administration18

  • animalGVS-111 shows antithrombotic effects upon peroral administration18

  • animalNoopept is 1000 times lower effective dose than pyracetam19

How the body handles it

Based on 1 human study finding, 19 animal findings, 2 in vitro findings, 3 expert opinion findings and 2 theoretical findings.

  • human studyNoopept is able to penetrate the blood-brain barrier (BBB) when administered orally1

  • animalNoopept retains activity upon parenteral introduction and peroral administration4

  • 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 serum6

  • 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 barrier6

  • animalThe half-life of Noopept is around 16 minutes in rats6

  • animalThere appear to be interspecies differences with rats having more rapid metabolism of Noopept in serum relative to humans6

  • animalAn oral dose is about the equivalent of one tenth an injected dose (10% bioavailability)6

  • animalNoopept per se is not reliably detectable in serum as it is rapidly metabolized within 25 minutes of oral ingestion6

Show 19 more findings

  • 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 serum6

  • animalCmax of 50mg/kg oral Noopept in rats in brain reaches 1.289mcg/mL at Tmax of 0.115 hours (7 minutes)6

  • animalNoopept can easily cross the blood brain barrier6

  • animalThe half-life of Noopept is around 16 minutes in rats6

  • animalNoopept is not detectable in serum 25 minutes following oral ingestion6

  • animalThere appear to be interspecies differences with rats having more rapid metabolism of Noopept in serum relative to humans6

  • animalNoopept activity is retained upon parenteral introduction and peroral administration19

  • 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) conditions20

  • animalThree substances corresponding to the three possible GVS-111 metabolites, namely phenylacetic acid, prolylglycine and cyclo-prolylglycine, were found in experimental rat brain samples20

  • animalOnly cyclo-prolylglycine concentration increased (2.5-fold) 1 h after GVS-111 administration20

  • animalNoopept has a short half-life (~5-10 minutes in rodents) and is not present in the brain one hour after administration21

  • animalNoopept crosses the blood brain barrier in rodents21

  • 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-drug6

  • 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)6

  • expert opinionMost nootropics do not have an immediate effect after a single dose, and therefore long-term use is necessary to achieve the desired results5

  • expert opinionNoopept appears to have bioactivity following oral ingestion in humans6

  • expert opinionAn oral dose appears to be about one tenth an injected dose (approximately 10% bioavailability)6

  • theoreticalDipeptides have oral bioavailability due to ability to penetrate biological barriers and absence of targets bounds for exopeptidases2

  • theoreticalNoopept is an orally available active pharmaceutical ingredient7

Safety and side effects

Based on 3 human study findings, 3 animal findings, 1 in vitro finding, 3 expert opinion findings and 1 theoretical finding.

  • human study75% of declared drug quantities on supplement labels were inaccurate10

  • human studyMultiple unapproved drugs were detected in cognitive enhancement supplements, with some not declared on labels and some declared drugs not detected10

  • human studyPossible side effects of noopept in clinical trial included sleep disturbances (5/31 patients), irritability (3/31), and increased blood pressure (7/31)21

  • animalNoopept (0.5 mg/kg, i.p.) does not possess anticonvulsant properties when given as single or repeated administration4

  • animalGVS-111 has low toxicity18

  • animalGVS-111 has absence of complications18

  • in vitroThe effect of tested substances on OATP1B1/OATP1B3 is clinically insignificant according to FDA approach C/I ratio calculation9

  • 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 mild5

Show 3 more findings

  • expert opinionThe long-term effects of nootropics on healthy individuals are still unknown5

  • expert opinionHealth effects of consuming untested combinations of unapproved drugs at unpredictable dosages without clinician oversight in supplements are unknown10

  • 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 dependence2

What people use it for

Based on 5 human study findings, 3 animal findings, 5 expert opinion findings and 7 theoretical findings.

  • human studyNoopept is a safe, nootropic compound that is commercially available to humans to enhance cognitive activity1

  • human studyNoopept is currently used in Europe to treat mild cognitive decline1

  • human studyNoopept tablets (5 and 10 mg) are under clinical assessment for treating cognitive deficiency of cerebrovascular and post-traumatic origin4

  • human studyOver-the-counter dietary supplements marketed for memory and cognitive function may contain unapproved pharmaceutical drugs including omberacetam, aniracetam, phenibut, vinpocetine, and picamilon10

  • human studyNoopept tablets (5 and 10 mg) are under clinical assessment for treating cognitive deficiency of cerebrovascular and post-traumatic origin19

  • animalNoopept produces selective anxiolytic action4

  • animalProlonged five-week preliminary administration of noopept enhanced the anticonvulsant activity of valproate in mice4

  • animalNoopept produces selective anxiolytic action19

Show 12 more findings

  • expert opinionNoopept is a nontoxic, orally available, highly effective dipeptide nootropic drug designed as a dipeptide analog of piracetam2

  • expert opinionNoopept is said to be anxiolytic and mildly psychostimulatory while promoting cognitive health and memory6

  • expert opinionNoopept is said to be anxiolytic and mildly psychostimulatory while promoting cognitive health and memory6

  • expert opinionTherapeutic effectiveness of Noopept should be evaluated at the initial stage of Alzheimer's disease16

  • expert opinionNoopept is not sold over the counter in the United States and is available with prescription in Russia21

  • theoreticalNootropics improve human thinking, learning, and memory, especially in cases where these functions are impaired5

  • theoreticalNoopept has neuroprotective properties7

  • theoreticalNoopept has ability to enhance cognitive function7

  • theoreticalNoopept holds much promise to prevent the development of Alzheimer's disease in patients with mild cognitive impairment16

  • 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 disorders17

  • theoreticalGVS-111 has neuroprotector properties18

  • theoreticalGVS-111 is a promising antistroke drug18

Other findings

Based on 1 in vitro finding, 4 expert opinion findings and 1 theoretical finding.

  • in vitroGVS-111 (Noopept) is a novel N-acylprolyl-containing dipeptide analog of Piracetam17

  • expert opinionDipeptides are more technically available in comparison to poly- and oligopeptides2

  • expert opinionNoopept belongs to nootropic family of drugs7

  • expert opinionVery little is known about Noopept's structural and physicochemical properties7

  • expert opinionNoopept is a nootropic developed at the Zakusov Institute of Pharmacology (Russian Academy of Medical Sciences)21

  • theoreticalNoopept was synthesized in 1996 and was based off of the endogenous neuropeptide cycloprolylglycine6

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.

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

Check a stack
  • 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 established

    Shares 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 established

    Shares anti inflammatory · BDNF signaling

  • 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 established

    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 established

    Shares mitochondrial function · anti inflammatory · BDNF signaling

  • DihexaComplementary

    May be complementary

    Noopept boosts BDNF/NGF and modulates AMPA/TrkB signaling for cognition, whereas Dihexa uses the HGF/c-Met synaptogenic route. Different mechanisms aimed at the same memory-enhancement and neuroprotection endpoint.

    Tier 4Theoretical — not established

    Shares BDNF signaling · anti inflammatory

  • 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 established

    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 established

    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 established

    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)21. 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.

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 dependence2. 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 unknown5. An animal study reported that chronic 28-day treatment did not produce tolerance16. 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(vendor claim).

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(vendor claim).

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 inaccurate10. 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 unknown10.

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. Antidiabetic and antithrombotic/anticoagulant findings — which bear on bleeding and glucose-related safety — come only from animal and in vitro work8,13,15,18.

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. 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(vendor claim).
  • An open-label study used 10 mg twice per day for 56 days in patients with mild cognitive disorders14,21.
  • 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.
  • An information site reports nootropic effects at approximately 10-30 mg/day, roughly 1000-fold lower than the multi-gram daily doses used for piracetam6.
  • 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(vendor claim).
  • A database summary4 notes tablets of 5 and 10 mg were under clinical assessment, with activity retained via both parenteral and peroral administration.

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 basis6. A community guide clarifies this refers to potency by dose — Noopept being active at tens of milligrams where piracetam is dosed in grams.

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. A community dosing guide notes vendors commonly claim roughly 98%+ purity by HPLC(vendor claim). 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 label10.

Sources

Ordered by evidence quality — the strongest first.

  1. Comparative studies of Noopept and piracetam in the ...(opens in a new tab)
    Tier 1Web · researchgate.net · 2024
  2. Current Pharmaceutical Design(opens in a new tab)
    Tier 2Web · pdfs.semanticscholar.org
  3. Molecular Mechanism Underlying the Action of Substituted ...(opens in a new tab)
    Tier 2Web · pmc.ncbi.nlm.nih.gov
  4. nootropic drug noopept: Topics by Science.gov(opens in a new tab)
    Tier 2Web · science.gov
  5. Nootropics as Cognitive Enhancers: Types, Dosage and Side ...(opens in a new tab)
    Tier 2Web · pmc.ncbi.nlm.nih.gov
  6. N-Phenylacetyl-L-prolylglycine ethyl ester(opens in a new tab)
    Tier 2Web · examine.com · 2025
  7. 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
  8. 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
  9. 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
  10. Five Unapproved Drugs Found in Cognitive Enhancement Supplements.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2021
  11. Cognitive Enhancer Noopept Activates Transcription Factor HIF-1.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2020
  12. Drug with Neuroprotective Properties Noopept Does Not Stimulate Cell Proliferation.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2019
  13. 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
  14. 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
  15. 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
  16. Noopept stimulates the expression of NGF and BDNF in rat hippocampus | Bulletin of Experimental Biology and Medicine | Springer Nature Link(opens in a new tab)
    Tier 2Web · link.springer.com · 2009
  17. 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
  18. [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
  19. [The original novel nootropic and neuroprotective agent noopept].(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2002
  20. 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
  21. Noopept(opens in a new tab)
    Tier 3Web · alzdiscovery.org
  22. 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

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