Noopept (Omberacetam): The Dipeptide That Is Not a Racetam, the 1,000x Claim Its Developers Made, and the One Human Trial Everyone Quotes Without Reading

Noopept (Omberacetam): The Dipeptide That Is Not a Racetam, the 1,000x Claim Its Developers Made, and the One Human Trial Everyone Quotes Without Reading

Noopept is sold as "the racetam that is a thousand times stronger than piracetam," and both halves of that sentence need an asterisk. It is not a racetam in any chemical sense: it has no 2-oxo-pyrrolidine ring, and the Warsaw group that solved its crystal structure in 2025 noted that its structure "is quite different than the other compounds from this group." It was designed to copy piracetam's shape with amino acids, which is why it is filed with the racetams, and that design history is also where the thousand-fold figure comes from. The developers compared their own doses in their own rat models, found Noopept active at far lower doses than piracetam, and wrote "1000 times lower" into their reviews. No independent group has run a dedicated potency study, and the few comparisons done outside Moscow had Zakusov co-authors. Then there is the human record. Almost every page about Noopept cites a 2009 clinical trial as proof that it works in people. That trial enrolled 53 patients with mild vascular or post-traumatic cognitive disorder, compared a Noopept arm with a piracetam arm, had no placebo arm, and recorded raised blood pressure in seven of the 31. It is a real study and a useful one. It is also the only trial against an active comparator, none of the handful of open studies around it was blinded or placebo-controlled, and the people quoting it almost never say either of those things. This reference goes through what the molecule is, what has been measured in cells and animals, what the single comparative trial actually reported, and where it sits legally in 2026.

Michael Phelps

Founder & Peptide Research Specialist, PrymaLab

Research reference · Last updated October 4, 2026 · ~36 min read

What Noopept is: a dipeptide built to look like piracetam

Start with the molecule, because the name misleads twice. Noopept is ethyl 1-(phenylacetyl)-L-prolylglycinate: a phenylacetyl group capping the nitrogen of L-proline, proline joined to glycine, glycine closed off as an ethyl ester. Formula C₁₇H₂₂N₂O₄, molecular weight 318.37 g/mol, CAS 157115-85-0, PubChem CID 180496.^[1][2] Two amino acids make it a dipeptide, so it qualifies under the definition in the peptide boundary guide, but a capped, esterified dipeptide behaves more like a small lipophilic drug than like the peptides on the rest of this site. The 2025 physicochemical study from the Medical University of Warsaw, which ran thermal analysis, solution and solid-state NMR, single-crystal and powder diffraction and a polymorph screen, put the point plainly: Noopept "is included in the group of racetams, although its chemical structure is quite different than the other compounds from this group, including the most popular one, piracetam."^[3] There is no 2-oxo-pyrrolidine ring. The "-racetam" in omberacetam is a pharmacological family name, not a chemical one.

The reason it carries the name anyway is its origin. In the early 1990s Tatiana Gudasheva, Rita Ostrovskaya, Tatiana Voronina and Sergei Seredenin at the Zakusov Institute of Pharmacology in Moscow were pursuing what they called "peptide design": take a known non-peptide psychotropic drug, work out which atoms constitute its pharmacophore, and rebuild that arrangement out of amino-acid residues so the result is a short peptide with the parent's activity.^[4] For GVS-111 the parent was piracetam. The group's 2016 paper in Acta Naturae states it in one sentence: "The non-peptide prototype of Noopept is the nootropic drug Piracetam."^[5] The originating patent is US 5,439,930, granted to Seredenin and colleagues in 1995, and the first analytical and rat pharmacokinetic papers appeared in 1996 and 1997.^[6][7][8]

The cycloprolylglycine connection

The second thing the design did, perhaps by intent and perhaps by luck, was to make a molecule whose main metabolite is something the brain already makes. Cyclo-prolylglycine, a diketopiperazine formed when proline and glycine close into a six-membered ring, is an endogenous cyclic dipeptide found in rat brain. In 1997 Gudasheva's group gave rats GVS-111 intraperitoneally and went looking for the parent and three candidate metabolites in brain at one hour. The parent was below the detection limit of their HPLC method. Of phenylacetic acid, prolylglycine and cycloprolylglycine, only the cyclic dipeptide rose, by 2.5-fold, and they showed the conversion in vitro with plasma and brain enzymes. Their conclusion: GVS-111 "is prodrug which converts in the body to cyclo-prolylglycine," a compound "identical to the endogenous cyclopeptide that produces the nootropic activity."^[9] Secondary summaries quote the absolute brain concentrations as 2.8 rising to 6.7 nmol/g.^[10]

That would make Noopept a delivery vehicle for cycloprolylglycine, and the same laboratory has spent years characterising what cycloprolylglycine does on its own: it raised BDNF in neuronal cultures at 10^-7 and 10^-3 M under normal, glutamate and 6-hydroxydopamine toxicity conditions,^[11] and its neuroprotective effect was abolished by AMPA-receptor blockers and by the Trk inhibitor K252a, which is the pattern of a positive AMPA modulator working through TrkB.^[12] But the prodrug story is not the whole story, and the developers said so themselves. In a one-session active-avoidance model, repeated Noopept increased the number of rats that learned, while cycloprolylglycine and piracetam did not; the 2001 paper says GVS-111 "principally differs from its main metabolite."^[13] So the parent compound, in the minutes it survives, does something the metabolite does not. Which of the two is responsible for which effect is one of the open questions at the end of this article.

The US detour that went nowhere

Russian sources record that the compound was licensed for Western development under the code SGS-111 by a company called Saegis Pharmaceuticals, and the 2003 University of Connecticut paper on oxidative neuroprotection refers to it as "GVS-111 (DVD-111/Noopept)."^[14][15] No Western registration followed, and I could not find any record of what the Saegis programme concluded. That absence matters for a reader in 2026: a molecule that was in Western hands twenty years ago and never reached a Phase 2 result outside Russia is a molecule whose Western efficacy has never been tested, not one that was tested and failed, and not one that was tested and passed.

Where it goes: minutes in the blood, cycloprolylglycine in the brain

The pharmacokinetics are mostly rat data from one laboratory, and the numbers are quoted inconsistently in the secondary literature, so it is worth setting them down carefully. The core study is Boiko and colleagues, 2000, in Bulletin of Experimental Biology and Medicine. The abstract establishes the qualitative result: after oral administration to rats, GVS-111 "is absorbed in the gastrointestinal tract, enters the circulation, and penetrates through the blood-brain barrier in an unmodified state."^[16] The numbers come from secondary readers of the full paper. Examine's breakdown reports that after oral administration, serum Tmax was 0.116 hours, about seven minutes, with a Cmax of 0.82 µg/mL; brain Cmax was 1.289 µg/g at essentially the same time; the elimination half-life was "around 16 minutes"; and oral exposure was roughly a tenth of an injected dose, which Examine itself flags with the caution that "a true bioavailability study has not been conducted."^[10] The Alzheimer's Drug Discovery Foundation, reading the same paper, gives the rodent half-life as 5 to 10 minutes.^[17] I could not obtain the primary PDF to adjudicate, so the honest statement is: minutes, not hours, with brain concentration at peak exceeding serum concentration.

Interspecies work from the same group in 2004 adds the only human pharmacokinetic observations I can find. In rats, metabolism after intravenous dosing was "very intensive," with a phenyl-ring hydroxylated metabolite formed presystemically. In rabbits the unchanged drug circulated longer and the hydroxylated metabolite was absent. In humans, elimination was "still slower," with "considerable individual variability," and "no drug metabolites are found in the human blood plasma, probably because of a relatively small dose and low concentration."^[18] No numeric human half-life appears in that abstract. The Russian prescribing monograph states a bioavailability of 99.7 percent, a Tmax of about 15 minutes and a plasma half-life of 0.38 hours, roughly 23 minutes, with metabolism to phenylacetic acid, phenylacetylproline and cycloprolylglycine.^[19] These are label values with no published method behind them, and 99.7 percent sits uncomfortably beside the ten-percent rat estimate. Wikipedia's summary, that human metabolism and half-life "were not well understood," is the fair one.^[1]

The 2018 paper from the same pharmacokinetics group closes the loop on the metabolite: cycloprolylglycine found in rat plasma and brain after Noopept "differed significantly in its pharmacokinetic parameters from noopept" while sharing its spectrum of memory effects.^[20] Put together, the picture is a parent compound with a lifetime of minutes that leaves behind a longer-lived active cyclic dipeptide.

How it is thought to work: neurotrophins, HIF-1, antioxidant and the missing receptor

Noopept has been given more mechanisms than most molecules its size, and they are not all equal. I will go through them in rough order of how much they explain, and end with the experiment that failed to find a receptor.

BDNF and NGF

The neurotrophin result is the one most often repeated, and it is a real finding. In 2008 Ostrovskaya's group ran Northern blots on rat brain after Noopept. After a single dose, NGF and BDNF mRNA rose in hippocampus while cortical expression actually fell below control; after 28 days of repeated treatment the hippocampal increase was larger with no tolerance, and cortex showed a slight BDNF rise.^[21] A 2010 follow-up with 28 days of intraperitoneal treatment found reduced stress-activated kinases, SAPK/JNK and phosphorylated ERK1/2, in hippocampus alongside higher BDNF mRNA in hippocampus and hypothalamus, with hypothalamic BDNF protein "somewhat increased."^[22] Two cautions. First, the acute cortical decrease is almost never mentioned on vendor pages, and it is in the same abstract as the hippocampal increase. Second, a 2021 paper in Heliyon on Noopept and spinal microglial BDNF is sometimes cited as corroboration; it was retracted the same year and should not be used.^[23] There is no human BDNF measurement.

HIF-1 and the search for a target

The most interesting mechanistic paper is the 2016 Acta Naturae study, because it reports a negative result most groups would have buried. The authors screened Noopept at the contract laboratory CEREP against more than 100 known receptors, and the screen "did not lead to the expected identification of the primary targets." They then ran a panel of transcription-factor reporter assays in HEK293 cells. At 10 µM, Noopept increased the DNA-binding activity of HIF-1 and of nothing else on the panel: not CREB, NFAT, NF-kappaB, p53, STAT1, GAS, VDR or HSF1. The effect was concentration-dependent and additive with the hypoxia mimetic cobalt chloride; piracetam at 1 mM did nothing; and docking suggested the L-isomer, but not the inactive D-isomer, fits prolyl hydroxylase 2, the oxygen sensor that marks HIF-1alpha for degradation.^[5] A 2020 paper confirmed in SH-SY5Y cells that Noopept raised basal and hypoxia-mimetic HIF-1 activity through prolyl-hydroxylase inhibition and increased HIF-1alpha protein.^[24] If this holds, Noopept is a mild hypoxia-response inducer, which would unify its neuroprotective, ischaemia and neurotrophin results under one mechanism. It is also, so far, the finding of one network of laboratories.

Antioxidant and anti-apoptotic

This is where the strongest independent data sit. In 2003 Alejandra Pelsman and Jorge Busciglio at the University of Connecticut, with the Moscow group as co-authors but in a US laboratory with its own cultures, exposed human cortical neurons to 50 µM hydrogen peroxide, which killed more than 60 percent of them. GVS-111 was protective from 10 nM up to 100 µM with a half-maximal concentration of 1.21 ± 0.07 µM, blocked free-radical accumulation and lipid peroxidation, outperformed piracetam, vitamin E, propyl gallate and the spin trap s-PBN in the same assay, and reduced degeneration in cortical cultures from Down syndrome fetal tissue.^[15] Earlier Moscow work had shown protection of cerebellar granule cells against oxygen-glucose deprivation, glutamate and oxidative stress, where piracetam did not block glutamate toxicity,^[25] and a 2016 study protected HT-22 hippocampal cells from 5 mM glutamate across 10^-11 to 10^-5 M.^[26] In PC12 cells pretreated with 10 µM Noopept for 72 hours before amyloid-beta 25-35, viability improved, early and late apoptosis fell, reactive oxygen species and intracellular calcium dropped, mitochondrial potential recovered, and tau phosphorylation at serine 396 was attenuated.^[27] An Umeå group found something different with alpha-synuclein: Noopept did not bind a specific site but, through hydrophobic interaction, pushed toxic oligomers into larger, less toxic fibrils, rescuing SH-SY5Y viability.^[28]

Glutamate, GABA, acetylcholine and calcium

The remaining mechanisms are smaller pieces. On AMPA receptors, radioligand work found Noopept competes at the [³H]Ro 48-8587 site with an IC50 of 80 µM, an order of magnitude weaker than the reference compound nooglutil; piracetam and phenylpiracetam had no effect at any concentration tested.^[29] EEG studies in rats given the compound subcutaneously found increased alpha and beta-1 power with a 30-minute latency; the acute effect was blocked by an NMDA antagonist and the tolerance that developed after eight or nine injections was reversed by an AMPA antagonist.^[30][31] In hippocampal slices, 1 µM Noopept increased the frequency of spontaneous inhibitory currents in CA1 pyramidal cells by activating interneurons,^[32] and a 2022 paper traced that to alpha-7 nicotinic receptors: 5 µM increased firing of stratum radiatum GABAergic interneurons, and alpha-bungarotoxin at 6 nM or methyllycaconitine at 20 nM abolished it.^[33] Behaviourally it reverses scopolamine amnesia in rats and mice and potentiates acetylcholine responses in snail neurons at picomolar to nanomolar concentrations.^[34][35][36] On ion channels, 2 µM GVS-111 cut calcium current by 39 percent in snail neurons where 2 mM piracetam managed 19 percent, and 0.1 µM reduced calcium-activated potassium current by 69 percent against 49 percent for 1 mM piracetam.^[37]

Finally there is a body of work on inflammation and immunity that rarely makes it into nootropic discussions. Noopept suppressed concanavalin-A inflammation dose-dependently by intravenous and oral routes, cut carrageenan paw oedema by 62 percent at 3 hours after intravenous administration, and reduced adjuvant arthritis scores by 94 percent after intramuscular administration.^[38] Five days of intraperitoneal treatment significantly reduced LPS-induced interleukin-6 and roughly halved TNF-alpha.^[39] It also has anticoagulant and fibrinolytic activity by intraperitoneal and oral routes, with cycloprolylglycine active in vitro down to 10^-10 M.^[40] None of these has been examined in people.

The animal record: memory, stroke, amyloid and anxious mice

The animal literature is extensive, almost entirely from the Zakusov Institute and its collaborators, and uses a handful of recurring doses. The Alzheimer's Drug Discovery Foundation's review summarised the problem in one sentence: "Almost all studies have been conducted in a single laboratory that used non-standard animal models and outcome measures."^[17] With that in mind, here is what the models showed.

Memory and the non-monotonic response

The anchor result is oral activity in passive avoidance. Ostrovskaya's 2001 paper established that GVS-111 given by mouth retained its antiamnesic activity in rats.^[13] Examine's reading of the series is that a low and a higher tested amount worked while two others did not, a non-monotonic pattern the developers have not explained.^[10] After frontal lobectomy, nine days of intraperitoneal treatment restored active and passive avoidance and open-field habituation.^[41] Against scopolamine, Noopept prevented the spatial-memory deficit in BALB/c mice.^[36] And the effect depends on who the mouse is: the same treatment improved long-term memory in BALB/c mice, which learn poorly at baseline, produced no further gain in C57BL/6J mice, which learn well, and did nothing in DBA/2J.^[42] That strain dependence is worth holding onto when reading claims about healthy humans.

Stroke models

Photochemical cortical stroke was the group's main ischaemia model. Nine days of intravenous treatment beginning one hour after the lesion attenuated the passive-avoidance deficit and "significantly diminished the volume of the infarcted area."^[43] Related papers found improvement across all three memory stages, strongest in the most impaired animals, and activity by both intraperitoneal and oral routes after compression injury.^[44][45] In a middle-cerebral-artery occlusion model from a different Moscow laboratory, repeated intraperitoneal treatment over the first 48 hours reduced infarct volume from 18.6 to 12.2 percent of the hemisphere, a 34.5 percent reduction with p below 0.05.^[46] In chronic bilateral carotid ligation, seven days of treatment improved survival and behaviour and blocked the build-up of lipid-peroxidation products.^[47]

Alzheimer's models

Three models have been used. In olfactory-bulbectomised NMRI mice, a model with amyloid pathology and spatial-memory loss, 21 days of treatment plus five training days restored Morris-maze performance and, unexpectedly, raised serum antibodies to amyloid-beta 25-35 oligomers; this appeared in the Journal of Psychopharmacology in 2007 with a British co-author.^[48][49] When amyloid-beta 25-35 was injected into the nucleus basalis of Meynert, seven days of prophylactic intraperitoneal treatment "completely prevented" the memory deficit, and treatment starting at day 15 also normalised it.^[50] In the intracerebroventricular streptozotocin model of sporadic Alzheimer's disease, Noopept reversed the loss of NGF and BDNF, the rise in malondialdehyde and the memory deficit.^[51] These are models of amyloid toxicity and cholinergic loss, not of the human disease, and none has been replicated outside Russia.

Anxiety, and a developmental warning

The developers describe Noopept as having an "additional selective anxiolytic action,"^[4] and the mouse data show where "selective" comes from. Anxiolytic and exploratory effects appeared only in high-anxiety BALB/c mice, not in C57BL/6, were maximal at day 7 of treatment, and tracked prefrontal benzodiazepine-receptor density.^[52][53] In learned-helplessness models, Noopept accelerated active-avoidance acquisition and 21 days of treatment eliminated the helplessness signs.^[54][55] The result that should be better known is from 2005: rats given Noopept subcutaneously on postnatal days 8 to 20 showed disturbed declarative and procedural learning as adults, with fewer successful learners among males.^[56] A companion study found no adult behavioural changes in females.^[57] Piracetam given in the same design also reduced the share of successful male learners. The Russian label contraindicates use under 18 without saying whether that reflects this finding or simply the absence of paediatric data, and it is the only place in the literature where Noopept made cognition worse.

The thousand-fold figure

Now the comparison that sells the product. The statement that Noopept is a thousand times more potent than piracetam originates with the developers: the 2002 review by Ostrovskaya, Gudasheva, Voronina and Seredenin says the effective dose is "1000 times lower for noopept than for pyracetam," and the 2016 Acta Naturae paper repeats "doses 1,000 times lower."^[4][5] The underlying comparison is their own, built from the effective amounts of each compound in their models and laid out in the manufacturer-affiliated monograph.^[58] It is a dose ratio in one laboratory's assays, not an independent potency study, and the ratio moves with the assay: about 1,000-fold on calcium current, about 10,000-fold on calcium-activated potassium current, about 2,000-fold on the EEG dose, and Examine notes figures "between 200 and 50,000" depending on the endpoint.^[10][30][37] Potency by weight also says nothing about maximal effect. A drug that does the same thing at a thousandth of the dose is more potent, not more effective, and the only human comparison, below, did not test equivalent effect at matched endpoints. PrymaLab's own product page uses the thousand-fold figure; this article is where the sourcing for it lives.

The human record: one active-comparator trial and a handful of open series

Here is the whole of the human efficacy literature that I could identify, and it is short enough to list.

The study every page cites is Neznamov and Teleshova, published in Russian in 2008 and in English translation in Neuroscience and Behavioral Physiology in 2009.^[59][60] It was an open, comparative trial at the Zakusov Institute's clinical laboratory with no placebo arm. Fifty-three patients with mild cognitive disorder of vascular origin, described as dyscirculatory encephalopathy with emotional lability, or of traumatic origin, post-concussion syndrome, were enrolled and 41 completed. Adverse events are reported for 31 Noopept-treated patients; the comparator group received piracetam; treatment ran 56 days. Mini-Mental State scores in the Noopept arm moved from 26 to 29.^[17] Responder rates were 42.9 percent in vascular and 70 percent in post-traumatic patients on Noopept, against 25 and 16.7 percent on piracetam.^[61] The adverse events recorded on Noopept were sleep disturbance in 5 of 31, irritability in 3 of 31 and raised blood pressure in 7 of 31, two of whom needed antihypertensive treatment; Examine summarises the overall side-effect rate as 1.8-fold lower than piracetam's.^[10][17][61] A companion EEG paper reported increased alpha and beta power and reduced delta, interpreted as "nonspecific activation and anxiolytic effect," clearer in the vascular group.^[62] Every one of those patient-level numbers reaches me through secondary sources, the ADDF review, ConsumerLab and Examine, because the primary abstract is not indexed and the full text is paywalled; I have not been able to read the trial itself, and neither, I suspect, have most of the people citing it.

The second-largest study is Amelin and colleagues, 2011: an open prospective study of 60 post-stroke patients, followed to 12 months. At two months there was significant improvement on MMSE and an association test against the control group; the authors reported "mild improvement" on global efficacy and a "high level of safety."^[63] Around these two sit a cluster of small Russian-language open series: dyscirculatory encephalopathy, neurasthenia, post-traumatic cognitive disorder, 30 tuberculosis patients studied for the neurotoxicity of chemotherapy, healthy volunteers aged 20 to 24 in a climate chamber for a "meteoadaptogenic" effect, and elderly teachers given Noopept plus self-massage, whose gains had faded by month three.^{[64][65][66][67][68][69]}

What is missing is more important than what is present. The Alzheimer's Drug Discovery Foundation counts "Clinical trials: 1 conducted, 0 ongoing" and concludes that "little clinical evidence supports its use."^[17] ConsumerLab notes that both human studies "did not include a placebo control" and that there is "no evidence that Noopept will improve cognition and memory in healthy individuals."^[61] I searched ClinicalTrials.gov and found no registration under Noopept, omberacetam or GVS-111. There is no Western trial, no double-blind trial, no placebo-controlled trial and no healthy-volunteer cognition trial, and the longest controlled treatment period is about two months (56 days in the comparator trial; two months in the post-stroke series). A reader who sees Noopept described as "clinically proven" should ask: proven against what, in how many people, and blinded by whom.

What Reddit adds, and what it cannot

Because "noopept reddit" is searched more often than "noopept dosage," the community record deserves a paragraph. The largest structured dataset is a 2014 survey of r/nootropics and Longecity users with 162 respondents, in which Noopept ranked in the middle to upper part of 28 substances for perceived benefit.^[70] The recurring complaints in community threads are headache, irritability and insomnia, which map closely onto the adverse events the 2009 trial recorded: irritability in 3 of 31, sleep disturbance in 5 of 31.^[17] The recurring benefit claims, sharper recall and faster verbal fluency within an hour, map onto nothing in the human literature, because no study has tested memory or cognition in healthy adults; the two healthy-volunteer reports measured climate adaptation and teachers' work performance. A survey of self-selected users who know what they took cannot separate the drug from the expectation, and a trial that could has not been run. That is the whole of what can be said.

What the Noopept studies measured

This section lists the systems the published studies used and what each measured. It is split by system because the gap between the cell, animal and human work is the point.

Three things stand out. The in-vitro effects span five orders of magnitude, from 10 nM protection to 80 µM receptor competition, and the concentration that activates HIF-1 is ten thousand times the lowest protective one. No bridging pharmacology between the rodent and human studies has been published. And the human studies all trace to the Russian label. Sublingual, intranasal and other routes discussed in forums have no peer-reviewed human source at all; the only intranasal data are in rats, in a forskolin co-formulation at 20 nM, from a laboratory with a declared industry interest.^[72] PrymaLab's 30 mg capsules are a research format; the studies above describe other people's experiments, not a use for them.

Noopept side effects and what toxicology exists

The human adverse-event data come from the trial already described: sleep disturbance in 5 of 31, irritability in 3 of 31, and raised blood pressure in 7 of 31, two requiring treatment.^[17][61] The blood-pressure finding, nearly a quarter of the treated group, has never been followed up in a dedicated study. The Russian label lists allergic reactions and possible blood-pressure elevation in people with severe hypertension; contraindicates severe hepatic or renal impairment, pregnancy, lactation, age under 18 and lactose intolerance; and lists insomnia among its cautions.^[19] The 2011 post-stroke series reported a "high level of safety" over a year of observation, in open-label conditions.^[63]

Toxicology is thinner than the marketing suggests and comes from two kinds of source. The peer-reviewed piece is a 2002 study in Experimental and Clinical Pharmacology: six months of oral Noopept at 10 or 100 mg/kg in rabbits produced "no irreversible pathologic changes," and no allergenic, immunotoxic or mutagenic activity, with no effect on reproduction or offspring development.^[71] The other figures circulate from a manufacturer-affiliated monograph: an intraperitoneal LD50 of 5,080 mg/kg in rodents, no deaths at oral doses up to 10,000 mg/kg, and reversible hepatic parenchymal changes at 100 mg/kg for 180 days, with no allergenicity, mutagenicity or reproductive toxicity.^[73] I have found no peer-reviewed LD50, and I flag the monograph as promotional. Drug-interaction data are essentially absent; the ADDF lists interactions as "unknown," and the one published interaction is potentiation of valproate's anticonvulsant effect in mice.^[17][74] No human exposure has ever been blinded; the longest controlled treatment period is about two months; and the one early-life animal study found lasting impairment.^[56][60]

Noopept vs piracetam, Semax, Selank and Cerebrolysin

Noopept is usually discussed alongside four other compounds: the drug it was designed from and the three Russian neuropeptides it is most often grouped with. The comparison below is about evidence shape, not about which "works better," because no head-to-head other than the piracetam trial exists.

Piracetam is a 142 Da pyrrolidone acetamide; it has decades of trials and a Cochrane review that found the evidence for dementia inconclusive. Noopept's relationship to it is one of design intent, developer-stated potency ratio and a single open trial. In that trial, Noopept produced higher responder rates than piracetam with fewer adverse events; the trial was unblinded and run by the developer's institute.^[60][61] The mechanistic contrast is cleaner: in the same assays, piracetam at millimolar concentrations does nothing to HIF-1 and does not block glutamate toxicity, where Noopept does both at micromolar.^[5][25]

Semax and Selank are heptapeptides from the Institute of Molecular Genetics in Moscow, given intranasally, with their own Russian open-label records and the same absence of Western placebo-controlled trials; the Semax versus Selank guide goes through them. Where Noopept differs is route and chemistry: it is an orally active small lipophilic ester that survives the gut, where the heptapeptides are given by nose precisely because they would not. Cerebrolysin is a porcine brain-peptide mixture given by injection, with a far larger stroke and dementia trial record, including placebo-controlled studies, and a correspondingly more contested interpretation; the Cerebrolysin reference covers it. If a reader wants the compound in this group with controlled human data, it is Cerebrolysin, not Noopept.

Regulatory status: OTC in Russia, Schedule 4 in Australia, unapproved in the US

Noopept's legal position is unusually scattered, which is why "is noopept legal" is a question people search for. Country by country, as of October 2026:

Russia. Noopept is a registered medicine, 10 mg tablets, developed at the Zakusov Institute and currently held by OTCPharm with a re-registration dated 20 March 2024; the label states it is dispensed without prescription.^[5][19] Indications are memory and attention disorders and emotional lability after brain injury, post-concussion syndrome, cerebrovascular insufficiency and asthenic states.^[19] The original approval year is often given as the late 1990s, but the developers' own 2002 review describes the tablets as still "under clinical assessment," so registration more plausibly dates to the mid-2000s.^[4]

United States. Not FDA approved and not a controlled substance. The FDA's position is that it is an unapproved new drug that cannot be a dietary-supplement ingredient. A warning letter to Peak Nootropics dated 4 February 2019 named Noopept among thirteen products marketed with disease claims, including Alzheimer's claims, and listed it among eight that "are not dietary supplements or conventional foods" and are unapproved and misbranded drugs.^[76] Import Alert 66-66, which covers bulk active ingredients that appear misbranded because they do not meet the research and manufacturing labelling exemptions in 21 CFR 201.122, lists Noopept from at least one Chinese supplier with the note that it "is an analog of Piracetam."^[77] The practical consequence showed up in Pieter Cohen's 2021 analysis of ten over-the-counter "cognitive enhancement" supplements: omberacetam was detected at up to 40.6 mg per serving, about four times what the paper calls a typical pharmacologic dose, and nine of twelve declared quantities were inaccurate.^[75] Research-grade material sold with a certificate of analysis for laboratory use is a different category from those supplements, and the FDA judges intended use from labelling, marketing and the circumstances of sale together, so a "research use only" label does not settle the question by itself.

Australia. Prescription only. After a November 2018 referral, the TGA created new Schedule 4 entries for "RACETAMS except when separately specified" and for "OMBERACETAM" by name, effective 1 June 2019.^[78][79] A 2025 market-surveillance study by twelve official medicines control laboratories from the European network and Australia reported Noopept intercepted "as large bulk quantities of raw material" among "non-authorised drugs only available on prescription in Russia."^[80]

United Kingdom. Not a controlled drug under the Misuse of Drugs Act. The Psychoactive Substances Act 2016 makes it an offence to produce, supply or import a substance that stimulates or depresses the central nervous system for human consumption; simple possession is not an offence except in a custodial institution, and medicinal products are exempt.^[81] No Home Office determination on Noopept exists, and the frequently repeated claim that it falls outside the Act is unsourced. The honest wording is that its status is untested.

Elsewhere. Hungary added omberacetam to its controlled new-psychoactive-substances list on 25 August 2020.^[1] The World Health Organization recommended the INN "omberacetam" in 2018.^[82] WADA does not name Noopept or omberacetam on the Prohibited List; a 2018 anti-doping commentary argued it "could perhaps be interpreted as prohibited" under catch-all language, but it has not been added by name as far as the lists I checked show, and the 2027 list should be re-checked before relying on that.^[83]

Research-grade omberacetam: what to verify

A research buyer has three practical questions about a Noopept lot, and the literature answers all three.

Identity and chirality. Omberacetam has one stereocentre, at the proline alpha-carbon, and the 2016 docking work found only the L-isomer fits the proposed prolyl-hydroxylase site while the D-isomer is inactive.^[5] A certificate should therefore confirm not just mass, 318.37 by HPLC-MS, but identity against a reference standard; the 2025 crystallographic paper provides the solid-state fingerprint, a single stable polymorph with characteristic powder-diffraction and solid-state NMR signatures, that a well-equipped laboratory can match.^[3] The purity testing guide explains why an HPLC trace alone does not establish identity.

Quantity. Cohen's 2021 finding that nine of twelve declared drug quantities in US supplements were inaccurate, and that recommended servings could deliver up to 40.6 mg of omberacetam, about four times what the paper calls a typical pharmacologic dose, is the reason to insist on a batch assay rather than a label.^[75] PrymaLab's 30mg capsules ship with a certificate of analysis for the lot; a laboratory planning quantitative work should still verify content on receipt.

Stability and handling. The solid is stable; the Warsaw group found no polymorphic transitions or hygroscopic behaviour of concern at ambient conditions.^[3] In solution the ethyl ester hydrolyses and the dipeptide cyclises, which is after all the point of the molecule, so aqueous solutions for cell work should be prepared immediately before use, and DMSO stocks kept frozen and used within the day once thawed. The general rules in the storage and stability guide apply, with the added note that the relevant degradation product here, cycloprolylglycine, is itself bioactive and will confound an assay that assumes the parent is what is in the well.

What this article does not settle

I would rather list the gaps than paper over them.

• What Noopept binds first. A screen of more than 100 targets found nothing; the HIF-1 and prolyl-hydroxylase hypothesis comes from one group; AMPA affinity is weak.^[5][29]
• Prodrug or drug. The parent is undetectable in brain at one hour yet behaves differently from its metabolite in avoidance tests.^[9][13]
• Human pharmacokinetics. One qualitative paper and a set of label values with no published method.^[18][19]
• The potency ratio. "1,000x" is a developer-stated dose ratio across their own models, ranging from 200 to 50,000 depending on endpoint.^[4][10]
• Efficacy in anyone. No blinded or placebo-controlled trial; no test of memory or cognition in healthy adults; outcome measures in open Russian series.^[17][61]
• Blood pressure. Seven of 31 treated patients; never studied again.^[17]
• The bent response curve. Active at two tested amounts and inactive at two others in between and above, unexplained.^[10][13]
• Long-term and developmental safety. No long-term human data; one rodent early-life study showing impairment.^[56]
• Replication. Nearly every in-vivo result is from one institute in Moscow.^[17]

Noopept, omberacetam, GVS-111 and "racetam": what the names refer to

Noopept is the registered Russian brand name and the term almost everyone searches for. Omberacetam is the international nonproprietary name recommended by the World Health Organization in 2018; it is the term used in the Australian Poisons Standard, the Hungarian schedule and Pieter Cohen's supplement analyses, and the one AI systems increasingly use.^[75][78][82] GVS-111 is the Zakusov Institute's development code and the name in the 1990s and early 2000s primary literature, occasionally mis-rendered as GBS-111 or GBC-111 in translated abstracts.^[8] SGS-111 and DVD-111 were codes used during the abandoned US development programme.^[14][15] N-phenylacetyl-L-prolylglycine ethyl ester and ethyl 1-(phenylacetyl)-L-prolylglycinate are the chemical names. Cycloprolylglycine is the metabolite, not a synonym. Racetam is a pharmacological family label that includes Noopept by convention but not by chemistry; a search for racetams on this site leads to the nootropics and cognitive compounds category, which is where the product sits.

Why this is not in the same category as stimulants

Omberacetam gets filed with modafinil, caffeine and amphetamine in most places it is discussed, and the pharmacology has nothing in common with any of them. Stimulants work on monoamine transmission: amphetamine reverses the dopamine transporter, methylphenidate blocks it, modafinil acts on it weakly, caffeine blocks adenosine receptors and raises arousal indirectly. None of that is proposed for this dipeptide. No monoamine transporter or receptor affinity has been reported for it or for its metabolite, and the subjective and physiological signatures of a stimulant, raised heart rate, suppressed appetite, delayed sleep onset, are not what the Russian literature reports.

What is proposed instead is neurotrophic. The recurring finding from the originating institute is that nerve growth factor and brain-derived neurotrophic factor expression rise in rat hippocampus, reported in 2008. Two details of that paper are usually dropped. It measured mRNA by Northern blot, not protein by western blot, so the result is a transcription finding and the protein-level confirmation a western blot would give was not part of it. And the hippocampal rise followed a single dose, with 28 days of dosing potentiating rather than producing it, while cortical expression after a single dose fell below control. Nerve growth factor supports cholinergic neurons and brain-derived neurotrophic factor supports synaptic plasticity, so a compound working this way would not produce an acute stimulant-like effect, which is one reason the subjective reports around it are so inconsistent.

The receptor question is less empty than it is often described, and also less settled than a single named target would be. No monoamine receptor or transporter affinity has been reported for omberacetam or for cycloprolylglycine, which is the pharmacological basis for saying this is not a stimulant. Several other sites have been proposed. A 2022 electrophysiology paper concluded that alpha-7 nicotinic acetylcholine receptors are an important site of action, because the compound's effects on CA1 interneuron firing and inhibitory current frequency were abolished by alpha-bungarotoxin and methyllycaconitine. The 2016 transcription-factor work docked it to prolyl hydroxylase 2. And cycloprolylglycine, the proposed metabolite, has been characterised separately as a positive modulator of AMPA receptors, enhancing transmembrane AMPA currents in rat cerebellar Purkinje cells. NMDA receptor involvement rests on weaker evidence: altered Bmax in radioligand binding to the NMDA receptor channel site and to benzodiazepine sites in hippocampus and prefrontal cortex, which is a change in receptor density rather than a demonstrated direct affinity.

The neuroprotection claims: amyloid, HIF-1 and the inflammation data

The animal work extends beyond memory tasks into models of neurodegeneration, and the findings are worth separating from what they would need to show to support claims about brain health in a person.

The amyloid work is routinely described backwards, so it is worth stating what it found. In rats given beta-amyloid 25-35 into the Meynert basal nuclei, not intracerebroventricularly, the compound prevented a long-term memory deficit, and the mechanism the authors proposed was stimulation of antibodies to the peptide rather than removal of it. In olfactory-bulbectomised mice it raised serum antibodies to prefibrillar beta-amyloid 25-35, a result the 2007 paper puts in its own title. No study of this compound has measured amyloid plaque burden at all, and the intracerebroventricular model in this literature uses streptozotocin rather than beta-amyloid. Anyone citing reduced amyloid burden here is citing something that was not measured.

Hypoxia-inducible factor 1 is the group's proposed primary mechanism and it is the best-supported part of the account. A 2016 screen of nine transcription factors found the compound raised DNA-binding activity of HIF-1 alone, with molecular docking to prolyl hydroxylase 2, and a 2020 paper repeated the HIF-1 activation finding. What does not follow, and what is often asserted anyway, is angiogenesis. HIF-1 drives vascular endothelial growth factor transcription in general biology, so new vessel growth is a reasonable thing to look for, but no published study has reported angiogenesis or a VEGF effect for this compound. The nearest relevant result points the other way: a 2019 paper titled to say so found no stimulation of cell proliferation, with no effect on Ki-67 or on cell-cycle distribution in two cell lines. Angiogenesis here is an untested inference from general HIF-1 biology, not a finding.

The anti-inflammatory data are real but belong to a different compartment than they are usually placed in. A 2012 mouse study reported that the compound cut serum interleukin-6 roughly 1.8-fold after concanavalin A and halved serum tumour necrosis factor alpha after lipopolysaccharide, in peripheral inflammation models including carrageenan paw oedema. Those are pro-inflammatory cytokines measured in blood, in peripheral models, not in brain tissue in an injury model. The one paper that claimed spinal microglial effects in an inflammation model was retracted in 2021 and should not be cited. None of these results has been reproduced outside the originating network, and none involves a model of a human neurodegenerative disease that progresses on its own rather than being induced.

The step the whole body of work does not take is into measured cognitive function in a healthy person. Cognitive performance in the human record comes from one active-comparator trial against piracetam in patients with mild cognitive disorders following vascular or traumatic brain injury, conducted at the compound's originating institute and published without an indexed abstract, so its sample size, randomisation and blinding cannot be verified from the published record. Brain health, as a phrase, does not correspond to any endpoint in any of it.

Frequently asked questions

References