Noopept

N-Phenylacetyl-L-prolylglycine ethyl ester

Noopept (N-Phenylacetyl-L-prolylglycine ethyl ester) is a cognitive & mood research compound. Dipeptide nootropic (piracetam family) — modulates AMPA/NMDA glutamate signaling and raises BDNF/NGF for fast-acting focus and memory.

How Noopept works

Dipeptide nootropic (piracetam family) — modulates AMPA/NMDA glutamate signaling and raises BDNF/NGF for fast-acting focus and memory.

Proposed benefits

Researched for focus, memory, neuroprotection, mood and stress resilience.

Where to get Noopept

Noopept is sold in 2 forms. They are not interchangeable — the dose and the route differ, so pick the one this page describes unless you know why you want another.

The evidence for Noopept

Graded by what exists behind each claim.

Human clinical evidence

• The human record is Soviet and post-Soviet clinical work — real patients and real endpoints, published in Russian and rarely replicated to Western standards.

📊 Correlative data

• Registered in Russia for cognitive impairment, with domestic trials reporting benefit in mild cognitive disorders and post-traumatic states.
• Very widely used in the nootropic community at microgram doses. Reported experience is variable — a meaningful minority report irritability or headache, which is more than most nootropics generate.

🧪 Theoretical / extrapolated

• A dipeptide often called a racetam by association, though structurally it is not one. It is metabolized to cycloprolylglycine, an endogenous neuropeptide, and increases NGF and BDNF expression in rodent brain.
• The NGF/BDNF mechanism predicts a cumulative rather than acute effect, which is at odds with how it is usually taken. It is roughly a thousand times more potent by weight than piracetam, which is why dosing errors here matter more than in the rest of the category.

How to read the Soviet clinical series →

How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →

What Noopept actually does

It is not a racetam and it was never meant to be one. Noopept (GVS-111, INN omberacetam) is N-phenylacetyl-L-prolylglycine ethyl ester, C17H22N2O4, 318.38 Da — a dipeptide designed at the Zakusov Institute as a topological analog of piracetam's beta-turn, which is a deliberate design strategy rather than a family resemblance. Three parts: a phenylacetyl cap, a Pro-Gly dipeptide, and an ethyl ester on the C-terminus.

The ester is the delivery device and the liability. Carboxylesterases — CES1 in liver, CES2 in intestinal wall, plus plasma esterase activity — cleave ethyl esters quickly. What survives cleavage and cyclization is cycloprolylglycine, a diketopiperazine of 154.17 Da that is not a xenobiotic at all: it is an endogenous neuropeptide the brain already makes. Metabolism study of the closely related dipeptide GZK-111 — N-phenylacetylglycyl-L-proline ethyl ester, the reversed sequence — found four biotransformation products in rat plasma by HPLC-mass spectrometry, with the main routes being esterase hydrolysis of the ester bond followed by degradation, plus reactions yielding phenylacetic acid and cycloprolylglycine Kolyvanov 2022. Both the forward and the reversed dipeptide converge on the same active metabolite, which tells you where the pharmacology actually lives.

What cycloprolylglycine does, at receptor level. At a physiological concentration of 10⁻⁶ M it significantly enhances transmembrane AMPA currents in rat cerebellar Purkinje cells; the authors conclude it is an endogenous positive modulator of AMPA receptors and propose that its effects run through BDNF accumulation downstream of AMPA receptor activation Gudasheva 2016. That is a specific ionotropic glutamate receptor, a specific concentration, and a specific downstream sequence.

And here is the finding that contradicts the standard description of this compound. In rat hippocampal slices, noopept at 5 µM increased the action-potential firing frequency of GABAergic interneurons in stratum radiatum of CA1, and increased the frequency of spontaneous inhibitory postsynaptic currents in CA1 pyramidal cells. Both effects were almost completely abolished by the alpha-7 nicotinic antagonists alpha-bungarotoxin at 6 nM and methyllycaconitine at 20 nM Kondratenko 2022. Read what that means: noopept's hippocampal action runs through alpha-7 nicotinic acetylcholine receptors on inhibitory interneurons, and its net effect on the principal cells is more inhibition, not more excitation. Every vendor description of this compound as a glutamatergic stimulant has the sign backwards, and the alpha-7 account is a far better explanation of why the subjective report is quiet, narrow-focus attention rather than stimulation.

The neurotrophin result, with the half nobody quotes. Northern blot in rats: after a single dose, NGF and BDNF mRNA in the cerebral cortex fell below control, while in the hippocampus both rose. After 28 days, cortical BDNF rose slightly and the hippocampal effect was not merely maintained but potentiated rather than tolerant Ostrovskaya 2008. A regional split with opposite signs in cortex and hippocampus is a strange and interesting result, it is in the abstract, and it appears on no page selling this compound.

The connection nobody has made. Cycloprolylglycine is the same molecule as cyclic glycine-proline, cGP, which has an entirely separate literature in marine natural products and neuroscience in which its principal described role is regulating insulin-like growth factor 1 homeostasis and bioavailability, alongside neuroprotective and neurotrophic effects Hu 2024. So noopept's active metabolite is, in another field, a modulator of the IGF-1 axis. The nootropic literature and the IGF literature describe the same compound and have never been put in the same sentence.

Cell, rodent, human — and where it stops

In slices and cells. Cycloprolylglycine at 1 µM on rat cerebellar Purkinje cells, whole-cell recording, AMPA currents enhanced Gudasheva 2016. Noopept at 5 µM on rat hippocampal slices, patch-clamp, interneuron firing and spontaneous IPSC frequency up, both abolished by alpha-7 antagonists at nanomolar concentrations Kondratenko 2022.

In rodents, pharmacokinetics first. GVS-111 given orally to rats and assayed by HPLC: the dipeptide is absorbed from the gastrointestinal tract, enters the circulation, and penetrates the blood-brain barrier in an unmodified state Boiko 2000. That is the whole result. The abstract reports no half-life, no Cmax and no brain-to-plasma ratio, which is why the arithmetic in the pharmacokinetics section below has to do the work.

In rodents, effects. Rat hippocampus, single dose and 28 days, NGF and BDNF mRNA by Northern blot, with the cortex-down/hippocampus-up split described above Ostrovskaya 2008. And an intranasal experiment worth reading carefully: PINK1-knockout rats given a formulation of forskolin 10 µM with noopept 20 nM intranasally showed reversal of motor symptoms and hind-limb strength loss, rescue of midbrain dopaminergic neurons, raised protein kinase A activity, BDNF and NGF, and a fall in cortical alpha-synuclein aggregates that the combination produced and forskolin alone did not Dagda 2022.

In humans. Noopept is registered in Russia for cognitive impairment and the trials supporting that registration are in the Russian-language clinical literature; a search of the English-indexed record turns up no randomized controlled trial of noopept. What the international literature does contain is enforcement data: European and Australian medicines control laboratories intercepted noopept as bulk raw material in a surveillance study covering 159 samples and 34 distinct molecules from 2020 to 2024 Vanhee 2025.

The obstacles, and the first is a concentration problem that runs the wrong way. (1) The slice experiment used 5 µM and a human oral dose cannot reach it. 20 mg of a 318 Da compound is 63 µmol; spread through 42 L of body water with nothing absorbed imperfectly and nothing cleared, that is 1.5 µM as an absolute ceiling — roughly three-fold below the concentration at which the alpha-7 effect was demonstrated Kondratenko 2022. The metabolite is the opposite case: cGP was active at 1 µM Gudasheva 2016, which the same arithmetic does reach. So the honest reading is that the parent's mechanism is out of range and the metabolite's is in range, which is another argument that this is a cGP prodrug. (2) The intranasal rodent result is a combination product. 20 nM noopept with 10 µM forskolin Dagda 2022; this site lists a nasal form of noopept alone, and the paper's own alpha-synuclein result required the pair. (3) The active metabolite is endogenous, so there is no clean baseline: you cannot measure the drug's cGP against zero, only against whatever the person already makes. (4) The best PK statement in the literature has no numbers in it Boiko 2000, and an ester that plasma esterases attack has to arrive before it is cut — a race whose result nobody has timed.

Noopept pharmacokinetics — how much of it actually gets in

The catalog says ~30–60 minutes with a longer-lasting active metabolite. That is the right shape; here is the arithmetic underneath it.

What degrades it, in order. First the ethyl ester, cleaved by carboxylesterases — CES2 in the intestinal wall on the way through, CES1 in the liver, plus plasma esterase activity. Then the exposed dipeptide cyclizes to cycloprolylglycine, and the phenylacetyl cap leaves as phenylacetic acid; both routes were identified for the reversed-sequence analog in rat plasma Kolyvanov 2022. The peptide bond itself is a target for aminopeptidases once the phenylacetyl cap is off, which is the ordinary fate of any uncapped dipeptide. Three enzyme classes, one molecule, and the last product in the chain is the one with the receptor activity.

The ceiling calculation, which is the number this page exists to give. 318.38 Da. A 10 mg dose is 31 µmol, 20 mg is 63 µmol, 30 mg is 94 µmol. Distributed through roughly 42 L of total body water with complete absorption and zero clearance — a ceiling nobody actually reaches — that is 0.75, 1.5 and 2.2 µM respectively. Set those against the two concentrations that produced the published mechanisms: noopept 5 µM for the alpha-7 interneuron effect Kondratenko 2022 and cGP 1 µM for the AMPA effect Gudasheva 2016. The metabolite's active concentration is reachable and the parent's is not. Nobody has written that down, and it is the strongest available argument for why the compound is best understood as an oral cycloprolylglycine prodrug.

The oral barrier. Intestinal CES2 and hepatic CES1 mean the dominant loss is first-pass ester hydrolysis rather than failure to absorb — the molecule gets in and then gets cut. Rat data confirm the getting-in half: absorbed from the gut, into the circulation, across the blood-brain barrier unmodified Boiko 2000. The nasal route on this site exists to skip that first pass, which is mechanistically sound and has no human data; the only nasal animal study is a co-formulation Dagda 2022.

Transporters, with the honest reading of a scary-sounding result. In HepG2 cells, omberacetam at 500 µM raised the content of both OATP1B1 and OATP1B3 and, from 100 µM upwards, reduced the uptake of atorvastatin; the authors evaluated it by the FDA's Cmax/IC50 approach and judged the effect clinically insignificant Erokhina 2023. Put that beside the ceiling above: 500 µM is more than 300-fold above the most a 20 mg oral dose could ever produce. This is a mechanism finding, not a warning, and the arithmetic is the reason to say so rather than leaving a reader to worry about their statin.

Route. Oral in the trials and in the registration; nasal on this site's variant list, with no human comparison of the two.

What would have to be true, and how you would know it was not

Four predictions. The second is the one nobody has ever run and it comes from joining two literatures.

1. Against the product: MoCA will not move in a healthy adult, and the mechanism explains why you should not expect it to. The demonstrated hippocampal action is an increase in inhibitory tone onto pyramidal cells via alpha-7 receptors on interneurons Kondratenko 2022; the neurotrophin effect is regional and, acutely, negative in cortex Ostrovskaya 2008. Neither predicts a bedside cognitive score change in an intact brain. Retest at 8 weeks if you want the number, but treat a null as expected rather than as disproof.

2. IGF-1 is the draw nobody has ever done on this compound. Cycloprolylglycine's described role in a separate literature is regulating IGF-1 homeostasis and bioavailability Hu 2024, and the ester-then-cyclization route that produces cGP was mapped for noopept’s reversed-sequence analog in rat plasma Kolyvanov 2022. Order IGF-1 (insulin-like growth factor 1) at baseline and at 8 weeks on a steady dose. The specific prediction: total IGF-1 will not change, because cGP's described action is on binding and availability rather than on hepatic production — so a total-IGF-1 shift would be the surprising result and would point at a growth-axis effect nobody is watching for. Hold protein intake, training load and sleep roughly constant, because all three move IGF-1 more than this will.

3. Prolactin should not move, and it is the cheapest dopaminergic control. Noopept is routinely described in dopaminergic terms it has never earned; the receptor evidence is alpha-7 nicotinic and AMPA Kondratenko 2022 Gudasheva 2016. Draw prolactin fasted before 10am at baseline and 8 weeks. No change is the prediction and it is a useful negative, because it would close off a mechanism that gets asserted constantly.

4. High-sensitivity CRP should be flat, and the irritability should be dose-dependent. hs-CRP is the systemic control at 8 weeks. The more interesting half is behavioral: if the alpha-7 interneuron account is right, the irritability and headache a meaningful minority report should scale with dose and should not improve with added choline — which is the opposite of the standard community advice, and is testable by anyone with two four-week blocks and a diary.

What nobody has tested yet

Five experiments. The first is embarrassing by its absence and the second would open a new question about the compound entirely.

1. No human plasma or CSF concentration of noopept or cycloprolylglycine has ever been published. Not at 10 mg, not at 30 mg, not by any route. The assay is described in the rat metabolism paper's methods Kolyvanov 2022. Six people, one 30 mg dose, eight timepoints, and the central question of this page — whether the parent or the metabolite is doing the work — stops being arithmetic and becomes data.

2. Nobody has drawn an IGF-1 panel on a noopept user. The active metabolite is a described regulator of IGF-1 homeostasis in a literature the nootropic field has never read Hu 2024. Total IGF-1, IGFBP-3 and, if available, free IGF-1, before and after eight weeks, in twenty people. This is the single most likely place a genuinely unknown systemic effect of this compound is hiding, and it costs a standard endocrine panel.

3. Nobody has compared nasal with oral in a person. This site sells both. The mechanistic rationale for nasal dosing is bypassing intestinal and hepatic carboxylesterases, which is sound; the only animal nasal study used a forskolin co-formulation Dagda 2022. A crossover with a pharmacokinetic endpoint would say whether the nasal route delivers more parent compound or simply more irritation.

4. Nobody has tested the alpha-7 prediction in a human, and there is a standard way to. Alpha-7 nicotinic receptor function in people is conventionally probed by the auditory P50 sensory-gating ratio — a thirty-minute EEG paradigm. If noopept works through alpha-7 receptors on inhibitory interneurons Kondratenko 2022, P50 suppression should improve on drug. That is a directly falsifiable human test of the compound's best-characterized mechanism and it has never been attempted.

5. Nobody has replicated the cortex-down/hippocampus-up split. Eighteen years after it was published Ostrovskaya 2008, the most counterintuitive result in noopept's literature — acute suppression of cortical neurotrophin message alongside hippocampal induction — has not been repeated in any other laboratory, and it is the result that would most change how the compound is dosed if it held.

Noopept — its own safety story, not its class's

The class block is written for racetams and tells you to cycle. Four things here belong to this molecule.

1. The irritability has a candidate mechanism now, and it predicts the opposite of the usual advice. A meaningful minority report irritability or headache on noopept — more than most compounds in this category generate. If the operative action is increased firing of GABAergic interneurons through alpha-7 nicotinic receptors Kondratenko 2022, that is a cholinergic effect, and adding a choline source should make it worse rather than better. The standard forum answer is to add choline. One of those two positions is wrong and the experiment to settle it takes eight weeks and a notebook.

2. The dose is small enough that a label error is a different drug. Noopept is taken at 10–30 mg. Analysis of cognitive-enhancement supplements found 75% of declared quantities inaccurate, with some products delivering up to four-fold more than a typical pharmacologic dose, and with drugs present but unlabelled or labeled but absent Cohen 2021; medicines control laboratories in Europe and Australia intercepted noopept specifically as bulk raw material Vanhee 2025. At this dose scale a four-fold error is the difference between 20 mg and 80 mg, and nobody has ever characterized 80 mg in a person.

3. The endogenous-metabolite argument cuts both ways. Cycloprolylglycine is a molecule the brain already makes Gudasheva 2016, which is genuinely reassuring about acute toxicity and says nothing at all about chronic supra-physiological exposure — particularly given that the same molecule is described elsewhere as a regulator of IGF-1 availability Hu 2024. A growth-axis modulator taken daily for months, with nobody measuring the growth axis, is the open question on this page.

4. The nasal route has no data and one specific hazard. The variant list includes nasal dosing. An ethyl ester in an unbuffered vehicle applied to respiratory epithelium is a mucosal-irritation and ciliary-function question with no published study for this molecule; the only nasal animal work used a different formulation containing a second active compound Dagda 2022. Choosing the nasal route to bypass first-pass esterases is mechanistically reasonable and is an experiment on yourself with no dose equivalence to the oral route.

Sources read for this page

• Kondratenko RV, Povarov IS, Kolbaev SN, Derevyagin VI, Ostrovskaya RU, Gudasheva TA, Sharonova IN, Skrebitsky VG. Effect of nootropic dipeptide noopept on CA1 pyramidal neurons involves α7AChRs on interneurons in hippocampal slices from rat. Neuroscience Letters 2022;790:136898 · PMID 36195298
• Gudasheva TA, Grigoriev VV, Koliasnikova KN, Zamoyski VL, Seredenin SB. Neuropeptide cycloprolylglycine is an endogenous positive modulator of AMPA receptors. Doklady Biochemistry and Biophysics 2016;471(1):387-389 · PMID 28058675
• Ostrovskaya RU, Gudasheva TA, Zaplina AP, Vahitova JV, Salimgareeva MH, Jamidanov RS, Seredenin SB. Noopept stimulates the expression of NGF and BDNF in rat hippocampus. Bulletin of Experimental Biology and Medicine 2008;146(3):334-337 · PMID 19240853
• Boiko SS, Ostrovskaya RU, Zherdev VP, Korotkov SA, Gudasheva TA, Voronina TA, Seredenin SB. Pharmacokinetics of new nootropic acylprolyldipeptide and its penetration across the blood-brain barrier after oral administration. Bulletin of Experimental Biology and Medicine 2000;129(4):359-361 · PMID 10977920
• Kolyvanov GB, Bochkov PO, Litvin AA, Shevchenko RV, Podol'ko AL, Kravtsova OY, Kolyasnikova KN, Zherdev VP. Metabolism of a New Dipeptide Neuroprotector in Rats. Bulletin of Experimental Biology and Medicine 2022;172(5):579-582 · PMID 35352249
• Hu L, Lin J, Qin F, Xu L, Luo L. Exploring Sources, Biological Functions, and Potential Applications of the Ubiquitous Marine Cyclic Dipeptide: A Concise Review of Cyclic Glycine-Proline. Marine Drugs 2024;22(6):271 · PMID 38921582
• Dagda RK, Dagda RY, Vazquez-Mayorga E, Martinez B, Gallahue A. Intranasal Administration of Forskolin and Noopept Reverses Parkinsonian Pathology in PINK1 Knockout Rats. International Journal of Molecular Sciences 2022;24(1):690 · PMID 36614135
• Erokhina PD, Abalenikhina YV, Mylnikov PY, Petrov AV, Ganina SO, Konyakhin EA, Shchulkin AV, Yakusheva EN. The Effect of Original Russian Neurotropic Drugs on Organic Anion Transporting Polypeptides OATP1B1 and OATP1B3. Bulletin of Experimental Biology and Medicine 2023;176(2):170 · PMID 38198100
• Vanhee C, Deconinck E, George M, Hansen A, Hackl A, Wollein U, El-Atma O, Beerbaum N, Aureli F, Borioni A, et al. The Occurrence of Illicit Smart Drugs or Nootropics in Europe and Australia and Their Associated Dangers: Results from a Market Surveillance Study by 12 Official Medicines Control Laboratories. Journal of Xenobiotics 2025;15(3):88 · PMID 40558871
• Cohen PA, Avula B, Wang YH, Zakharevich I, Khan I. Five Unapproved Drugs Found in Cognitive Enhancement Supplements. Neurology: Clinical Practice 2021;11(3):e303-e307 · PMID 34484905

Noopept — safety, predicted from mechanism

Noopept — interference & stacking

Bloodwork to run alongside Noopept

Baseline first, then again at 8–12 weeks.

The Brain Fog & Cognition panel covers these in one order — 12 markers, $233.06 with the discount applied.

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Noopept — frequently asked questions

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