Noopept
Arkham Labs editorial/Published 8 September 2026/Revised 12 September 2026/Corrections policy
on a narrow and explicitly stated basis. See the note below
01 · What it is
Noopept is the only compound in this project that twelve national medicines control laboratories went looking for and found being shipped as bulk raw material.
It is not a peptide. Noopept is N-phenylacetyl-L-prolylglycine ethyl ester 35 — a dipeptide ethyl ester, which is to say a small molecule built from two amino acids with the carboxyl end esterified and a phenylacetyl group on the front. Its own literature calls it a substituted Pro-Gly dipeptide 21 and a dipeptide analogue of piracetam 22. The ester is what makes it orally active and what makes it, pharmacologically, a prodrug: rat pharmacokinetics identify cycloprolylglycine as its active metabolite 24. A reader evaluating Noopept is evaluating two molecules, and the literature is much clearer about the first than the second.
Where it comes from. Noopept, originally GVS-111, was designed at the Zakusov Institute of Pharmacology in Moscow by a group building nootropic drugs from dipeptide scaffolds 1,3,23. It is a prescription medicine in Russia 36. Essentially the entire efficacy literature comes from that one institute, under the recurring names Gudasheva, Ostrovskaya, Seredenin and Voronina — the founding pharmacology 2, the neurotrophin work 10, the diabetes programme 16,17,18, the mechanism papers 21,25,28, and the reviews 23.
The sourcing evidence is unusually good, and unusually bad news. Two independent analyses exist, which is more than almost any compound in this project has.
A 2021 study bought ten over-the-counter cognitive-enhancement supplements in the United States and analysed them by mass spectrometry 31. Products labelled as containing omberacetam — Noopept’s other name — delivered up to 40.6 mg per recommended serving against a typical pharmacologic dose of 10 mg. Drugs were detected that were not on the label, and drugs on the label were not detected. Of the products that stated a quantity, 75% — nine of twelve — were inaccurate 31.
A market-surveillance study by the General European Official Medicines Control Laboratory Network and Australia documented 159 samples between January 2020 and September 2024, identifying 34 distinct molecules. Sixty-nine per cent came from the illegal market. Noopept was among a small group — with phenylpiracetam and phenibut — intercepted as large bulk quantities of raw material 36.
And one of its papers has been retracted. A 2021 study on Noopept, spinal microglia and BDNF expression was withdrawn by the journal three months after publication 29,30.
The compound is a Russian prescription drug with a large single-institute animal literature, no controlled human trial that this guide could locate in English indexing, a retracted paper, and documented product mislabelling at four times the pharmacologic dose.
02 · Evidence at a glance
- Evidence grade
- Approved Pharma — on a narrow and explicitly stated basis. See the note below
- Chemical class
- Not a peptide. A dipeptide ethyl ester — N-phenylacetyl-L-prolylglycine ethyl ester 35
- Active metabolite
- Cycloprolylglycine 24 — the parent behaves as a prodrug
- Regulatory status, Russia
- Prescription medicine 36
- US status
- Not approved for human use; not a lawful dietary supplement ingredient 31
- Research concentration
- One institute produced almost the entire efficacy literature 1,2,3,4,9,10,16,17,18,19,20,21,22,23,24,25,27,28
- Controlled human trials located
- None in English indexing. See Limitation 2
- Label accuracy, US supplements
- 75% of declared quantities inaccurate (9 of 12) 31
- Highest measured serving
- 40.6 ± 0.4 mg omberacetam against a typical pharmacologic dose of 10 mg 31
- European/Australian surveillance
- 159 samples, 34 molecules, 69% from the illegal market; Noopept found as bulk raw material 36
- Published toxicology
- Limited; a genotoxicity-adjacent study exists 27
On the grade. Approved Pharma requires a marketing authorisation in at least one jurisdiction. The sole basis here is the European medicines control laboratory network’s description of Noopept as a drug available on prescription in Russia 36. This guide has not consulted a Russian regulatory record, and no registration number, indication or authorisation date is stated anywhere in it. The grade also carries no implication about evidence quality: authorisation in one jurisdiction is not the same as having satisfied any particular regulator’s evidentiary standard, and the rubric grades the state of the literature, not the strength of a compound.
03 · Mechanism of action
A prodrug, and the literature mostly studies the parent
Noopept’s ester is cleaved in vivo, and rat pharmacokinetic work identifies cycloprolylglycine as the active metabolite 24. That paper is in Russian and is cited here on its title and English abstract alone.
Almost every mechanistic experiment in this file administers Noopept and measures an outcome. Very few establish which of the two molecules produced it. That is a structural gap in the mechanism literature rather than a criticism of any single paper.
Neurotrophin expression is the headline claim
Noopept is reported to stimulate expression of both nerve growth factor and brain-derived neurotrophic factor in rat hippocampus 10. This is the mechanism most often cited for the compound and the one that connects it to the neuroprotection and memory findings.
It is also the mechanism of the retracted paper 29,30, which concerned spinal microglia-dependent BDNF and pro-BDNF expression. The retraction does not touch the 2008 hippocampal result, which stands 10, but a reader assembling the BDNF case should know that one of its bricks was removed.
Receptor and channel-level findings
Work in hippocampal slices reports that Noopept’s effect on CA1 pyramidal neurons involves α7 nicotinic acetylcholine receptors on interneurons 32, and separately that it enhances inhibitory synaptic transmission in the hippocampus 20. Behavioural work reports prevention of memory deficit under both muscarinic and nicotinic receptor blockade 9.
Acting through interneuron α7 receptors to change inhibition is a specific, testable proposal, and it is the most mechanistically concrete thing in the file. It also sits awkwardly beside a behavioural claim of efficacy during nicotinic blockade 9, and no paper here addresses the tension.
Transcriptional and cellular effects
A molecular mechanism study frames the compound as a substituted Pro-Gly dipeptide with defined cellular actions 21. Noopept has been reported to activate the transcription factor HIF-1 28, to improve viability of HT-22 hippocampal neurons under glutamate toxicity 22, and to attenuate apoptosis and tau hyperphosphorylation in a cellular Alzheimer’s model 19.
Reported separately by the same institute, and worth noting because HIF-1 activation is a double-edged finding — it is protective in ischaemia and is also a pathway tumours exploit.
A negative result the developers published themselves
A 2019 study from the originating group is titled to report that Noopept does not stimulate cell proliferation 25.
A laboratory publishing a paper whose entire point is that its compound lacks a growth-promoting property is publishing an inconvenient result, and in a compound class where proliferation is the standing safety question it is a useful one. It deserves credit and it is cited here for that reason.
04 · Key research findings
Founding pharmacology, 2002–2003. The original characterisation of Noopept as a nootropic and neuroprotective agent 2, its anti-inflammatory properties under the designation GVS-111 1, and the design rationale for building neuropsychotropic drugs from dipeptides 3. All Russian-language.
This guide has not read them. Three of the founding papers for this compound are in a language its author cannot check, which is the same limitation that constrains the Semax, Selank, Vilon and Pinealon guides.
Developmental and early-life dosing, 2005 and 2007. Effects of early postnatal Noopept and piracetam on declarative and procedural memory in adult male and female rats 4, and a comparison of Noopept against the brain extract Cortexin in rats treated with corticoliberin or 70-kDa heat shock proteins during early ontogeny 6.
Dosing during early development is a serious design choice, and it appears here in 2005 without any supporting reproductive-toxicity work anywhere in this file. The Cortexin comparison also places Noopept directly against the animal-tissue extracts covered elsewhere in this project.
Cerebral ischaemia, 2006 and 2009. Neuroprotective activity in middle cerebral artery occlusion 5, and reduction of postischemic functional and metabolic disorders in rats of differing hypoxia sensitivity 11.
Alzheimer’s model, 2007. Restoration of spatial memory and increased immunoreactivity to amyloid in an Alzheimer’s disease model, published in a Western journal with a mixed Russian and British author list 8.
One of the few early studies to reach a journal outside the Russian pharmacology literature.
Neurotrophins, 2008. Stimulation of NGF and BDNF expression in rat hippocampus 10.
Anticonvulsant interaction, 2009. Potentiation of the anticonvulsant activity of valproate in mice 12.
A drug-drug interaction finding, in Russian, never followed up in humans anywhere in this file. It is the same shape as the Selank–diazepam finding elsewhere in this family: a compound sold for everyday use that modifies the action of a prescription central nervous system drug, with no human interaction study.
Independent work on amyloid, 2011. A group at Umeå in Sweden reported that Noopept rescues α-synuclein amyloid cytotoxicity, published in the Journal of Molecular Biology 14.
Genuinely independent, in a structural biology journal, on a protein unrelated to the compound’s marketed positioning.
Independent electrophysiology, 2011. Effects of nootropics on the EEG of conscious rats and their modification by glutamatergic inhibitors, from a group including a Cardiff co-author 13.
The diabetes programme, 2013–2014. Efficacy in streptozotocin-induced diabetes 16; a direct comparison against the dipeptidyl peptidase-4 inhibitor sitagliptin in a model of developing diabetes 17; and normalisation of incretin-system parameters 18.
A proline-containing dipeptide compared against a DPP-4 inhibitor is a chemically motivated experiment rather than an opportunistic one, and the incretin work connects this compound to Family K in a way nothing else in Family F does.
Genotoxicity-adjacent evidence, 2019. Prevention of DNA damage in mice with modelled prediabetes 27.
The nearest thing to a safety study in the file, and it is framed as protection rather than as a toxicology assessment.
Independent Parkinson’s work, 2022. Intranasal forskolin and Noopept reported to reverse parkinsonian pathology in PINK1 knockout rats, from a group at the University of Nevada, Reno 33.
Independent, and a combination design — the contribution attributable to Noopept alone is not separable from the abstract.
The retracted paper, 2021. A study on Noopept, persistent inflammation, spinal microglia and BDNF/pro-BDNF expression through the apoptotic process, published in Heliyon in February 2021 29 and retracted by the journal in May 2021 30. The retraction notice states only that it retracts the article.
Three months from publication to withdrawal. As with Dihexa, the notice gives no grounds, so this guide states the fact and nothing more. It is the second retraction found in this family.
Drug transporter interaction, 2023. An examination of the effect of Russian neurotropic drugs, Noopept among them, on the organic anion transporting polypeptides OATP1B1 and OATP1B3 34.
Transporter effects are the mechanism behind a large share of clinical drug-drug interactions, and this is the only paper in the file that looks for them.
Structural characterisation, 2025. A physicochemical and structural analysis of N-phenylacetyl-L-prolylglycine ethyl ester as an active pharmaceutical ingredient, from a Polish and Greek group 35.
Independent confirmation of what the molecule actually is — which, after the P21 guide in this same family, is not something to take for granted.
The two product analyses, 2021 and 2025. Ten US supplements analysed by mass spectrometry: up to 40.6 mg omberacetam per serving against a 10 mg pharmacologic dose, undeclared drugs present, declared drugs absent, and 75% of stated quantities inaccurate 31. And 159 samples across Europe and Australia over nearly five years, 69% from the illegal market, with Noopept intercepted as bulk raw material 36.
These are the most important papers in the file for anyone handling this compound, and neither is about pharmacology. The first was published by a neurology journal and the second by twelve official medicines control laboratories.
05 · Evidence overview
| Dimension | Status |
|---|---|
| Controlled human trials located | None in English indexing |
| Human pharmacokinetics | Not located; rat pharmacokinetics published 24 |
| Animal efficacy studies | Extensive — ischaemia 5,11, Alzheimer’s models 8,19, diabetes 16,17,18, Parkinson’s 33 |
| Independent replication | Yes, in mechanism and structure 13,14,33,35 |
| Independent efficacy replication in a disease model | Partial — one combination study 33 |
| Research concentration | One Moscow institute on the large majority of papers |
| Russian-language sources unread here | At least six 1,2,3,5,12,24 |
| Retracted publications | One 29,30 |
| Active metabolite identified | Yes — cycloprolylglycine 24 |
| Which molecule produces the effects | Not established |
| Drug interaction data | Valproate potentiation in mice 12; OATP transporter work 34; no human studies |
| Product identity in the market | Poor — 75% of declared quantities inaccurate 31 |
06 · Safety profile
Animal data. The compound has been dosed across many rodent studies without adverse findings being reported in the abstracts, including chronic diabetes protocols 16,17,18 and early postnatal administration 4. A study in mice with modelled prediabetes reports prevention of DNA damage 27, and the originating group has published that Noopept does not stimulate cell proliferation 25. Immunopharmacological and anti-inflammatory properties have been examined 7,15.
Two findings bear on interaction risk. Noopept potentiates the anticonvulsant activity of valproate in mice 12, and Russian neurotropic drugs including Noopept have been assessed for effects on the OATP1B1 and OATP1B3 transporters 34.
Human data. This guide located no controlled human trial in English indexing. One 2019 paper in Georgian Medical News concerns management of amnestic and behavioural disorders after ketamine anaesthesia 26; whether it is a human study, and what it found, cannot be established from the indexed record available here, and it is cited for existence only.
That absence sits oddly beside prescription status in Russia 36. Russian-language clinical literature very likely exists and is simply not reachable through the indexing this guide uses. The honest statement is that the trials were not located, not that they do not exist.
What is genuinely unknown. Which molecule is responsible for the effects — parent or cycloprolylglycine metabolite 24. Human pharmacokinetics, at any dose. What the valproate interaction 12 and the transporter findings 34 mean for anyone taking prescription medication. Long-term exposure of any duration. And carcinogenicity, which is worth naming specifically because the compound is reported to activate HIF-1 28 and to raise neurotrophin expression 10 — the developers’ own negative proliferation result 25 is relevant reassurance but is not a carcinogenicity study.
The exposure risk that is actually documented. Everything above concerns the molecule. The measured hazard concerns the products. A consumer taking a labelled serving of a US supplement could receive four times a pharmacologic dose of this drug, alongside up to three other unapproved drugs not named on the label 31. That is not a theoretical gap in the literature; it is a measured finding, in ten products, published in a neurology journal.
07 · US regulatory status
Current as of 6 September 2026. Noopept is not approved for human use in the United States and is not a lawful dietary supplement ingredient. The 2021 analysis identifies omberacetam explicitly as one of four drugs not approved for human use in the US that were nonetheless found in products sold as supplements 31. It is not a controlled substance.
In Russia it is a prescription medicine 36. This guide has not consulted the Russian regulatory record, and states no registration number, indication or date. In the European Union and Australia, the medicines control laboratory network treats Noopept as an unauthorised medicine, and the majority of the samples it documented came from the illegal market 36.
Under the World Anti-Doping Code, Noopept does not appear as a named prohibited substance in the classes reviewed for this guide. Competitors should consult the current Prohibited List directly rather than rely on secondary summaries, including this one.
08 · Limitations of the evidence
- A paper in this file has been retracted. The 2021 Heliyon study on Noopept, spinal microglia and BDNF was withdrawn three months after publication 29,30. The notice gives no grounds. This is the second retraction found in Family F, and it was found the same way as the first — by noticing a flag in a search result rather than by any systematic check.
- No controlled human trial was located, in a compound that is prescribed to humans. The absence is in English indexing, not necessarily in the world. Russian-language clinical literature probably exists; this guide cannot read it and does not assert what it contains. Every efficacy claim reported above is an animal or cell claim.
- Research concentration is close to total. One Moscow institute produced the founding chemistry, the pharmacology, the neurotrophin work, the diabetes programme, the mechanism papers and the reviews. Independent work exists 13,14,33,35 but addresses structure and mechanism, not whether the compound does what it is sold to do.
- At least six primary sources are Russian-language and unread here 1,2,3,5,12,24. Two of them carry findings the guide reports — the valproate interaction 12 and the identification of the active metabolite 24 — on the basis of their titles and English abstracts alone.
- The active molecule is not established. Noopept is a prodrug whose metabolite is cycloprolylglycine 24, and the mechanistic literature overwhelmingly administers the parent and measures an outcome. Attributing any reported effect to Noopept specifically is not supported by the material cited here.
- Animal-to-human translation is unattempted and the models are heterogeneous. Streptozotocin diabetes, middle cerebral artery occlusion, PINK1 knockout and amyloid models each have their own poor track record of predicting human results, and nothing in this file bridges any of them to a person.
- Publication bias cannot be assessed. A single-institute literature spanning two decades, much of it in journals published in the same country, provides no way to estimate what was run and not published. The developers’ own negative proliferation paper 25 is a point in the opposite direction and is noted as such.
- Two mechanistic claims are in tension and nobody has resolved them. Efficacy under nicotinic receptor blockade 9 versus an effect requiring α7 nicotinic receptors on interneurons 32.
- Interaction risk is documented in animals and unstudied in humans. Valproate potentiation 12 and OATP transporter effects 34 are exactly the findings that would trigger interaction studies for a regulated drug. None exists here.
- Product identity in the market is measurably poor. Seventy-five per cent of declared quantities inaccurate, undeclared drugs present, declared drugs absent, and servings delivering four times a pharmacologic dose 31; bulk raw material intercepted across Europe and Australia 36. Whatever the pharmacology says, this is what is actually in circulation.
- This guide has read abstracts, not full texts, for every source cited.
- Dihexathe family’s other non-peptide, and its other retraction.
- Selankanother compound from the same Russian pharmacological tradition, with the same unfollowed benzodiazepine-interaction problem.
- Semaxthe family’s clearest case of an evidence base sitting with one national research programme.
- Family F · Cognitive and neuroactive peptidesthe family index.
09 · References
Kovalenko LP, Miramedova MG, Alekseeva SV, Gudasheva TA, Ostrovskaia RU, Seredenin SB. [Anti-inflammatory properties of noopept (dipeptide nootropic agent GVS-111)]. Eksp Klin Farmakol. 2002 Mar–Apr;65(2):53–55. Russian.
PMID 12109295 ↗Ostrovskaia RU, Gudasheva TA, Voronina TA, Seredenin SB. [The original novel nootropic and neuroprotective agent noopept]. Eksp Klin Farmakol. 2002 Sep–Oct;65(5):66–72. Russian. Review.
PMID 12596521 ↗Gudasheva TA, Skoldinov AP. [Design of the novel dipeptide neuropsychotropic drug preparations]. Eksp Klin Farmakol. 2003 Mar–Apr;66(2):15–19. Russian. Review.
PMID 12962042 ↗Trofimov SS, Voronina TA, Guzevatykh LS. Early postnatal effects of noopept and piracetam on declarative and procedural memory of adult male and female rats. Bull Exp Biol Med. 2005 Jun;139(6):683–687.
PMID 16224581 ↗Gavrilova SA, Us KS, Ostrovskaia RU, Koshelev VB. [Neuroprotective activity of the proline-containing dipeptide noopept on the model of brain ischemia induced by the middle cerebral artery occlusion]. Eksp Klin Farmakol. 2006 Jul–Aug;69(4):16–18. Russian.
PMID 16995431 ↗Shabanov PD, Lebedev AA, Stetsenko VP, Lavrov NV, Sablina GV, Gudasheva TA, Ostrovaskaia RU. [Effects of noopept and cortexin on the behavior of matured rats treated with corticoliberin or 70-kDa heat shock proteins in early ontogeny]. Eksp Klin Farmakol. 2007 Jan–Feb;70(1):6–10. Russian.
PMID 17402584 ↗Kovalenko LP, Shipaeva EV, Alekseeva SV, Pronin AV, Durnev AD, Gudasheva TA, Ostrovskaja RU, Seredenin SB. Immunopharmacological properties of noopept. Bull Exp Biol Med. 2007 Jul;144(1):49–52.
PMID 18256750 ↗Ostrovskaya RU, Gruden MA, Bobkova NA, Sewell RD, Gudasheva TA, Samokhin AN, Seredinin SB, Noppe W, Sherstnev VV, Morozova-Roche LA. The nootropic and neuroprotective proline-containing dipeptide noopept restores spatial memory and increases immunoreactivity to amyloid in an Alzheimer’s disease model. J Psychopharmacol. 2007 Aug;21(6):611–619.
PMID 17092975 ↗Radionova KS, Belnik AP, Ostrovskaya RU. Original nootropic drug noopept prevents memory deficit in rats with muscarinic and nicotinic receptor blockade. Bull Exp Biol Med. 2008 Jul;146(1):59–62.
PMID 19145351 ↗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. Bull Exp Biol Med. 2008 Sep;146(3):334–337.
PMID 19240853 ↗Zarubina IV, Shabanov PD. Noopept reduces the postischemic functional and metabolic disorders in the brain of rats with different sensitivity to hypoxia. Bull Exp Biol Med. 2009 Mar;147(3):339–344.
PMID 19529857 ↗Kravchenko EV, Ponteleeva IV, Trofimov SS, Lapa VI, Ostrovskaia RU, Voronina TA. [The original nootropic and neuroprotective drug noopept potentiates the anticonvulsant activity of valproate in mice]. Eksp Klin Farmakol. 2009 Nov–Dec;72(6):15–17. Russian.
PMID 20095393 ↗Vorobyov V, Kaptsov V, Kovalev G, Sengpiel F. Effects of nootropics on the EEG in conscious rats and their modification by glutamatergic inhibitors. Brain Res Bull. 2011 May 30;85(3–4):123–132.
PMID 21414388 ↗Jia X, Gharibyan AL, Öhman A, Liu Y, Olofsson A, Morozova-Roche LA. Neuroprotective and nootropic drug noopept rescues alpha-synuclein amyloid cytotoxicity. J Mol Biol. 2011 Dec 16;414(5):699–712.
PMID 21986202 ↗Alekseeva SV, Kovalenko LP, Tallerova AV, Gudasheva TA, Durnev AD. [An experimental study of the anti-inflammatory action of noopept and its effect on the level of cytokines]. Eksp Klin Farmakol. 2012;75(9):25–27. Russian.
PMID 23156084 ↗Ostrovskaya RU, Ozerova IV, Gudascheva TA, Kapitsa IG, Ivanova EA, Voronina TA, Seredenin SB. Efficiency of noopept in streptozotocin-induced diabetes in rats. Bull Exp Biol Med. 2013 Jan;154(3):334–338.
PMID 23484194 ↗Ostrovskaya RU, Ozerova IV, Gudascheva TA, Kapitsa IG, Ivanova EA, Voronina TA, Seredenin SB. Comparative activity of proline-containing dipeptide noopept and inhibitor of dipeptidyl peptidase-4 sitagliptin in a rat model of developing diabetes. Bull Exp Biol Med. 2014 Jan;156(3):342–346.
PMID 24771372 ↗Ostrovskaya RU, Zolotov NN, Ozerova IV, Ivanova EA, Kapitsa IG, Taraban KV, Michunskaya AM, Voronina TA, Gudasheva TA, Seredenin SB. Noopept normalizes parameters of the incretin system in rats with experimental diabetes. Bull Exp Biol Med. 2014 Jul;157(3):344–349.
PMID 25065315 ↗Ostrovskaya RU, Vakhitova YV, Kuzmina USh, Salimgareeva MKh, Zainullina LF, Gudasheva TA, Vakhitov VA, Seredenin SB. Neuroprotective effect of novel cognitive enhancer noopept on AD-related cellular model involves the attenuation of apoptosis and tau hyperphosphorylation. J Biomed Sci. 2014 Aug 6;21(1):74.
PMID 25096780 ↗Povarov IS, Kondratenko RV, Derevyagin VI, Ostrovskaya RU, Skrebitskii VG. Nootropic dipeptide noopept enhances inhibitory synaptic transmission in the hippocampus. Bull Exp Biol Med. 2015 Jan;158(3):349–351.
PMID 25573367 ↗Vakhitova YV, Sadovnikov SV, Borisevich SS, Ostrovskaya RU, Gudasheva TA, Seredenin SB. Molecular mechanism underlying the action of substituted Pro-Gly dipeptide noopept. Acta Naturae. 2016 Jan–Mar;8(1):82–89.
PMID 27099787 ↗Antipova TA, Nikolaev SV, Ostrovskaya PU, Gudasheva TA, Seredenin SB. Dipeptide piracetam analogue noopept improves viability of hippocampal HT-22 neurons in the glutamate toxicity model. Bull Exp Biol Med. 2016 May;161(1):58–60.
PMID 27265136 ↗Gudasheva TA, Ostrovskaya RU, Seredenin SB. Novel technologies for dipeptide drugs design and their implantation. Curr Pharm Des. 2018;24(26):3020–3027. Review.
PMID 30295186 ↗Boyko SS, Zherdev VP, Shevchenko RV. [Pharmacokinetics of noopept and its active metabolite cycloprolyl glycine in rats]. Biomed Khim. 2018 Sep;64(5):455–458. Russian.
PMID 30378564 ↗Zainullina LF, Ivanova TV, Ostrovskaya RU, Gudasheva TA, Vakhitova YV, Seredenin SB. Drug with neuroprotective properties noopept does not stimulate cell proliferation. Bull Exp Biol Med. 2019 Feb;166(4):466–468.
PMID 30788746 ↗Belenichev I, Burlaka B, Puzyrenko A, Ryzhenko O, Kurochkin M, Yusuf J. Management of amnestic and behavioral disorders after ketamine anesthesia. Georgian Med News. 2019 Sep;(294):141–145. Study design not established from the indexed record..
PMID 31687967 ↗Ostrovskaya RU, Yagubova SS, Zhanataev AK, Anisina EA, Gudasheva TA, Durnev AD. Neuroprotective dipeptide noopept prevents DNA damage in mice with modeled prediabetes. Bull Exp Biol Med. 2019 Dec;168(2):233–237.
PMID 31776952 ↗Zainullina LF, Ivanova TV, Sadovnikov SV, Vakhitova YV, Seredenin SB. Cognitive enhancer noopept activates transcription factor HIF-1. Dokl Biochem Biophys. 2020 Sep;494(1):256–260.
PMID 33119829 ↗Taghizadeh M, Maghsoudi N, Manaheji H, Akparov V, Baniasadi M, Mohammadi M, Danyali S, Ghasemi R, Zaringhalam J. Noopept; a nootropic dipeptide, modulates persistent inflammation by effecting spinal microglia dependent brain derived neurotropic factor (BDNF) and pro-BDNF expression throughout apoptotic process. Heliyon. 2021 Feb 12;7(2):e06219. RETRACTED — see reference 30..
PMID 33644478 ↗Retraction notice to “Noopept; a nootropic dipeptide, modulates persistent inflammation by effecting spinal microglia dependent brain derived neurotropic factor (BDNF) and pro-BDNF expression throughout apoptotic process” [Heliyon (2021) e06219]. Heliyon. 2021 May 17;7(5):e06981.
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PMID 36195298 ↗Dagda RK, Dagda RY, Vazquez-Mayorga E, Martinez B, Gallahue A. Intranasal administration of forskolin and noopept reverses parkinsonian pathology in PINK1 knockout rats. Int J Mol Sci. 2022 Dec 30;24(1):690.
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PMID 40558871 ↗
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