Nooglutyl (nooglutil)

updated

Nooglutyl (nooglutil, ONK-10) is a research compound from Russian pharmacology, sold for memory enhancement and neuroprotection. Its published work is rat and mouse studies, mostly Russian-language papers from one network of laboratories between 1990 and 2013, with one 2019 paper on a calcium salt, and no controlled human study exists: a PubMed query on 10 October 2026 returned 27 records and none reports nooglutil given to a person. The doses in those studies, 20 to 50 mg/kg and up, are not comparable to any human use.

Nicotinoyl-glutamic acid nootropic (AMPA label unsettled)

  • Nooglutyl is PubChem CID 147523, C11H12N2O6, molecular weight 268.22, N-(5-hydroxynicotinoyl)-L-glutamic acid; the literature also writes nooglutil, noogluthyl and ONK-10, and a 2019 paper tested a separate calcium salt.
  • At 50 mg/kg intraperitoneally nooglutil prevented retrograde amnesia produced by electromagnetic exposure, motion sickness and electroconvulsive shock in rodents.
  • After distal middle cerebral artery occlusion in rats, nooglutyl 10 mg/kg limited the affected zone from 22.51% to 7.6% of the ipsilateral hemisphere, against 9.55% for mexidol and 12.8% for phenyl-tert-butylnitrone.
  • The abstracts describe the mechanism three ways: an AMPA receptor modulator with no stated basis, AMPA binding competition at an IC50 of 6.4 micromolar, and NMDA-mediated suppression in slices at high concentrations.
  • Of the 27 PubMed records, 23 are marked as Russian-language articles and 3 are English-language papers in Bulletin of Experimental Biology and Medicine.
  • DailyMed returned no label and ClinicalTrials.gov no study on 10 October 2026, and no Russian register was read, so status in Russia is not established here.

What is nooglutyl, and what is its regulatory status?

Nooglutyl, also written nooglutil and ONK-10, is N-(5-hydroxynicotinoyl)-L-glutamic acid, PubChem CID 147523, a research compound from Russian pharmacology. It has no FDA label and no registered study, a calcium salt studied in 2019 is a separate form, and its status in Russia is not established here.

Nooglutyl is PubChem CID 147523, C11H12N2O6, 268.22 g/mol, CAS 112193-35-8 among the synonyms, (2S)-2-[(5-hydroxypyridine-3-carbonyl)amino]pentanedioic acid, which is N-(5-hydroxynicotinoyl)-L-glutamic acid. The papers also write it N-(5-oxynicotinoyl)-L-glutamic acid, ONC-10 and OHK-10, and the literature uses nooglutil, nooglutyl, noogluthyl and ONK-10 interchangeably, so searches need all of them.

A 2019 paper tested the calcium salt of the same acid, named Ampasse there, which is a separate salt form. The free acid and the calcium salt should not be treated as the same product. No public record ties any vendor material, free acid or salt, to the studied compound.

On 10 October 2026 DailyMed returned no label under either spelling, an openFDA Drugs@FDA query returned no match, and ClinicalTrials.gov queries for nooglutil, nooglutyl, the chemical name and ONK-10 spelling variants, and Ampasse returned no studies. A web search for the name returned no Russian leaflet or registration entry, which is not proof, and no Russian register was read, so status in Russia is not established here.

PubChem: nooglutyl identity, spellings, and the calcium salt flag

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 147523, (2S)-2-[(5-hydroxypyridine-3-carbonyl)amino]pentanedioic acid (nooglutyl, nooglutil).

Nooglutyl (also nooglutil, noogluthyl, ONK-10) is PubChem CID 147523, C11H12N2O6, 268.22 g/mol, CAS 112193-35-8 (listed among the synonyms), IUPAC name (2S)-2-[(5-hydroxypyridine-3-carbonyl)amino]pentanedioic acid, which is N-(5-hydroxynicotinoyl)-L-glutamic acid. The papers also write it N-(5-oxynicotinoyl)-L-glutamic acid, 'ONC-10' and 'OHK-10'. A 2019 paper tested the calcium salt of the same acid, named 'Ampasse' there, a separate salt form (PMID 31745682). The literature uses nooglutil, nooglutyl and ONK-10 interchangeably, so searches need all of them.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule; free acid and calcium salt
Follow-up
Not applicable
Study design
Chemical database record; original reports
Funding
not stated in the source

Identity record only. No public record ties any vendor material, free acid or salt, to the studied compound.

Read the original source
Label and registry searches, 10 October 2026: no label, no match, no study

Regulatory record

U.S. Food and Drug Administration (DailyMed label search; openFDA Drugs@FDA query) and ClinicalTrials.gov. Searches for nooglutil, nooglutyl, the chemical name and ONK-10 spelling variants, and Ampasse, run 10 October 2026.

ClinicalTrials.gov queries for nooglutil, nooglutyl, the chemical name and ONK-10 spelling variants, and 'Ampasse' returned no studies, DailyMed returned no label under either spelling, and the openFDA Drugs@FDA query returned no match. A web search for the name returned no Russian leaflet or registration entry, which is not proof, and no Russian register was read.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated label, application and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026. It covers United States label, application and registry records and one web search; the Russian state register was not read.

Read the original source
Rat pups and mice: prenatal alcohol and hypoxia, dopamine efflux with opposite effects, calcium salt

Animal study

Kovalev GI et al. Biull Eksp Biol Med. 1993;116(7):56-8. PMID 8400184.

Given to rat pups from day 8 to 20 at 25 mg/kg/day, nooglutyl prevented learning and memory disorders after prenatal alcohol exposure (PMID 1305426) and after intrauterine hypoxia (PMID 8704601). In a dopamine release study of alcohol-exposed pups, nooglutil at 25 mg/kg subcutaneously normalized the reduced dopamine efflux, while its effects in pups of non-alcoholized rats were opposite. The calcium salt at 30 mg/kg showed antidepressant-like activity in the mouse forced swim test and at 0.1 mg/kg alleviated MPTP-induced parkinsonian signs in mice and haloperidol catalepsy in rats (PMID 31745682).

Participants / model
Rat pups; mice; rats
Treatment
Subcutaneous and other routes; calcium salt in the 2019 paper
Follow-up
Day 8 to 20 of life in the pup studies
Study design
Original preclinical studies
Funding
not stated in the source

The two dopamine results suggest the direction of effect depends on the animal's starting state, which is an inference from those two results and not a conclusion stated in the abstract.

Read the original source

What did the rat and mouse studies find?

In rats and mice nooglutyl prevented memory loss from several insults, including electromagnetic exposure, motion sickness, electroconvulsive shock and hypoxia, and improved behavior in aged SAMP10 mice and rat pups. Every result is an induced or strain-based deficit in rodents, mostly in Russian-language papers from one network of laboratories, at doses of 20 to 50 mg/kg and up, and no controlled human study exists.

The founding paper, from the originating institute, reports that in mice and rats ONK-10 had pronounced antiamnestic and antihypoxic effects, did not disturb conditioned reflex activity or orientation behavior, had no anxiolytic or anticonvulsant activity, caused no disorder of movement coordination and was low toxic. The authors report it was superior in antiamnestic and antihypoxic effects to piracetam, meclofenoxate and demanol aceglumate and not inferior to aniracetam. The abstract gives no doses, routes or toxicity figures, so low toxic is an unquantified statement.

In operant learning, nooglutil enhanced escape and avoidance responses in a Skinner box where piracetam improved only escape, and neither changed shuttle-box avoidance or water-reward T-maze behavior. At 50 mg/kg i.p. nooglutil prevented retrograde amnesia produced by electromagnetic exposure, motion sickness and electroconvulsive shock, and a 2013 rat paper finds marked antiamnestic effects on microwave, acute hypoxia and motion-sickness models. In 9-month-old SAMP10 mice, 20 mg/kg improved open field activity, anxiety in the plus maze and passive avoidance retrieval. In BALB/c mice, nooglutil improved exploratory behavior in the cross-maze, and in C57BL/6 mice it did not. Hypoxia and ischemia models by the same Russian groups reached similar conclusions.

Given to rat pups from day 8 to 20 at 25 mg/kg/day, nooglutyl prevented learning and memory disorders after prenatal alcohol exposure and after intrauterine hypoxia. In a dopamine release study of alcohol-exposed pups, nooglutil at 25 mg/kg subcutaneously normalized the reduced dopamine efflux, while its effects in pups of non-alcoholized rats were opposite, so the direction of effect may depend on the animal's starting state, which is an inference from the two results and not a stated conclusion. The calcium salt at 30 mg/kg showed antidepressant-like activity in the mouse forced swim test and at 0.1 mg/kg alleviated MPTP-induced parkinsonian signs in mice and haloperidol catalepsy in rats.

Every result is an induced or strain-based deficit in rats or mice. None is a healthy-person outcome, and the doses used, 20 to 50 mg/kg and up, are not comparable to any human use. Of the 27 PubMed records, 23 are marked as Russian-language articles and 3 are English-language papers in Bulletin of Experimental Biology and Medicine.

Founding paper from the originating institute: antiamnestic and antihypoxic, 'low toxic', no doses in the abstract

Animal study

Voronina TA et al. Farmakol Toksikol. 1990;53(4):13-6. PMID 1977613.

In mice and rats ONK-10 had pronounced antiamnestic and antihypoxic effects, did not disturb conditioned reflex activity or orientation behavior, had no anxiolytic or anticonvulsant activity, caused no disorder of movement coordination, and was 'low toxic'; the authors report it was superior in antiamnestic and antihypoxic effects to piracetam, meclofenoxate and demanol aceglumate and not inferior to aniracetam. The abstract gives no doses, no routes and no toxicity figures. A 2003 review from the same school (Voronina TA) lists nooglutyl among drugs created at the Institute of Pharmacology from Zakusov's synaptic ideas, alongside mexidol, noopept and beglimin (PMID 12962041).

Participants / model
Mice and rats
Treatment
Not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study; review
Funding
not stated in the source

'Low toxic' is an unquantified statement. The paper is from the originating institute.

Read the original source
Rodent deficits: electromagnetic exposure, motion sickness, shock, hypoxia, aged SAMP10 mice, strain differences

Animal study

Iasnetsov VV et al. Eksp Klin Farmakol. 1996;59(3):20-3. PMID 8974577.

In operant learning, nooglutil enhanced escape and avoidance responses in a Skinner box where piracetam improved only escape, and neither changed shuttle-box avoidance or water-reward T-maze behavior (PMID 8348043). At 50 mg/kg i.p. nooglutil prevented retrograde amnesia produced by electromagnetic exposure, motion sickness and electroconvulsive shock, and a 2013 rat paper finds marked antiamnestic effects on microwave, acute hypoxia and motion-sickness models (PMID 24555225). In 9-month-old SAMP10 mice, 20 mg/kg improved open field activity, anxiety in the plus maze and passive avoidance retrieval (PMID 18078032). In BALB/c mice, nooglutil improved exploratory behavior in the cross-maze, and in C57BL/6 mice it did not (PMID 23025044). Hypoxia and ischemia models by the same Russian groups reached similar conclusions (PMID 9606516, PMID 11055197).

Participants / model
Rats; mice including SAMP10, BALB/c and C57BL/6
Treatment
Intraperitoneal in some studies, 50 mg/kg in the amnesia models and 20 mg/kg in SAMP10 mice; route not stated in others
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

Every result is an induced or strain-based deficit in rats or mice; none is a healthy-person outcome, and the doses used (20 to 50 mg/kg and up) are not comparable to any human use.

Read the original source
Rat pups and mice: prenatal alcohol and hypoxia, dopamine efflux with opposite effects, calcium salt

Animal study

Kovalev GI et al. Biull Eksp Biol Med. 1993;116(7):56-8. PMID 8400184.

Given to rat pups from day 8 to 20 at 25 mg/kg/day, nooglutyl prevented learning and memory disorders after prenatal alcohol exposure (PMID 1305426) and after intrauterine hypoxia (PMID 8704601). In a dopamine release study of alcohol-exposed pups, nooglutil at 25 mg/kg subcutaneously normalized the reduced dopamine efflux, while its effects in pups of non-alcoholized rats were opposite. The calcium salt at 30 mg/kg showed antidepressant-like activity in the mouse forced swim test and at 0.1 mg/kg alleviated MPTP-induced parkinsonian signs in mice and haloperidol catalepsy in rats (PMID 31745682).

Participants / model
Rat pups; mice; rats
Treatment
Subcutaneous and other routes; calcium salt in the 2019 paper
Follow-up
Day 8 to 20 of life in the pup studies
Study design
Original preclinical studies
Funding
not stated in the source

The two dopamine results suggest the direction of effect depends on the animal's starting state, which is an inference from those two results and not a conclusion stated in the abstract.

Read the original source
PubMed, 10 October 2026: 27 records from 1990 to 2019, mostly Russian-language, none gives nooglutil to a person

PubMed search record

PubMed search run 10 October 2026: nooglutil[tiab] OR nooglutyl[tiab] OR noogluthyl[tiab] OR ONK-10[tiab] and the chemical name variants, with a follow-up query adding patients, volunteers, clinical, trial, human, humans, toxicity or toxic.

The search returned 27 records dated 1990 to 2019, and abstracts were read for 26 (record 7579248, on an antimotion-sickness effect, has no abstract and was judged by its title). Twenty-three are marked as Russian-language articles, one (7579248) has a bracketed title in a Russian journal, and three are English-language papers in Bulletin of Experimental Biology and Medicine, so the claim that the literature is mainly Russian is accurate. Adding patients, volunteers, clinical, trial, human, humans, toxicity or toxic returned 8 records, all read, and none reports nooglutil given to a person; the matches were reviews, rat studies and a mouse study. No controlled human trial exists in the records reviewed.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished, unindexed or Russian-register material exists.

Read the original source

Does nooglutyl protect the brain after injury in rats?

In rat injury models given by injection, yes. Nooglutyl 10 mg/kg limited the affected zone after artery occlusion from 22.51% to 7.6% of the ipsilateral hemisphere, and it reduced deficits after hematoma and protected mitochondrial function after trauma. All of it is rat work from Russian laboratories between 1997 and 2007, with no replication outside that network and no human outcome.

After distal middle cerebral artery occlusion in rats, nooglutyl 10 mg/kg intravenously at occlusion and intraperitoneally for two days limited the affected zone from 22.51 +/- 3.0% of the ipsilateral hemisphere to 7.6 +/- 2.28%, against 9.55 +/- 1.9% for mexidol and 12.8 +/- 1.7% for phenyl-tert-butylnitrone, and improved passive avoidance retrieval.

In rats with a posttraumatic intracerebral hematoma, single i.p. doses of 10 and 20 mg/kg 3 to 4 hours after surgery decreased neurological deficit, restored coordination, improved retrieval and prevented loss of animals. In rat brain trauma models, nooglutil at 50 mg/kg (and 25 mg/kg in immature rats) protected mitochondrial oxidative phosphorylation and did better than the comparators tested, which included picamilon and pyriditol, and in a trauma model it showed a moderate antiischemic, antihypoxic and antiamnestic action.

All of this is in rats, by injection, from Russian laboratories between 1997 and 2007. No replication outside that network was found, and none of it reaches a human outcome.

Rat injury models by injection: infarct zone 22.51% to 7.6%, hematoma, trauma, mitochondria

Animal study

Povarova OV et al. Eksp Klin Farmakol. 2004;67(1):3-6. PMID 15079898.

After distal middle cerebral artery occlusion in rats, nooglutyl 10 mg/kg intravenously at occlusion and intraperitoneally for two days limited the affected zone from 22.51 +/- 3.0% of the ipsilateral hemisphere to 7.6 +/- 2.28%, against 9.55 +/- 1.9% for mexidol and 12.8 +/- 1.7% for phenyl-tert-butylnitrone, and improved passive avoidance retrieval. In rats with a posttraumatic intracerebral hematoma, single i.p. doses of 10 and 20 mg/kg 3 to 4 hours after surgery decreased neurological deficit, restored coordination, improved retrieval and prevented loss of animals (PMID 12924225). In rat brain trauma models, nooglutil at 50 mg/kg (and 25 mg/kg in immature rats) protected mitochondrial oxidative phosphorylation and did better than the comparators tested, which included picamilon and pyriditol (PMID 9162289, PMID 9621180), and in a trauma model it showed a moderate antiischemic, antihypoxic and antiamnesic action (PMID 18074799).

Participants / model
Rats
Treatment
Intravenous and intraperitoneal injection
Follow-up
Two days after occlusion in the artery occlusion study; single doses in the hematoma study
Study design
Original preclinical studies
Funding
not stated in the source

All in rats, by injection, from Russian laboratories between 1997 and 2007; no replication outside that network was found, and none reaches a human outcome.

Read the original source

How does nooglutyl act, and is it an AMPA modulator?

The mechanism is not settled. A 2002 abstract calls nooglutil a positive modulator of AMPA receptors without giving the basis, a binding study shows it competes with an AMPA receptor agonist at an IC50 of 6.4 micromolar, which is binding competition and not modulation, and slice work found NMDA-mediated suppression at high concentrations. The AMPA label is the research group's working description.

A 2002 abstract calls nooglutil a positive modulator of AMPA receptors for glutamate without giving the basis. In the same paper 50 mg/kg increased the dissociation constant and density of D2 dopamine receptors in rat striatum while 100 mg/kg abolished the effect, and 70 mg/kg i.p. reduced anxiety in rats in the Vogel conflict test 24 hours after stopping chronic diazepam.

A radioligand study found that nooglutil competes with a selective AMPA receptor agonist for binding sites with an IC50 of 6.4 +/- 0.2 micromolar (noopept 80 +/- 5.6 micromolar) in rat brain, which shows binding competition and not modulation. A 2013 abstract says the antiamnestic effect of nooglutil was caused to a significant degree by activation of non-NMDA receptors, mostly AMPA.

Hippocampal slice work found that high concentrations of nooglutil suppressed CA1 responses through NMDA receptors, an effect blocked by AP7. The AMPA label is the research group's working description, and the data are indirect or conflicting.

Unsettled mechanism: AMPA binding competition (IC50 6.4 micromolar), D2 receptors, NMDA-mediated slice effects

Animal study

Firstova IuIu et al. Eksp Klin Farmakol. 2011;74(1):6-10. PMID 21476267.

A 2002 abstract calls nooglutil 'a positive modulator of AMPA receptors for glutamate' without giving the basis, and in the same paper 50 mg/kg increased the dissociation constant and density of D2 dopamine receptors in rat striatum while 100 mg/kg abolished the effect, and 70 mg/kg i.p. reduced anxiety in rats in the Vogel conflict test 24 hours after stopping chronic diazepam (PMID 12802448). A radioligand study found nooglutil competes with a selective AMPA receptor agonist for binding sites with an IC50 of 6.4 +/- 0.2 micromolar (noopept 80 +/- 5.6 micromolar) in rat brain, which shows binding competition and not modulation. A 2013 abstract says the antiamnestic effect of nooglutil was caused to a significant degree by activation of non-NMDA receptors, mostly AMPA (PMID 24555225), while hippocampal slice work found high concentrations of nooglutil suppressed CA1 responses through NMDA receptors, an effect blocked by AP7 (PMID 11177255).

Participants / model
Rat brain tissue; rat hippocampal slices; rats
Treatment
Radioligand binding; tissue bath; intraperitoneal in rats
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

The AMPA label is the research group's working description, and the data are indirect or conflicting.

Read the original source

Does nooglutyl improve memory and protect neurons?

In rodents, yes in the narrow sense. Memory is supported as rescue of drug-, hypoxia-, trauma- and age-model deficits at 20 to 50 mg/kg, neuroprotection only as smaller lesions and better mitochondrial function in rat injury models given by injection, and the literature is mainly Russian. Nothing shows either effect in a person.

Sellers describe memory enhancement and neuroprotection, supported mainly by Russian literature. The memory claim is supported as rescue of deficits caused by drugs, hypoxia, trauma and age-related or strain-based changes in rats and mice at 20 to 50 mg/kg and up. The neuroprotection claim is supported only as smaller lesions and better mitochondrial function in rat injury models given by injection.

The claim that the literature is mainly Russian is accurate. A PubMed query on 10 October 2026 for nooglutil, nooglutyl, noogluthyl and ONK-10 returned 27 records dated 1990 to 2019, and abstracts were read for 26 of them, with the 27th, which has no abstract, judged by its title. Twenty-three are marked as Russian-language articles, one has a bracketed title in a Russian journal, and three are English-language papers in Bulletin of Experimental Biology and Medicine.

No person has been given nooglutil in the records reviewed. Adding patients, volunteers, clinical, trial, human, humans, toxicity or toxic returned 8 records, all read, and none reports nooglutil given to a person; the matches were reviews, rat studies and a mouse study. No controlled human trial exists in the records reviewed.

Rodent deficits: electromagnetic exposure, motion sickness, shock, hypoxia, aged SAMP10 mice, strain differences

Animal study

Iasnetsov VV et al. Eksp Klin Farmakol. 1996;59(3):20-3. PMID 8974577.

In operant learning, nooglutil enhanced escape and avoidance responses in a Skinner box where piracetam improved only escape, and neither changed shuttle-box avoidance or water-reward T-maze behavior (PMID 8348043). At 50 mg/kg i.p. nooglutil prevented retrograde amnesia produced by electromagnetic exposure, motion sickness and electroconvulsive shock, and a 2013 rat paper finds marked antiamnestic effects on microwave, acute hypoxia and motion-sickness models (PMID 24555225). In 9-month-old SAMP10 mice, 20 mg/kg improved open field activity, anxiety in the plus maze and passive avoidance retrieval (PMID 18078032). In BALB/c mice, nooglutil improved exploratory behavior in the cross-maze, and in C57BL/6 mice it did not (PMID 23025044). Hypoxia and ischemia models by the same Russian groups reached similar conclusions (PMID 9606516, PMID 11055197).

Participants / model
Rats; mice including SAMP10, BALB/c and C57BL/6
Treatment
Intraperitoneal in some studies, 50 mg/kg in the amnesia models and 20 mg/kg in SAMP10 mice; route not stated in others
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

Every result is an induced or strain-based deficit in rats or mice; none is a healthy-person outcome, and the doses used (20 to 50 mg/kg and up) are not comparable to any human use.

Read the original source
Rat injury models by injection: infarct zone 22.51% to 7.6%, hematoma, trauma, mitochondria

Animal study

Povarova OV et al. Eksp Klin Farmakol. 2004;67(1):3-6. PMID 15079898.

After distal middle cerebral artery occlusion in rats, nooglutyl 10 mg/kg intravenously at occlusion and intraperitoneally for two days limited the affected zone from 22.51 +/- 3.0% of the ipsilateral hemisphere to 7.6 +/- 2.28%, against 9.55 +/- 1.9% for mexidol and 12.8 +/- 1.7% for phenyl-tert-butylnitrone, and improved passive avoidance retrieval. In rats with a posttraumatic intracerebral hematoma, single i.p. doses of 10 and 20 mg/kg 3 to 4 hours after surgery decreased neurological deficit, restored coordination, improved retrieval and prevented loss of animals (PMID 12924225). In rat brain trauma models, nooglutil at 50 mg/kg (and 25 mg/kg in immature rats) protected mitochondrial oxidative phosphorylation and did better than the comparators tested, which included picamilon and pyriditol (PMID 9162289, PMID 9621180), and in a trauma model it showed a moderate antiischemic, antihypoxic and antiamnesic action (PMID 18074799).

Participants / model
Rats
Treatment
Intravenous and intraperitoneal injection
Follow-up
Two days after occlusion in the artery occlusion study; single doses in the hematoma study
Study design
Original preclinical studies
Funding
not stated in the source

All in rats, by injection, from Russian laboratories between 1997 and 2007; no replication outside that network was found, and none reaches a human outcome.

Read the original source
PubMed, 10 October 2026: 27 records from 1990 to 2019, mostly Russian-language, none gives nooglutil to a person

PubMed search record

PubMed search run 10 October 2026: nooglutil[tiab] OR nooglutyl[tiab] OR noogluthyl[tiab] OR ONK-10[tiab] and the chemical name variants, with a follow-up query adding patients, volunteers, clinical, trial, human, humans, toxicity or toxic.

The search returned 27 records dated 1990 to 2019, and abstracts were read for 26 (record 7579248, on an antimotion-sickness effect, has no abstract and was judged by its title). Twenty-three are marked as Russian-language articles, one (7579248) has a bracketed title in a Russian journal, and three are English-language papers in Bulletin of Experimental Biology and Medicine, so the claim that the literature is mainly Russian is accurate. Adding patients, volunteers, clinical, trial, human, humans, toxicity or toxic returned 8 records, all read, and none reports nooglutil given to a person; the matches were reviews, rat studies and a mouse study. No controlled human trial exists in the records reviewed.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished, unindexed or Russian-register material exists.

Read the original source
Label and registry searches, 10 October 2026: no label, no match, no study

Regulatory record

U.S. Food and Drug Administration (DailyMed label search; openFDA Drugs@FDA query) and ClinicalTrials.gov. Searches for nooglutil, nooglutyl, the chemical name and ONK-10 spelling variants, and Ampasse, run 10 October 2026.

ClinicalTrials.gov queries for nooglutil, nooglutyl, the chemical name and ONK-10 spelling variants, and 'Ampasse' returned no studies, DailyMed returned no label under either spelling, and the openFDA Drugs@FDA query returned no match. A web search for the name returned no Russian leaflet or registration entry, which is not proof, and no Russian register was read.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated label, application and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026. It covers United States label, application and registry records and one web search; the Russian state register was not read.

Read the original source

What is known about the safety of nooglutyl?

No human safety, pharmacokinetic or toxicology data exist for nooglutyl. The founding paper calls it low toxic without giving toxicity figures, and no abstract gives a half-life, absolute bioavailability, LD50, repeat-dose toxicology or genotoxicity result. The free acid and the calcium salt are separate forms, and the identity of vendor material is not established.

No record reports nooglutil given to a person, so no human adverse event, tolerability, pharmacokinetic or interaction information exists. The founding paper calls the compound low toxic, but its abstract gives no doses, routes or toxicity figures, so that statement is unquantified.

Pharmacokinetic data are thin. In rabbits, one tablet form containing tween-80 had a bioavailability of 104.3% relative to the drug substance, a relative figure that says nothing about absolute oral absorption. In progeny of alcoholized and intact rats, repeated dosing changed plasma levels, clearance, volume of distribution and the main metabolite compared with a single dose. No abstract gives half-life, absolute bioavailability, LD50, repeat-dose toxicology, genotoxicity or human pharmacokinetics.

Two rodent results point to context dependence. The effect on dopamine efflux in pups of non-alcoholized rats was opposite to the effect in alcohol-exposed pups, and in hippocampal slices high concentrations of nooglutil suppressed CA1 responses through NMDA receptors.

Product identity is a separate concern. The free acid and the calcium salt are different forms and should not be treated as the same product, and no public record ties vendor material to the studied compound.

PubMed, 10 October 2026: 27 records from 1990 to 2019, mostly Russian-language, none gives nooglutil to a person

PubMed search record

PubMed search run 10 October 2026: nooglutil[tiab] OR nooglutyl[tiab] OR noogluthyl[tiab] OR ONK-10[tiab] and the chemical name variants, with a follow-up query adding patients, volunteers, clinical, trial, human, humans, toxicity or toxic.

The search returned 27 records dated 1990 to 2019, and abstracts were read for 26 (record 7579248, on an antimotion-sickness effect, has no abstract and was judged by its title). Twenty-three are marked as Russian-language articles, one (7579248) has a bracketed title in a Russian journal, and three are English-language papers in Bulletin of Experimental Biology and Medicine, so the claim that the literature is mainly Russian is accurate. Adding patients, volunteers, clinical, trial, human, humans, toxicity or toxic returned 8 records, all read, and none reports nooglutil given to a person; the matches were reviews, rat studies and a mouse study. No controlled human trial exists in the records reviewed.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished, unindexed or Russian-register material exists.

Read the original source
Founding paper from the originating institute: antiamnestic and antihypoxic, 'low toxic', no doses in the abstract

Animal study

Voronina TA et al. Farmakol Toksikol. 1990;53(4):13-6. PMID 1977613.

In mice and rats ONK-10 had pronounced antiamnestic and antihypoxic effects, did not disturb conditioned reflex activity or orientation behavior, had no anxiolytic or anticonvulsant activity, caused no disorder of movement coordination, and was 'low toxic'; the authors report it was superior in antiamnestic and antihypoxic effects to piracetam, meclofenoxate and demanol aceglumate and not inferior to aniracetam. The abstract gives no doses, no routes and no toxicity figures. A 2003 review from the same school (Voronina TA) lists nooglutyl among drugs created at the Institute of Pharmacology from Zakusov's synaptic ideas, alongside mexidol, noopept and beglimin (PMID 12962041).

Participants / model
Mice and rats
Treatment
Not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study; review
Funding
not stated in the source

'Low toxic' is an unquantified statement. The paper is from the originating institute.

Read the original source
Thin pharmacokinetics: one relative bioavailability figure in rabbits, repeated-dose changes in rat progeny

Animal study

Chesnokova EA et al. Eksp Klin Farmakol. 1998;61(4):48-50. PMID 9783110.

In rabbits, one tablet form containing tween-80 had a bioavailability of 104.3% relative to the drug substance, a relative figure that says nothing about absolute oral absorption. In progeny of alcoholized and intact rats, repeated dosing changed plasma levels, clearance, volume of distribution and the main metabolite compared with a single dose (PMID 1786827). No abstract gives half-life, absolute bioavailability, LD50, repeat-dose toxicology, genotoxicity or human pharmacokinetics.

Participants / model
Rabbits; rat progeny
Treatment
Oral tablets in rabbits; route not stated in the rat study; doses not stated in the abstracts
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

A relative figure only. No absolute oral absorption, half-life or toxicology figure is available.

Read the original source
Rat pups and mice: prenatal alcohol and hypoxia, dopamine efflux with opposite effects, calcium salt

Animal study

Kovalev GI et al. Biull Eksp Biol Med. 1993;116(7):56-8. PMID 8400184.

Given to rat pups from day 8 to 20 at 25 mg/kg/day, nooglutyl prevented learning and memory disorders after prenatal alcohol exposure (PMID 1305426) and after intrauterine hypoxia (PMID 8704601). In a dopamine release study of alcohol-exposed pups, nooglutil at 25 mg/kg subcutaneously normalized the reduced dopamine efflux, while its effects in pups of non-alcoholized rats were opposite. The calcium salt at 30 mg/kg showed antidepressant-like activity in the mouse forced swim test and at 0.1 mg/kg alleviated MPTP-induced parkinsonian signs in mice and haloperidol catalepsy in rats (PMID 31745682).

Participants / model
Rat pups; mice; rats
Treatment
Subcutaneous and other routes; calcium salt in the 2019 paper
Follow-up
Day 8 to 20 of life in the pup studies
Study design
Original preclinical studies
Funding
not stated in the source

The two dopamine results suggest the direction of effect depends on the animal's starting state, which is an inference from those two results and not a conclusion stated in the abstract.

Read the original source

Why does nooglutyl sit in C tier?

Nooglutyl has a defined structure, a plausible glutamatergic story and more than two decades of rodent work showing rescue of induced deficits and smaller infarcts, with no harm and no failed trial in the records reviewed, but nearly all of it is Russian-language work from one network, with no human exposure, no quantified toxicology and a mechanism the abstracts describe three ways.

The compound has a defined structure, a plausible glutamatergic story, and more than two decades of rat and mouse work showing rescue of induced deficits and smaller infarcts, with no harm and no failed trial in the records reviewed.

The data are thin in the C sense. Nearly all of it is Russian-language work from one network of laboratories, from 1990 to 2013 with one 2019 salt paper, in rodents and rabbits, with no human exposure, no human pharmacokinetics, no quantified toxicology, no registered study, and a mechanism that the abstracts describe three different ways.

Founding paper from the originating institute: antiamnestic and antihypoxic, 'low toxic', no doses in the abstract

Animal study

Voronina TA et al. Farmakol Toksikol. 1990;53(4):13-6. PMID 1977613.

In mice and rats ONK-10 had pronounced antiamnestic and antihypoxic effects, did not disturb conditioned reflex activity or orientation behavior, had no anxiolytic or anticonvulsant activity, caused no disorder of movement coordination, and was 'low toxic'; the authors report it was superior in antiamnestic and antihypoxic effects to piracetam, meclofenoxate and demanol aceglumate and not inferior to aniracetam. The abstract gives no doses, no routes and no toxicity figures. A 2003 review from the same school (Voronina TA) lists nooglutyl among drugs created at the Institute of Pharmacology from Zakusov's synaptic ideas, alongside mexidol, noopept and beglimin (PMID 12962041).

Participants / model
Mice and rats
Treatment
Not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study; review
Funding
not stated in the source

'Low toxic' is an unquantified statement. The paper is from the originating institute.

Read the original source
Rodent deficits: electromagnetic exposure, motion sickness, shock, hypoxia, aged SAMP10 mice, strain differences

Animal study

Iasnetsov VV et al. Eksp Klin Farmakol. 1996;59(3):20-3. PMID 8974577.

In operant learning, nooglutil enhanced escape and avoidance responses in a Skinner box where piracetam improved only escape, and neither changed shuttle-box avoidance or water-reward T-maze behavior (PMID 8348043). At 50 mg/kg i.p. nooglutil prevented retrograde amnesia produced by electromagnetic exposure, motion sickness and electroconvulsive shock, and a 2013 rat paper finds marked antiamnestic effects on microwave, acute hypoxia and motion-sickness models (PMID 24555225). In 9-month-old SAMP10 mice, 20 mg/kg improved open field activity, anxiety in the plus maze and passive avoidance retrieval (PMID 18078032). In BALB/c mice, nooglutil improved exploratory behavior in the cross-maze, and in C57BL/6 mice it did not (PMID 23025044). Hypoxia and ischemia models by the same Russian groups reached similar conclusions (PMID 9606516, PMID 11055197).

Participants / model
Rats; mice including SAMP10, BALB/c and C57BL/6
Treatment
Intraperitoneal in some studies, 50 mg/kg in the amnesia models and 20 mg/kg in SAMP10 mice; route not stated in others
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

Every result is an induced or strain-based deficit in rats or mice; none is a healthy-person outcome, and the doses used (20 to 50 mg/kg and up) are not comparable to any human use.

Read the original source
Rat injury models by injection: infarct zone 22.51% to 7.6%, hematoma, trauma, mitochondria

Animal study

Povarova OV et al. Eksp Klin Farmakol. 2004;67(1):3-6. PMID 15079898.

After distal middle cerebral artery occlusion in rats, nooglutyl 10 mg/kg intravenously at occlusion and intraperitoneally for two days limited the affected zone from 22.51 +/- 3.0% of the ipsilateral hemisphere to 7.6 +/- 2.28%, against 9.55 +/- 1.9% for mexidol and 12.8 +/- 1.7% for phenyl-tert-butylnitrone, and improved passive avoidance retrieval. In rats with a posttraumatic intracerebral hematoma, single i.p. doses of 10 and 20 mg/kg 3 to 4 hours after surgery decreased neurological deficit, restored coordination, improved retrieval and prevented loss of animals (PMID 12924225). In rat brain trauma models, nooglutil at 50 mg/kg (and 25 mg/kg in immature rats) protected mitochondrial oxidative phosphorylation and did better than the comparators tested, which included picamilon and pyriditol (PMID 9162289, PMID 9621180), and in a trauma model it showed a moderate antiischemic, antihypoxic and antiamnesic action (PMID 18074799).

Participants / model
Rats
Treatment
Intravenous and intraperitoneal injection
Follow-up
Two days after occlusion in the artery occlusion study; single doses in the hematoma study
Study design
Original preclinical studies
Funding
not stated in the source

All in rats, by injection, from Russian laboratories between 1997 and 2007; no replication outside that network was found, and none reaches a human outcome.

Read the original source
Unsettled mechanism: AMPA binding competition (IC50 6.4 micromolar), D2 receptors, NMDA-mediated slice effects

Animal study

Firstova IuIu et al. Eksp Klin Farmakol. 2011;74(1):6-10. PMID 21476267.

A 2002 abstract calls nooglutil 'a positive modulator of AMPA receptors for glutamate' without giving the basis, and in the same paper 50 mg/kg increased the dissociation constant and density of D2 dopamine receptors in rat striatum while 100 mg/kg abolished the effect, and 70 mg/kg i.p. reduced anxiety in rats in the Vogel conflict test 24 hours after stopping chronic diazepam (PMID 12802448). A radioligand study found nooglutil competes with a selective AMPA receptor agonist for binding sites with an IC50 of 6.4 +/- 0.2 micromolar (noopept 80 +/- 5.6 micromolar) in rat brain, which shows binding competition and not modulation. A 2013 abstract says the antiamnestic effect of nooglutil was caused to a significant degree by activation of non-NMDA receptors, mostly AMPA (PMID 24555225), while hippocampal slice work found high concentrations of nooglutil suppressed CA1 responses through NMDA receptors, an effect blocked by AP7 (PMID 11177255).

Participants / model
Rat brain tissue; rat hippocampal slices; rats
Treatment
Radioligand binding; tissue bath; intraperitoneal in rats
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

The AMPA label is the research group's working description, and the data are indirect or conflicting.

Read the original source
PubMed, 10 October 2026: 27 records from 1990 to 2019, mostly Russian-language, none gives nooglutil to a person

PubMed search record

PubMed search run 10 October 2026: nooglutil[tiab] OR nooglutyl[tiab] OR noogluthyl[tiab] OR ONK-10[tiab] and the chemical name variants, with a follow-up query adding patients, volunteers, clinical, trial, human, humans, toxicity or toxic.

The search returned 27 records dated 1990 to 2019, and abstracts were read for 26 (record 7579248, on an antimotion-sickness effect, has no abstract and was judged by its title). Twenty-three are marked as Russian-language articles, one (7579248) has a bracketed title in a Russian journal, and three are English-language papers in Bulletin of Experimental Biology and Medicine, so the claim that the literature is mainly Russian is accurate. Adding patients, volunteers, clinical, trial, human, humans, toxicity or toxic returned 8 records, all read, and none reports nooglutil given to a person; the matches were reviews, rat studies and a mouse study. No controlled human trial exists in the records reviewed.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished, unindexed or Russian-register material exists.

Read the original source

Studies and sources

PubChem: nooglutyl identity, spellings, and the calcium salt flag

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 147523, (2S)-2-[(5-hydroxypyridine-3-carbonyl)amino]pentanedioic acid (nooglutyl, nooglutil).

Nooglutyl (also nooglutil, noogluthyl, ONK-10) is PubChem CID 147523, C11H12N2O6, 268.22 g/mol, CAS 112193-35-8 (listed among the synonyms), IUPAC name (2S)-2-[(5-hydroxypyridine-3-carbonyl)amino]pentanedioic acid, which is N-(5-hydroxynicotinoyl)-L-glutamic acid. The papers also write it N-(5-oxynicotinoyl)-L-glutamic acid, 'ONC-10' and 'OHK-10'. A 2019 paper tested the calcium salt of the same acid, named 'Ampasse' there, a separate salt form (PMID 31745682). The literature uses nooglutil, nooglutyl and ONK-10 interchangeably, so searches need all of them.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule; free acid and calcium salt
Follow-up
Not applicable
Study design
Chemical database record; original reports
Funding
not stated in the source

Identity record only. No public record ties any vendor material, free acid or salt, to the studied compound.

Read the original source
Founding paper from the originating institute: antiamnestic and antihypoxic, 'low toxic', no doses in the abstract

Animal study

Voronina TA et al. Farmakol Toksikol. 1990;53(4):13-6. PMID 1977613.

In mice and rats ONK-10 had pronounced antiamnestic and antihypoxic effects, did not disturb conditioned reflex activity or orientation behavior, had no anxiolytic or anticonvulsant activity, caused no disorder of movement coordination, and was 'low toxic'; the authors report it was superior in antiamnestic and antihypoxic effects to piracetam, meclofenoxate and demanol aceglumate and not inferior to aniracetam. The abstract gives no doses, no routes and no toxicity figures. A 2003 review from the same school (Voronina TA) lists nooglutyl among drugs created at the Institute of Pharmacology from Zakusov's synaptic ideas, alongside mexidol, noopept and beglimin (PMID 12962041).

Participants / model
Mice and rats
Treatment
Not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study; review
Funding
not stated in the source

'Low toxic' is an unquantified statement. The paper is from the originating institute.

Read the original source
Rodent deficits: electromagnetic exposure, motion sickness, shock, hypoxia, aged SAMP10 mice, strain differences

Animal study

Iasnetsov VV et al. Eksp Klin Farmakol. 1996;59(3):20-3. PMID 8974577.

In operant learning, nooglutil enhanced escape and avoidance responses in a Skinner box where piracetam improved only escape, and neither changed shuttle-box avoidance or water-reward T-maze behavior (PMID 8348043). At 50 mg/kg i.p. nooglutil prevented retrograde amnesia produced by electromagnetic exposure, motion sickness and electroconvulsive shock, and a 2013 rat paper finds marked antiamnestic effects on microwave, acute hypoxia and motion-sickness models (PMID 24555225). In 9-month-old SAMP10 mice, 20 mg/kg improved open field activity, anxiety in the plus maze and passive avoidance retrieval (PMID 18078032). In BALB/c mice, nooglutil improved exploratory behavior in the cross-maze, and in C57BL/6 mice it did not (PMID 23025044). Hypoxia and ischemia models by the same Russian groups reached similar conclusions (PMID 9606516, PMID 11055197).

Participants / model
Rats; mice including SAMP10, BALB/c and C57BL/6
Treatment
Intraperitoneal in some studies, 50 mg/kg in the amnesia models and 20 mg/kg in SAMP10 mice; route not stated in others
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

Every result is an induced or strain-based deficit in rats or mice; none is a healthy-person outcome, and the doses used (20 to 50 mg/kg and up) are not comparable to any human use.

Read the original source
Rat injury models by injection: infarct zone 22.51% to 7.6%, hematoma, trauma, mitochondria

Animal study

Povarova OV et al. Eksp Klin Farmakol. 2004;67(1):3-6. PMID 15079898.

After distal middle cerebral artery occlusion in rats, nooglutyl 10 mg/kg intravenously at occlusion and intraperitoneally for two days limited the affected zone from 22.51 +/- 3.0% of the ipsilateral hemisphere to 7.6 +/- 2.28%, against 9.55 +/- 1.9% for mexidol and 12.8 +/- 1.7% for phenyl-tert-butylnitrone, and improved passive avoidance retrieval. In rats with a posttraumatic intracerebral hematoma, single i.p. doses of 10 and 20 mg/kg 3 to 4 hours after surgery decreased neurological deficit, restored coordination, improved retrieval and prevented loss of animals (PMID 12924225). In rat brain trauma models, nooglutil at 50 mg/kg (and 25 mg/kg in immature rats) protected mitochondrial oxidative phosphorylation and did better than the comparators tested, which included picamilon and pyriditol (PMID 9162289, PMID 9621180), and in a trauma model it showed a moderate antiischemic, antihypoxic and antiamnesic action (PMID 18074799).

Participants / model
Rats
Treatment
Intravenous and intraperitoneal injection
Follow-up
Two days after occlusion in the artery occlusion study; single doses in the hematoma study
Study design
Original preclinical studies
Funding
not stated in the source

All in rats, by injection, from Russian laboratories between 1997 and 2007; no replication outside that network was found, and none reaches a human outcome.

Read the original source
Unsettled mechanism: AMPA binding competition (IC50 6.4 micromolar), D2 receptors, NMDA-mediated slice effects

Animal study

Firstova IuIu et al. Eksp Klin Farmakol. 2011;74(1):6-10. PMID 21476267.

A 2002 abstract calls nooglutil 'a positive modulator of AMPA receptors for glutamate' without giving the basis, and in the same paper 50 mg/kg increased the dissociation constant and density of D2 dopamine receptors in rat striatum while 100 mg/kg abolished the effect, and 70 mg/kg i.p. reduced anxiety in rats in the Vogel conflict test 24 hours after stopping chronic diazepam (PMID 12802448). A radioligand study found nooglutil competes with a selective AMPA receptor agonist for binding sites with an IC50 of 6.4 +/- 0.2 micromolar (noopept 80 +/- 5.6 micromolar) in rat brain, which shows binding competition and not modulation. A 2013 abstract says the antiamnestic effect of nooglutil was caused to a significant degree by activation of non-NMDA receptors, mostly AMPA (PMID 24555225), while hippocampal slice work found high concentrations of nooglutil suppressed CA1 responses through NMDA receptors, an effect blocked by AP7 (PMID 11177255).

Participants / model
Rat brain tissue; rat hippocampal slices; rats
Treatment
Radioligand binding; tissue bath; intraperitoneal in rats
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

The AMPA label is the research group's working description, and the data are indirect or conflicting.

Read the original source
Rat pups and mice: prenatal alcohol and hypoxia, dopamine efflux with opposite effects, calcium salt

Animal study

Kovalev GI et al. Biull Eksp Biol Med. 1993;116(7):56-8. PMID 8400184.

Given to rat pups from day 8 to 20 at 25 mg/kg/day, nooglutyl prevented learning and memory disorders after prenatal alcohol exposure (PMID 1305426) and after intrauterine hypoxia (PMID 8704601). In a dopamine release study of alcohol-exposed pups, nooglutil at 25 mg/kg subcutaneously normalized the reduced dopamine efflux, while its effects in pups of non-alcoholized rats were opposite. The calcium salt at 30 mg/kg showed antidepressant-like activity in the mouse forced swim test and at 0.1 mg/kg alleviated MPTP-induced parkinsonian signs in mice and haloperidol catalepsy in rats (PMID 31745682).

Participants / model
Rat pups; mice; rats
Treatment
Subcutaneous and other routes; calcium salt in the 2019 paper
Follow-up
Day 8 to 20 of life in the pup studies
Study design
Original preclinical studies
Funding
not stated in the source

The two dopamine results suggest the direction of effect depends on the animal's starting state, which is an inference from those two results and not a conclusion stated in the abstract.

Read the original source
Thin pharmacokinetics: one relative bioavailability figure in rabbits, repeated-dose changes in rat progeny

Animal study

Chesnokova EA et al. Eksp Klin Farmakol. 1998;61(4):48-50. PMID 9783110.

In rabbits, one tablet form containing tween-80 had a bioavailability of 104.3% relative to the drug substance, a relative figure that says nothing about absolute oral absorption. In progeny of alcoholized and intact rats, repeated dosing changed plasma levels, clearance, volume of distribution and the main metabolite compared with a single dose (PMID 1786827). No abstract gives half-life, absolute bioavailability, LD50, repeat-dose toxicology, genotoxicity or human pharmacokinetics.

Participants / model
Rabbits; rat progeny
Treatment
Oral tablets in rabbits; route not stated in the rat study; doses not stated in the abstracts
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

A relative figure only. No absolute oral absorption, half-life or toxicology figure is available.

Read the original source
PubMed, 10 October 2026: 27 records from 1990 to 2019, mostly Russian-language, none gives nooglutil to a person

PubMed search record

PubMed search run 10 October 2026: nooglutil[tiab] OR nooglutyl[tiab] OR noogluthyl[tiab] OR ONK-10[tiab] and the chemical name variants, with a follow-up query adding patients, volunteers, clinical, trial, human, humans, toxicity or toxic.

The search returned 27 records dated 1990 to 2019, and abstracts were read for 26 (record 7579248, on an antimotion-sickness effect, has no abstract and was judged by its title). Twenty-three are marked as Russian-language articles, one (7579248) has a bracketed title in a Russian journal, and three are English-language papers in Bulletin of Experimental Biology and Medicine, so the claim that the literature is mainly Russian is accurate. Adding patients, volunteers, clinical, trial, human, humans, toxicity or toxic returned 8 records, all read, and none reports nooglutil given to a person; the matches were reviews, rat studies and a mouse study. No controlled human trial exists in the records reviewed.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished, unindexed or Russian-register material exists.

Read the original source
Label and registry searches, 10 October 2026: no label, no match, no study

Regulatory record

U.S. Food and Drug Administration (DailyMed label search; openFDA Drugs@FDA query) and ClinicalTrials.gov. Searches for nooglutil, nooglutyl, the chemical name and ONK-10 spelling variants, and Ampasse, run 10 October 2026.

ClinicalTrials.gov queries for nooglutil, nooglutyl, the chemical name and ONK-10 spelling variants, and 'Ampasse' returned no studies, DailyMed returned no label under either spelling, and the openFDA Drugs@FDA query returned no match. A web search for the name returned no Russian leaflet or registration entry, which is not proof, and no Russian register was read.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated label, application and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026. It covers United States label, application and registry records and one web search; the Russian state register was not read.

Read the original source

Why is Nooglutyl (nooglutil) in C tier?

C fits a compound with a defined structure, a plausible glutamatergic story and more than two decades of rat and mouse work showing rescue of induced deficits and smaller infarcts, with no harm and no failed trial in the records reviewed. The data are thin: nearly all of it is Russian-language work from one network of laboratories, in rodents and rabbits, with no human exposure, no human pharmacokinetics, no quantified toxicology, no registered study and a mechanism that the abstracts describe three different ways.