Nooglutyl

Nooglutyl, also spelled nooglutil and known by the code ONK-10, is a nootropic developed at the Zakusov Institute of Pharmacology (formerly the Institute of Pharmacology of the Russian Academy of Medical Sciences) in Moscow, the research center associated with Noopept and Semax. Chemically it is a nicotinoyl-glutamic acid derivative, described as N-(5-hydroxynicotinoyl)-L-glutamic acid, which places it structurally alongside other nicotinoyl-amino acid conjugates ^[2][3].

Its principal pharmacological identity is that of a positive modulator of AMPA-subtype glutamate receptors, the receptors that mediate fast excitatory neurotransmission and are central to memory encoding and synaptic plasticity ^[2]. Comparative animal studies of nootropic agents attributed nooglutyl's anti-amnesic action largely to activation of non-NMDA (chiefly AMPA) receptors for excitatory amino acids, distinguishing its mechanism from agents that work through GABA-A or other systems ^[1].

The preclinical literature emphasizes both memory enhancement and neuroprotection. Nooglutyl produced marked anti-amnesic effects across several distinct models of amnesia, including deficits induced by microwave irradiation, acute hypoxia, and motion sickness ^[1], and it corrected cognitive disturbances in rats subjected to intrauterine hypoxia ^[4]. It also showed pronounced neuroprotective activity in a model of hemorrhagic stroke, reducing neurological deficit and preventing loss of animals when given after injury ^[5]. Additional work characterized its anti-motion-sickness effect and its neuronal basis ^[6], and its favorable oral pharmacokinetics; a tableted formulation achieved essentially complete bioavailability relative to the pure substance in rabbits ^[7].

Nooglutyl is a research compound rather than an approved medication and is not widely available commercially. Its body of evidence is largely preclinical and originates from a single Russian research network, which places it among the more exploratory, frontier nootropics aimed specifically at memory and neuroprotection.

MEASURED ADVERSE EFFECTS (calcium salt, intravenous, only). In the 124-patient phase III trial adverse events occurred in 14.52% on drug versus 8.06% on placebo, a non-significant difference (p=0.395), with no dropouts (PMID 34184474). The approved Russian label lists dizziness in 0.8% and mild drowsiness in 0.8%, plus possible allergic reactions to components. Label contraindications: hypersensitivity, pregnancy, breastfeeding, age under 18, and renal or hepatic impairment.

SEIZURE SIGNAL, the one real mechanistic red flag. The calcium salt at 10 mM in rat hippocampal slices provoked epileptiform activity, blocked by the NMDA antagonist MK-801 (PMID 29797131); high-concentration nooglutil separately suppressed CA1 responses through an AP7-sensitive NMDA-dependent mechanism (PMID 11177255). These are in vitro concentrations far above the therapeutic range, and no seizures were reported in any human study, but potentiating AMPA receptors carries a recognised theoretical convulsant risk and this is the only ceiling evidence that exists. It matters most for anyone self-dosing an oral powder for which no human ceiling has ever been established.

REPRODUCTIVE. The calcium salt at 6.7 mg/kg in rats, stated as 10 times the maximum human therapeutic dose, did not affect reproductive function and was not embryotoxic or teratogenic (PMID 22550856). Only a 10-fold margin was tested, and the label still contraindicates pregnancy.

UNKNOWN. No drug interaction studies of any kind exist. No human overdose data. No safety data beyond 15-day courses. No published carcinogenicity or genotoxicity. Total human exposure across the entire published record is roughly 650 patients, all Russian, all intravenous, all short-course, essentially all with developer involvement. Nothing is known about oral free-acid safety in humans.

REGULATORY. Nooglutyl free acid: never approved by any regulator, anywhere, in 36 years. Not scheduled under the US Controlled Substances Act, not FDA-approved, and not a lawful dietary supplement ingredient (no NDI notification, no pre-DSHEA status); it is sold as a research chemical. Nooglutyl calcium is approved in Russia as Ampasse, prescription-only IV solution 5 mg/mL, registration ЛП-006394 (2020), current registration ЛП-№(002862)-(РГ-RU) 2023, marketing authorisation holder OOO TAVITA, manufactured by OOO Ellara, indicated for chronic cerebrovascular insufficiency. It has no FDA, EMA or MHRA approval.

WADA. Not named on the Prohibited List, and there is no ampakine or AMPA-modulator category on it. The live question is the S0 non-approved-substances catch-all, which prohibits at all times any substance "with no current approval by any governmental regulatory health authority for human therapeutic use." Russian approval of the calcium salt arguably lifts that salt out of S0, while the free acid sold as Nooglutyl powder has no approval anywhere and would sit squarely in S0. This is genuinely unsettled; a tested athlete should obtain a ruling rather than assume either reading.

Nooglutyl, chemically N-(5-hydroxynicotinoyl)-L-glutamic acid, was developed at the Zakusov Research Institute of Pharmacology in Moscow, the same laboratory associated with Noopept and Semax. It was investigated principally during the 1990s and 2000s as a memory-oriented nootropic and neuroprotective agent, with radioligand studies identifying it as a positive modulator of AMPA-subtype glutamate receptors. Its documented characterization rests almost entirely on Russian preclinical research in rodent models of amnesia and cerebral ischemia. It has not undergone the large controlled human trials required for regulatory approval, and it remains an investigational compound.

Nooglutyl is discussed within nootropic circles as an intriguing, mechanistically direct ampakine, valued for engaging the AMPA-receptor signaling that underlies learning and synaptic plasticity comparatively directly. Its appeal rests on a consistent record of anti-amnesic and neuroprotective effects across diverse rodent models, including amnesia induced by hypoxia, electroconvulsive shock, and cerebral trauma, and on reports of benefit in senescence-accelerated mice. Enthusiasts are drawn to this combination of memory-encoding support and antihypoxic protection. Honesty requires noting that essentially all of this evidence is preclinical, and much of it published in Russian, with little independent human data. Reported subjective effects, where described, are modest and centered on cognitive sharpening.