Nooglutyl Technical Data Sheet Specification Matrix
| Property / Identifier | Value / Specification |
|---|---|
| Product Name | Nooglutyl (Synonyms: Nooglutil, ONK-10) |
| CAS Number | 112193-35-8 |
| Chemical Formula | C11H12N2O6 |
| Molecular Weight | 268.22 g/mol |
| IUPAC Chemical Name | (2S)-2-[(5-hydroxypyridine-3-carbonyl)amino]pentanedioic acid |
| InChIKey | XFZGYOJFPGPYCS-QMMMGPOBSA-N |
| SMILES Code | C1=C(C=NC=C1O)C(=O)N[C@@H](CCC(=O)O)C(=O)O |
| Appearance | White to off-white crystalline solid powder |
| Purity Standard | ≥ 99.5% (Analytical / Reference Grade) |
Nooglutyl: Glutamatergic Research Compound
Nooglutyl is a high-potency, synthetic glutamatergic reference compound structurally derived from L-glutamic and nicotinic acids. Developed for neuroscience research, it operates primarily as a positive allosteric modulator of AMPA-type glutamate receptors. In laboratory test models, Nooglutyl demonstrates robust neuroprotective, anti-hypoxic, and memory-consolidation properties, making it a primary asset for institutions investigating cognitive impairment, ischemic brain injury recovery, and vestibular system modulation.
In the field of experimental neuroscience, Nooglutyl (N-(5-hydroxynicotinoyl)-L-glutamic acid) stands out as one of the most promising central nervous system agents. Originally synthesized by prominent Russian pharmacological institutions, this compound bridges the gap between classic neurotransmitter analogues and advanced cellular protectants. By targeting glutamate-mediated signaling pathways, Nooglutyl allows researchers to map out structural responses to oxidative stress, mechanical trauma, and chemical amnesia models.
Core Research Mechanisms & Pharmacological Targets
Nooglutyl acts predominantly on the brain’s primary excitatory pathways. Unlike non-selective stimulants, its mechanism relies heavily on modulating AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors. By altering receptor affinity, it increases cellular responsiveness to endogenous glutamate without inducing excitotoxic over-saturation.
A milestone review published in Vestnik Rossiskoi Akademii Meditsinskikh Nauk (PMID: 9889699) highlights Nooglutyl’s multi-modal nature. The peer-reviewed data demonstrates its deep efficacy in reversing memory deficits caused by scopolamine, electroshock, and direct physical trauma, while actively safeguarding fragile neuronal structures from severe ischemic damage.
Nooglutyl vs. Leading Neuroscience Reference Compounds
To assist laboratory teams in optimizing their research outcomes, the table below outlines how Nooglutyl compares structurally and functionally to other core compounds available for acquisition.
| Compound | Primary Pathway / Target | Standout Research Utility |
|---|---|---|
| Noopept | BDNF & NGF Genetic Expression / Cycloprolylglycine Prodrug | Structural neuroplasticity, long-term memory architecture, and cellular repair models. |
| CMS-121 | Fatty Acid Synthase (FASN) Inhibition / Mitochondrial Protection | Geroprotective anti-aging pathways, lipid peroxidation defense, and advanced Alzheimer’s models. |
| PRL-8-53 | Cholinergic Hyper-Potentiation / Hyper-Specific Recall Activation | Short-term verbal retention, immediate cognitive processing, and high-volume acquisition models. |
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Frequently Asked Questions (Research FAQ)
What is the primary chemical definition of Nooglutyl?
Nooglutyl is a synthetic glutamate derivative, chemically identified as N-(5-hydroxynicotinoyl)-L-glutamic acid, primarily studied for its positive allosteric modulation of AMPA receptors.
Is Nooglutyl suitable for human dietary or therapeutic applications?
No. Nooglutyl is strictly classified as a research chemical for laboratory, in vitro, and animal testing use only. It is explicitly not approved for human consumption, medical treatment, or clinical administration.
How does Nooglutyl protect against hypoxic conditions in laboratory models?
Research shows Nooglutyl enhances tissue resilience by stabilizing glutamate signaling pathways during drops in oxygen levels, preventing the accelerated cell death typically caused by ischemic events.
