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Noopept 20mg – 60 capsules

Noopept 20 mg — 60 oral research capsules. Noopept (N-phenylacetyl-L-prolylglycine ethyl ester, GVS-111) is the most extensively characterized member of the second-g...

Noopept 20mg – 60 capsules Product Information

Noopept 20 mg — 60 oral research capsules. Noopept (N-phenylacetyl-L-prolylglycine ethyl ester, GVS-111) is the most extensively characterized member of the second-generation racetam-derived nootropic class. Originally developed and clinically registered in the Russian Federation, it is roughly 1,000-fold more potent on a per-milligram basis than the parent compound piracetam, with documented activity at concentrations as low as 10 nM. Its proximal active metabolite — cycloprolylglycine (CPG) — is itself a naturally occurring endogenous neuropeptide, a property unique among synthetic nootropics. The 20 mg per-capsule dose mirrors the standard clinical-research range used in published Russian-language clinical pharmacology. RESEARCH USE ONLY  ·  Not for human or veterinary use. For laboratory and collector purposes only. Purity ≥ 99 % (HPLC) — third-party tested, CoA on file Form Research capsules Content 20 mg Noopept per capsule Total 60 capsules per bottle (1.2 g total) Packaging Sealed bottle with tamper-evident closure Storage Room temperature, dry, protected from light Molecular formula C₁₇H₂₂N₂O₄ Molecular weight ≈ 318.37 g·mol⁻¹ IUPAC name Ethyl 2-{[(2S)-1-(2-phenylacetyl)pyrrolidin-2-yl]carbonylamino}acetate CAS number 157115-85-0 Synonyms GVS-111; N-phenylacetyl-L-prolylglycine ethyl ester; Omberacetam Research Overview Noopept is a peptide-derived nootropic that crosses the blood–brain barrier rapidly after oral administration and is hydrolyzed to its endogenous active metabolite cycloprolylglycine (CPG), which is itself a naturally occurring brain neuropeptide [1,2]. In rodent models, Noopept reliably enhances performance in passive-avoidance, conditioned-fear and spatial-memory paradigms across a remarkably wide dose range, with documented effects on hippocampal LTP, NGF and BDNF expression, and cholinergic, glutamatergic and α-adrenergic signaling tone [1,2]. Russian-language clinical literature reports cognitive-improvement effects in mild cognitive impairment of vascular and post-traumatic origin, with the molecule registered for clinical use in the Russian Federation under the name Noopept since 2002 [3]. Across the published preclinical record, Noopept exhibits anxiolytic, neuroprotective and antioxidant activity in addition to its core nootropic phenotype, and is widely used as a tool compound in mechanistic studies of CPG-mediated neuropeptide signaling. Primary Research Areas Memory and learning research — consistent enhancement of acquisition, consolidation and retrieval in rodent paradigms; one of the most pharmacologically robust pro-cognitive tool compounds available [1]. BDNF / NGF and neurotrophic signaling — documented upregulation of brain neurotrophin expression, of interest in research on neuroplasticity and cognitive resilience [2]. Hippocampal LTP and synaptic plasticity — facilitates LTP induction and maintenance — the cellular substrate of declarative-memory consolidation [1,2]. Neuroprotection and ischemia models — evaluated in cerebral ischemia, hypoxic injury and neurodegeneration paradigms with reproducible protective signals [2,3]. Anxiolytic and stress-response research — probed in elevated-plus-maze, forced-swim and chronic-stress paradigms; the anxiolytic phenotype is dissociable from the cognitive phenotype [3]. References Ostrovskaya RU, Gudasheva TA, Zaplina AP, et al. Noopept stimulates the expression of NGF and BDNF in rat hippocampus. Bull Exp Biol Med. 2008;146(3):334–337. Ostrovskaya RU, Belnik AP, Storozheva ZI. Noopept efficiency in experimental Alzheimer disease (cognitive deficiency caused by β-amyloid 25–35 injection into Meynert basal nuclei of rats). Bull Exp Biol Med. 2008;146(1):77–80. Neznamov GG, Teleshova ES. Comparative studies of Noopept and piracetam in the treatment of patients with mild cognitive disorders in organic brain diseases of vascular and traumatic origin. Neurosci Behav Physiol. 2009;39(3):311–321.