NoopeptNootropic and neuroprotective agent CAS# 157115-85-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 157115-85-0 | SDF | Download SDF |
PubChem ID | 180496 | Appearance | Powder |
Formula | C17H22N2O4 | M.Wt | 318.37 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | GVS-111; SGS-111; Omberacetam | ||
Solubility | DMSO : ≥ 100 mg/mL (314.10 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | ethyl 2-[[(2S)-1-(2-phenylacetyl)pyrrolidine-2-carbonyl]amino]acetate | ||
SMILES | CCOC(=O)CNC(=O)C1CCCN1C(=O)CC2=CC=CC=C2 | ||
Standard InChIKey | PJNSMUBMSNAEEN-AWEZNQCLSA-N | ||
Standard InChI | InChI=1S/C17H22N2O4/c1-2-23-16(21)12-18-17(22)14-9-6-10-19(14)15(20)11-13-7-4-3-5-8-13/h3-5,7-8,14H,2,6,9-12H2,1H3,(H,18,22)/t14-/m0/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Noopept (GVS-111) is a medication promoted and prescribed in Russia and neighbouring countries as a nootropic.
IC50 Value:
Target:
in vitro: Nooglutil exhibits pharmacologically significant competition with a selective agonist of AMPA receptors ([G-3H]Ro 48-8587) for the receptor binding sites (with IC50 = 6.4 +/- 0.2 microM), while the competition of noopept for these receptor binding sites was lower by an order of magnitude (IC50 = 80 +/- 5.6 microM) [1]. GVS-111 significantly increased neuronal survival after H(2)O(2)-treatment displaying a dose-dependent neuroprotective activity from 10 nM to 100 microM, and an IC(50) value of 1.21+/-0.07 microM. GVS-111 inhibited the accumulation of intracellular free radicals and lipid peroxidation damage in neurons treated with H(2)O(2) or FeSO(4), suggesting an antioxidant mechanism of action [2].
in vivo: N-Phenylacetyl-L-prolylglycine ethyl ester (GVS-111) administered intravenously at a dose of 0.5 mg/kg/day, for the first time 1 h after ischaemic lesion and then for 9 post-operative days, with the last administration 15 min before testing, attenuated the deficit [3]. GVS-111 itself was not found in rat brain 1 h after 5 mg/kg i.p. administration up to limit of detection (LOD) under high performance liquid chromatography (HPLC) conditions [4]. The most pronounced antiinflammatory effect of dipeptide was observed on the model of adjuvant arthritis in rats, where the drug administered over 25 days in a daily dose of 0.5 mg/kg (i.m.) or 5 mg/kg (p.o.) significantly reduced the chronic immune inflammation (on the 12th day, by 94.0 and 74.1%, respectively) [5].
Toxicity: Noopept administered in this dose range induced no irreversible pathologic changes in the organs and systems studied and exhibited no allergenic, immunotoxic, and mutagen activity [6].
Clinical trial: Discontinued References: |
Noopept Dilution Calculator
Noopept Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.141 mL | 15.705 mL | 31.41 mL | 62.82 mL | 78.525 mL |
5 mM | 0.6282 mL | 3.141 mL | 6.282 mL | 12.564 mL | 15.705 mL |
10 mM | 0.3141 mL | 1.5705 mL | 3.141 mL | 6.282 mL | 7.8525 mL |
50 mM | 0.0628 mL | 0.3141 mL | 0.6282 mL | 1.2564 mL | 1.5705 mL |
100 mM | 0.0314 mL | 0.157 mL | 0.3141 mL | 0.6282 mL | 0.7852 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Description: IC50 Value: N/A Noopept (GVS-111) is a medication promoted and prescribed in Russia and neighbouring countries as a nootropic. in vitro: Nooglutil exhibits pharmacologically significant competition with a selective agonist of AMPA receptors ([G-3H]Ro 48-8587) for the receptor binding sites (with IC50 = 6.4 +/- 0.2 microM), while the competition of noopept for these receptor binding sites was lower by an order of magnitude (IC50 = 80 +/- 5.6 microM) [1]. GVS-111 significantly increased neuronal survival after H(2)O(2)-treatment displaying a dose-dependent neuroprotective activity from 10 nM to 100 microM, and an IC(50) value of 1.21+/-0.07 microM. GVS-111 inhibited the accumulation of intracellular free radicals and lipid peroxidation damage in neurons treated with H(2)O(2) or FeSO(4), suggesting an antioxidant mechanism of action [2]. in vivo: N-Phenylacetyl-L-prolylglycine ethyl ester (GVS-111) administered intravenously at a dose of 0.5 mg/kg/day, for the first time 1 h after ischaemic lesion and then for 9 post-operative days, with the last administration 15 min before testing, attenuated the deficit [3]. GVS-111 itself was not found in rat brain 1 h after 5 mg/kg i.p. administration up to limit of detection (LOD) under high performance liquid chromatography (HPLC) conditions [4]. The most pronounced antiinflammatory effect of dipeptide was observed on the model of adjuvant arthritis in rats, where the drug administered over 25 days in a daily dose of 0.5 mg/kg (i.m.) or 5 mg/kg (p.o.) significantly reduced the chronic immune inflammation (on the 12th day, by 94.0 and 74.1%, respectively) [5]. Toxicity: Noopept administered in this dose range induced no irreversible pathologic changes in the organs and systems studied and exhibited no allergenic, immunotoxic, and mutagen activity [6]. Clinical trial: Discontinued
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Neuroprotective effect of novel cognitive enhancer noopept on AD-related cellular model involves the attenuation of apoptosis and tau hyperphosphorylation.[Pubmed:25096780]
J Biomed Sci. 2014 Aug 6;21:74.
BACKGROUND: Noopept (N-phenyl-acetyl-L-prolylglycine ethyl ester) was constructed as a dipeptide analog of the standard cognition enhancer, piracetam. Our previous experiments have demonstrated the cognition restoring effect of Noopept in several animal models of Alzheimer disease (AD). Noopept was also shown to prevent ionic disbalance, excitotoxicity, free radicals and pro-inflammatory cytokines accumulation, and neurotrophine deficit typical for different kinds of brain damages, including AD. In this study, we investigated the neuroprotective action of Noopept on cellular model of AD, Abeta 25-35-induced toxicity in PC12 cells and revealed the underlying mechanisms. RESULTS: The neuroprotective effect of Noopept (added to the medium at 10 muM concentration, 72 hours before capital A, Cyrillicbeta 25-35) was studied on capital A, Cyrillicbeta 25-35-induced injury (5 muM for 24 h) in PC12 cells. The ability of drug to protect the impairments of cell viability, calcium homeostasis, ROS level, mitochondrial function, tau phosphorylation and neurite outgrowth caused by capital A, Cyrillicbeta 25-35 were evaluated. Following the exposure of PC12 cells to capital A, Cyrillicbeta 25-35 an increase of the level of ROS, intracellular calcium, and tau phosphorylation at Ser396 were observed; these changes were accompanied by a decrease in cell viability and an increase of apoptosis. Noopept treatment before the amyloid-beta exposure improved PC12 cells viability, reduced the number of early and late apoptotic cells, the levels of intracellular reactive oxygen species and calcium and enhanced the mitochondrial membrane potential. In addition, pretreatment of PC12 cell with Noopept significantly attenuated tau hyperphosphorylation at Ser396 and ameliorated the alterations of neurite outgrowth evoked by capital A, Cyrillicbeta25-35. CONCLUSIONS: Taken together, these data provide evidence that novel cognitive enhancer Noopept protects PC12 cell against deleterious actions of Abeta through inhibiting the oxidative damage and calcium overload as well as suppressing the mitochondrial apoptotic pathway. Moreover, neuroprotective properties of Noopept likely include its ability to decrease tau phosphorylation and to restore the altered morphology of PC12 cells. Therefore, this nootropic dipeptide is able to positively affect not only common pathogenic pathways but also disease-specific mechanisms underlying Abeta-related pathology.
Molecular Mechanism Underlying the Action of Substituted Pro-Gly Dipeptide Noopept.[Pubmed:27099787]
Acta Naturae. 2016 Jan-Mar;8(1):82-9.
This study was performed in order to reveal the effect of Noopept (ethyl ester of N-phenylacetyl-Lprolylglycine, GVS-111) on the DNA-binding activity of transcriptional factors (TF) in HEK293 cells transiently transfected with luciferase reporter constructs containing sequences for CREB, NFAT, NF-kappaB, p53, STAT1, GAS, VDR, HSF1, and HIF-1. Noopept (10 muM) was shown to increase the DNA-binding activity of HIF-1 only, while lacking the ability to affect that of CREB, NFAT, NF-kappaB, p53, STAT1, GAS, VDR, and HSF1. Noopept provoked an additional increase in the DNA-binding activity of HIF-1 when applied in conditions of CoCl2-induced HIF- 1 stabilization. The degree of this HIF-positive effect of Noopept was shown to be concentration-dependent. Piracetam (1 mM) failed to affect significantly any of the TF under study. The results of molecular docking showed that Noopept (L-isomer), as well as its metabolite, L-isomer of N-phenyl-acetylprolyl, unlike its pharmacologically ineffective D-isomer, is able to bind to the active site of prolyl hydroxylase 2. Taking into account the important role of the genes activated by HIF-1 in the formation of an adaptive response to hypoxia, data on the ability of Noopept to provoke a selective increase in the DNA-binding activity of HIF-1 explain the wide spectrum of neurochemical and pharmacological effects of Noopept revealed before. The obtained data allow one to propose the HIF-positive effect as the primary mechanism of the activity of this Pro-Gly-containing dipeptide.
Nootropic dipeptide noopept enhances inhibitory synaptic transmission in the hippocampus.[Pubmed:25573367]
Bull Exp Biol Med. 2015 Jan;158(3):349-51.
Application of nootropic agent Noopept on hippocampal slices from Wistar rats enhanced the inhibitory component of total current induced by stimulation of Shaffer collaterals in CA1 pyramidal neurons, but did not affect the excitatory component. A direct correlation between the increase in the amplitude of inhibitory current and agent concentration was found. The substance did not affect the release of inhibitory transmitters from terminals in the pyramidal neurons, which indicated changes in GABAergic interneurons.
Dipeptide Piracetam Analogue Noopept Improves Viability of Hippocampal HT-22 Neurons in the Glutamate Toxicity Model.[Pubmed:27265136]
Bull Exp Biol Med. 2016 May;161(1):58-60.
Effect of Noopept (N-phenylacetyl-prolylglycine ethyl ester) on viability of neurons exposed to neurotoxic action of glutamic acid (5 mM) was studied in vitro in immortalized mouse hippocampal HT-22 neurons. Noopept added to the medium before or after glutamic acid improved neuronal survival in a concentration range of 10-11-10-5 M. Comparison of the effective Noopept concentrations determined in previous studies on cultured cortical and cerebellar neurons showed that hippocampal neurons are more sensitive to the protective effect of Noopept.