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Purity: ≥98%
| Targets |
NMDA receptor subunit 2A (NR2A) - No specific IC50/Ki/EC50 provided in this paper; the compound is described as an inhibitor of NR2A. [1]
PEAQX targets the N-methyl-D-aspartate (NMDA) receptor, an ionotropic glutamate receptor that plays a critical role in synaptic plasticity, learning, and memory. It acts as a competitive antagonist, binding to the glutamate binding site and blocking the receptor's activation. It has a preference for NMDA receptors containing the NR2A subunit over those containing NR2B. |
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| ln Vitro |
Inhibition of Src and NR2A with PP2 and NVP-AAM077 respectively not only down-regulated the levels of p-Src and p-NR2A, but also ameliorated hippocampal neurons apoptosis and long-term cognitive impairment after HIR
In vitro, PEAQX is a potent NMDA receptor antagonist with an IC₅₀ of 270 nM for hNMDR 1A/2A and 29.6 μM for hNMDR 1A/2B. It shows a 15-fold preference for the 1A/2A over 1A/2B subtype. It is a competitive antagonist, inhibiting glutamate-induced calcium influx and neuronal excitation. |
| ln Vivo |
In young C57BL/6 mice subjected to 70% hepatic ischemia reperfusion (HIR), pre-treatment with PEAQX (10 mg/kg i.p. daily for 3 days before surgery) significantly decreased the tyrosine phosphorylation of NR2A (p-NR2A) and Src (p-Src) in the hippocampus at 3 days after reperfusion compared to the HIR group (P < 0.05). [1]
PEAQX pre-treatment also decreased the interactions between Src and NR2A, as well as between Src and PSD95, as measured by immunoprecipitation at 3 days after HIR (P < 0.05). [1] PEAQX pre-treatment attenuated hippocampal neuron apoptosis (decreased apoptosis index by TUNEL staining) and reduced cleaved caspase-3 expression in the hippocampus at 3 days after HIR (P < 0.05). [1] In Morris water maze tests performed 1 month after HIR, PEAQX pre-treatment significantly increased the percentage of time spent in the target quadrant during probe trials compared to the HIR group (P < 0.05), indicating improvement of long-term cognitive impairment. [1] PEAQX pre-treatment did not affect serum levels of ALT, AST, TNF-α, IFN-γ, or IL-6 at 3 days after HIR, nor did it affect liver function or inflammatory cytokine levels at 1 month after HIR. [1] In sham-operated mice, PEAQX pre-treatment (10 mg/kg i.p. for 3 days) did not significantly alter the levels of p-Src, p-NR2A, c-Src, or NR2A in the hippocampus compared to vehicle-treated sham mice. [1] In vivo, PEAQX is orally active and has been shown to be a potent anticonvulsant in animal tests. It has potential therapeutic applications in conditions involving excessive NMDA receptor activity, such as epilepsy, neuropathic pain, and neurodegenerative diseases. However, specific in vivo efficacy data in animal models are not extensively detailed in the available literature. |
| Enzyme Assay |
In vitro NMDA receptor binding assays for PEAQX are performed using membrane preparations from cells expressing recombinant NMDA receptor subunits (e.g., NR1/NR2A or NR1/NR2B). Radioligand binding studies employ [³H]-MK-801 or [³H]-glutamate as tracers. Membranes are incubated with varying concentrations of PEAQX, and bound and free ligands are separated by filtration. IC₅₀ or Kᵢ values are calculated from competition binding curves.
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| Cell Assay |
In vitro cell-based assays for PEAQX are performed using cells expressing recombinant NMDA receptors. Cells are cultured in appropriate media and treated with PEAQX at various concentrations. Receptor activation is assessed by measuring calcium influx using fluorescent indicators (e.g., Fluo-4) in response to glutamate or NMDA stimulation. IC₅₀ values are calculated from dose-response curves.
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| Animal Protocol |
Animal model: 2-week-old C57BL/6 mice (weight 4-6 g) were subjected to 70% hepatic ischemia reperfusion (HIR) by clamping the left hepatic artery and portal vein for 1 hour, followed by reperfusion. Sham-operated mice underwent vessel isolation without clamping. PEAQX (NVP-AAM077) was dissolved in DMSO and diluted with sterile saline. Mice in the NVP group received intraperitoneal injections of PEAQX at a dose of 10 mg/kg once daily for 3 days before the HIR surgery. The sham(NVP) group received the same pre-treatment before sham operation. [1]
For assessment of short-term effects, mice were killed 3 days after reperfusion; for long-term cognitive assessment, Morris water maze tests were performed 1 month after HIR. [1] In vivo animal studies for PEAQX are conducted in rodent models of epilepsy, such as the maximal electroshock seizure (MES) test or pentylenetetrazol (PTZ) seizure test. The compound is administered orally or intraperitoneally, and the latency to seizure onset or the percentage of animals protected from seizures is measured. |
| ADME/Pharmacokinetics |
Specific pharmacokinetic properties of PEAQX, such as half-life and oral bioavailability, are not extensively detailed in the available literature. It is described as being orally active. As a small molecule with a molecular weight of 454.21 g/mol, it is expected to have good oral bioavailability and brain penetration. It is soluble in DMSO.
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| Toxicity/Toxicokinetics |
Comprehensive toxicological data for PEAQX are not widely available in public literature. As a research compound, it is intended for laboratory use only and is not for human therapeutic use. Standard safety precautions should be followed when handling this compound. The compound is supplied with a purity of ≥98%.
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| References | |
| Additional Infomation |
PEAQX (NVP-AAM077) is a selective antagonist of the NMDA receptor subunit 2A (NR2A). In this study, it was used to demonstrate that HIR-induced hippocampal injury and long-term cognitive impairment are mediated via the Src-PSD95-NR2A signaling pathway. Pre-treatment with PEAQX inhibited the tyrosine phosphorylation of NR2A and Src, reduced interactions among Src, PSD95 and NR2A, attenuated hippocampal neuron apoptosis, and improved long-term memory recall without affecting liver function or systemic inflammation. The results suggest that NR2A is a potential therapeutic target for preventing cognitive deficits after pediatric liver transplantation. [1]
PEAQX is a potent, orally active, and competitive NMDA receptor antagonist. It is also known as NVP-AAM077. It has a preference for the NMDA 1A/2A subunit over 1A/2B, with IC₅₀ values of 270 nM and 29.6 μM, respectively. It is a potent anticonvulsant. This product is for research use only. |
| Molecular Formula |
C17H15BRN3NA4O6P
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|---|---|
| Molecular Weight |
560.1543
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| Exact Mass |
453.008
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| CAS # |
459836-30-7
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| Related CAS # |
PEAQX tetrasodium hydrate
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| PubChem CID |
9868551
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| Appearance |
Typically exists as solid at room temperature
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| Density |
1.6±0.1 g/cm3
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| Index of Refraction |
1.647
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| LogP |
0.8
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| Hydrogen Bond Donor Count |
5
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
27
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| Complexity |
622
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| Defined Atom Stereocenter Count |
1
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| SMILES |
BrC1C([H])=C([H])C(=C([H])C=1[H])[C@]([H])(C([H])([H])[H])N([H])C([H])(C1C([H])=C([H])C([H])=C2C=1N=C(C(=N2)[O-])[O-])P(=O)([O-])[O-].[Na+].[Na+].[Na+].[Na+].O([H])[H]
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| InChi Key |
SMGAGBKXHAHCGQ-VSYRWHDMSA-J
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| InChi Code |
InChI=1S/C17H17BrN3O5P.4Na.H2O/c1-9(10-5-7-11(18)8-6-10)19-17(27(24,25)26)12-3-2-4-13-14(12)21-16(23)15(22)20-13;;;;;/h2-9,17,19H,1H3,(H,20,22)(H,21,23)(H2,24,25,26);;;;;1H2/q;4*+1;/p-4/t9-,17?;;;;;/m0...../s1
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| Chemical Name |
sodium ((((S)-1-(4-bromophenyl)ethyl)amino)(2,3-dioxidoquinoxalin-5-yl)methyl)phosphonate hydrate .
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| Synonyms |
NVP-AAM077; NVP-AAM 077; NVP AAM 077; NVP-AAM-077; AAM-077; AAM077; AAM 077
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.7852 mL | 8.9262 mL | 17.8524 mL | |
| 5 mM | 0.3570 mL | 1.7852 mL | 3.5705 mL | |
| 10 mM | 0.1785 mL | 0.8926 mL | 1.7852 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Products are for research use only; We do not sell to patients
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