Gavestinel

CAS# 153436-38-5

Gavestinel

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Chemical structure

Gavestinel

3D structure

Chemical Properties of Gavestinel

Cas No. 153436-38-5 SDF Download SDF
PubChem ID 16759177 Appearance Powder
Formula C18H11Cl2N2O3Na M.Wt 397.19
Type of Compound N/A Storage Desiccate at -20°C
Synonyms GV 150526A
Solubility Soluble to 40 mM in DMSO
Chemical Name sodium;3-[(E)-3-anilino-3-oxoprop-1-enyl]-4,6-dichloro-1H-indole-2-carboxylate
SMILES C1=CC=C(C=C1)NC(=O)C=CC2=C(NC3=CC(=CC(=C32)Cl)Cl)C(=O)[O-].[Na+]
Standard InChIKey GRSDSTMFQHAESM-UHDJGPCESA-M
Standard InChI InChI=1S/C18H12Cl2N2O3.Na/c19-10-8-13(20)16-12(17(18(24)25)22-14(16)9-10)6-7-15(23)21-11-4-2-1-3-5-11;/h1-9,22H,(H,21,23)(H,24,25);/q;+1/p-1/b7-6+;
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.
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.
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.

Biological Activity of Gavestinel

DescriptionHighly potent and selective non-competitive antagonist acting at the strychnine-insensitive glycine binding site of the NMDA receptor-channel complex (Kd = 0.8 nM). Displays > 1000-fold selectivity over NMDA, AMPA and kainate binding sites. Orally bioavailable and active in vivo.

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Preparing Stock Solutions of Gavestinel

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.5177 mL 12.5884 mL 25.1769 mL 50.3537 mL 62.9422 mL
5 mM 0.5035 mL 2.5177 mL 5.0354 mL 10.0707 mL 12.5884 mL
10 mM 0.2518 mL 1.2588 mL 2.5177 mL 5.0354 mL 6.2942 mL
50 mM 0.0504 mL 0.2518 mL 0.5035 mL 1.0071 mL 1.2588 mL
100 mM 0.0252 mL 0.1259 mL 0.2518 mL 0.5035 mL 0.6294 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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References on Gavestinel

The selective glycine antagonist gavestinel lacks phencyclidine-like behavioral effects.[Pubmed:12409996]

Behav Pharmacol. 2002 Nov;13(7):583-92.

Gavestinel [GV150526A; ( E)-3[(phenylcarbamoil)ethenyl]-4,6-dichloroindole-2-carboxylic acid sodium salt] is a selective antagonist at the strychnine-insensitive glycine site of the -methyl-D-aspartate (NMDA) receptor. It was tested for its ability to substitute for phencyclidine (PCP) in rats and rhesus monkeys trained to discriminate PCP from saline, under a two-lever fixed-ratio (FR) food reinforcement schedule, and for its ability to maintain responding in rhesus monkeys trained to self-administer PCP under a FR reinforcement schedule. No PCP-lever responding was observed after Gavestinel (1-56 mg/kg i.p.) administration to rats discriminating PCP (2.0 mg/kg i.p.) from saline. The highest dose of Gavestinel (100 mg/kg i.p.) tested eliminated responding. Likewise, no PCP-lever responding was observed after Gavestinel (1-30 mg/kg s.c.) administration to rhesus monkeys discriminating PCP (0.08 or 0.1 mg/kg i.m.) from saline; the highest dose of Gavestinel (30 mg/kg s.c.) tested reduced response rates to approximately 50% of those observed after its vehicle ( -cyclodextrin in 0.9% saline). Gavestinel (0.1-1 mg/kg per i.v. infusion) was not self-administered by rhesus monkeys that reliably self-administered PCP (0.0056 or 0.01 mg/kg per i.v. infusion). Infusion rates at the highest dose were typically lower than those for vehicle or saline, suggesting behavioral activity. Together, these results suggest that at behaviorally active doses Gavestinel is not PCP-like and is likely to have low abuse liability.

How a sequential design would have affected the GAIN International Study of gavestinel in stroke.[Pubmed:14707409]

Cerebrovasc Dis. 2004;17(2-3):111-7.

While planning the GAIN International Study of Gavestinel in acute stroke, a sequential triangular test was proposed but not implemented. Before the trial commenced it was agreed to evaluate the sequential design retrospectively to evaluate the differences in the resulting analyses, trial durations and sample sizes in order to assess the potential of sequential procedures for future stroke trials. This paper presents four sequential reconstructions of the GAIN study made under various scenarios. For the data as observed, the sequential design would have reduced the trial sample size by 234 patients and shortened its duration by 3 or 4 months. Had the study not achieved a recruitment rate that far exceeded expectation, the advantages of the sequential design would have been much greater. Sequential designs appear to be an attractive option for trials in stroke.

Gavestinel does not improve outcome after acute intracerebral hemorrhage: an analysis from the GAIN International and GAIN Americas studies.[Pubmed:15831831]

Stroke. 2005 May;36(5):1006-10.

BACKGROUND AND PURPOSE: Glycine Antagonist in Neuroprotection (GAIN) International and GAIN Americas trials were prospectively designed, randomized, placebo-controlled trials of Gavestinel, a glycine-site antagonist and putative neuroprotectant drug administered within 6 hours of suspected ischemic or hemorrhagic stroke. Both trials reported that Gavestinel was ineffective in ischemic stroke. This analysis reports the results in those with primary intracerebral hemorrhage. METHODS: The primary hypothesis was that Gavestinel treatment did not alter outcome, measured at 3 months by the Barthel Index (BI), from acute intracerebral hemorrhage, based on pooled results from both trials. The BI scores were divided into 3 groups: 95 to 100 (independent), 60 to 90 (assisted independence), and 0 to 55 (dependent) or dead. RESULTS: In total, 3450 patients were randomized in GAIN International (N=1804) and GAIN Americas (N=1646). Of these, 571 were ultimately identified to have spontaneous intracerebral hematoma on baseline head computerized tomography scan. The difference in distribution of trichotomized BI scores at 3 months between Gavestinel and placebo was not statistically significant (P=0.09). Serious adverse events were reported at similar rates in the 2 treatment groups. CONCLUSIONS: These observations from the combined GAIN International and GAIN Americas trials suggest that Gavestinel is not of substantial benefit or harm to patients with primary intracerebral hemorrhage. These findings are similar to results previously reported in patients with ischemic stroke.

Effect of the Glycine Antagonist Gavestinel on cerebral infarcts in acute stroke patients, a randomized placebo-controlled trial: The GAIN MRI Substudy.[Pubmed:16340185]

Cerebrovasc Dis. 2006;21(1-2):106-11.

BACKGROUND AND PURPOSE: Gavestinel, GV150526, is a selective antagonist at the glycine site of the N-methyl-D-aspartate receptor. The safety and efficacy of GV150526 were studied in two phase III randomized placebo-controlled clinical trials of acute ischemic stroke patients within 6 h from onset [The Glycine Antagonist in Neuroprotection (GAIN) International and GAIN Americas Trials]. A planned MRI substudy within these trials investigated the effect of Gavestinel on infarct volume. METHODS: Patients enrolled in the GAIN trials at designated MRI substudy sites were eligible if they had a pretreatment acute cortical lesion on diffusion-weighted MRI of at least 1.5 cm diameter or 5 cm(3). Final lesion assessment was performed on T(2)-weighted MRI at month 3. Blinded image analysis was performed centrally. The primary hypothesis was that Gavestinel would attenuate lesion growth from baseline relative to placebo. RESULTS: A total of 106 patients were eligible, 75 (34 Gavestinel, 41 placebo) of whom had month 3 scans (primary analysis population). No effects of Gavestinel on infarct volume were observed in the primary or other analyses. However, significant associations of lesion volume to clinical severity and outcomes were observed. Ischemic lesion volume decrease was predictive of substantial clinical improvement. CONCLUSION: Consistent with the clinical outcomes in the GAIN trials, no effects of Gavestinel on ischemic infarction was observed. Concordance of results of the clinical outcome trials with those of this infarct volume substudy as well the associations of infarct volume to clinical outcomes further support the potential role of infarct volume as a marker of outcome in dose finding and proof of principle acute stroke trials.

Pharmacokinetics, metabolism and excretion of the glycine antagonist GV150526A in rat and dog.[Pubmed:12745876]

Xenobiotica. 2003 Apr;33(4):415-28.

1. The pharmacokinetics, metabolic fate and excretion of 3-[-2(phenylcarbamoyl) ethenyl-4,6-dichloroindole-2-carboxylic acid (GV150526), a novel glycine antagonist for stroke, in rat and dog following intravenous administration of [C14]-GV150526A were investigated. 2. Studies were also performed in bile duct-cannulated animals to confirm the route of elimination and to obtain more information on metabolite identity. 3. Metabolites in plasma, urine and bile were identified by HPLC-MS/MS and NMR spectroscopy. 4. GV150526A was predominantly excreted in the faeces via the bile, with only trace metabolites of radioactivity in urine (< 5%). Radioactivity in rat bile was predominantly due to metabolites, whereas approximately 50% of the radioactivity in dog bile was due to parent GV150526. 5. The principal metabolites in bile were identified as glucuronide conjugates of the carboxylic acid, whereas in rat urine the main metabolite was a sulphate conjugate of an aromatic oxidation metabolite. Multiple glucuronide peaks were observed and identified as isomeric glucuronides and their anomers arising from acyl migration and muta-rotation.

Receptor binding characteristics of the novel NMDA receptor glycine site antagonist [3H]GV150526A in rat cerebral cortical membranes.[Pubmed:10729363]

Eur J Pharmacol. 2000 Mar 17;391(3):233-41.

Binding of the glycine site antagonist 3-[2-(Phenylamino-carbonyl)ethenyl]-4,6-dichloro-indole-2-carboxylic acid sodium salt ([3H]GV150526A) was characterised in rat cerebral cortical membranes. Saturation experiments indicated the existence of a high affinity binding site, with a pK(d) value of 9.08 (K(d)=0. 8 nM) and a B(max) of 3.4 pmol/mg of protein. A strong linear correlation was observed between the displacement potencies for [3H]GV150526A and [3H]glycine of 13 glycine site ligands (r=0.991). The association kinetics of [3H]GV150526A binding was monophasic, with a k(on) value of 0.047 (nM)(-1) min(-1). Dissociation was induced by the addition of an excess of glycine, GV150526A, or 5,7-dichlorokynurenic acid (DCKA), another glycine antagonist. With GV150526A and DCKA, the dissociation curves presented similar k(off) values (0.068 and 0.069 min(-1), respectively), as expected from ligands binding to the same site. Conversely, a significantly lower k(off) value (0.027 min(-1)) was found with glycine. Although these data may suggest that glycine agonists and antagonists bind to discrete sites with an allosteric linkage (rather than interacting competitively), the reason for this difference remains to be elucidated. It is concluded that [3H]GV150526A can be considered a new valuable tool to further investigate the properties of the glycine site of the NMDA receptor.

Substituted indole-2-carboxylates as in vivo potent antagonists acting as the strychnine-insensitive glycine binding site.[Pubmed:9083472]

J Med Chem. 1997 Mar 14;40(6):841-50.

A series of indole-2-carboxylates bearing suitable chains at the C-3 position of the indole nucleus was synthesized and evaluated in terms of in vitro affinity using [3H]glycine binding assay and in vivo potency by inhibition of convulsions induced by N-methyl-D-aspartate (NMDA) in mice. 3-[2-[(Phenylamino)carbonyl]ethenyl]-4,6-dichloroindole-2-carboxyl ic acid (8) was an antagonist at the strychnine-insensitive glycine binding site (noncompetitive inhibition of the binding of [3H]TCP, pA2 = 8.1) displaying nanomolar affinity for the glycine binding site (pKi = 8.5), coupled with high glutamate receptor selectivity (> 1000-fold relative to the affinity at the NMDA, AMPA, and kainate binding sites). This indole derivative inhibited convulsions induced by NMDA in mice, when administered by both iv and po routes (ED50 = 0.06 and 6 mg/kg, respectively). The effect of the substituents on the terminal phenyl ring of the C-3 side chain was investigated. QSAR analysis suggested that the pKi value decreases with lipophilicity and steric bulk of substituents and increases with the electron donor resonance effect of the groups present in the para position of the terminal phenyl ring. According to these results the terminal phenyl ring of the C-3 side chain should lie in a nonhydrophobic pocket of limited size, refining the proposed pharmacophore model of the glycine binding site associated with the NMDA receptor.

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