EtifoxineGABAA receptor potentiator CAS# 21715-46-8 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 21715-46-8 | SDF | Download SDF |
PubChem ID | 30768 | Appearance | Powder |
Formula | C17H17ClN2O | M.Wt | 300.78 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | DMSO : 100 mg/mL (332.47 mM; Need ultrasonic) | ||
Chemical Name | 6-chloro-N-ethyl-4-methyl-4-phenyl-3,1-benzoxazin-2-amine | ||
SMILES | CCNC1=NC2=C(C=C(C=C2)Cl)C(O1)(C)C3=CC=CC=C3 | ||
Standard InChIKey | IBYCYJFUEJQSMK-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C17H17ClN2O/c1-3-19-16-20-15-10-9-13(18)11-14(15)17(2,21-16)12-7-5-4-6-8-12/h4-11H,3H2,1-2H3,(H,19,20) | ||
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. |
Etifoxine Dilution Calculator
Etifoxine Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.3247 mL | 16.6234 mL | 33.2469 mL | 66.4938 mL | 83.1172 mL |
5 mM | 0.6649 mL | 3.3247 mL | 6.6494 mL | 13.2988 mL | 16.6234 mL |
10 mM | 0.3325 mL | 1.6623 mL | 3.3247 mL | 6.6494 mL | 8.3117 mL |
50 mM | 0.0665 mL | 0.3325 mL | 0.6649 mL | 1.3299 mL | 1.6623 mL |
100 mM | 0.0332 mL | 0.1662 mL | 0.3325 mL | 0.6649 mL | 0.8312 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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Etifoxine is potentiator of GABAA receptor function in cultured neurons. Etifoxine preferentially acts on β2 or β3 subunit-containing GABAA receptors. Etifoxine exhibits anxiolytic activity in rodents and humans with no sedative, myorelaxant or mnesic side effects. Etifoxine acts as a ligand of the translocator protein (TSPO); promotes axonal regeneration.
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Differential efficacy of the TSPO ligands etifoxine and XBD-173 in two rodent models of Multiple Sclerosis.[Pubmed:27039042]
Neuropharmacology. 2016 Sep;108:229-37.
Neurosteroids such as progesterone and allopregnanolone have been shown to exert neuroprotective effects under a variety of pathological or insult conditions, and there is evidence that the neurosteroid system is perturbed in Multiple Sclerosis (MS) patients. Neurosteroids are synthesized in the central nervous system (CNS) through a series of metabolic transformations, beginning with a rate-limiting step of cholesterol transport through the outer mitochondrial membrane via the transporter translocator protein (TSPO). We examined the effects of Etifoxine and XBD-173, two different brain penetrant TSPO agonists, for their ability to ameliorate clinical signs in two different experimental autoimmune encephalitis (EAE) models. Etifoxine, as previously reported, was efficacious in EAE, while XBD-173 was not. Surprisingly, XBD-173, but not Etifoxine elevated relevant neurosteroids in brain of female rats and differed in its ability to exert anti-inflammatory and direct neuroprotective effects in vitro as compared to Etifoxine. We conclude that the neurosteroid elevations produced in brain by XBD-173 are not sufficient to ameliorate EAE and suggest that Etifoxine may have additional mechanisms of action that provide therapeutic benefit in this model system.
A microPET comparison of the effects of etifoxine and diazepam on [(11)C]flumazenil uptake in rat brains.[Pubmed:26644334]
Neurosci Lett. 2016 Jan 26;612:74-79.
Using positron emission tomography (PET), the present study assessed the binding of [(11)C]flumazenil to GABA-A receptors in anesthetized rats following a single intravenous injection of an active dose of either Etifoxine (25mg/kg) or diazepam (1mg/kg), which are both anxiolytic drugs. [(11)C]flumazenil binding was measured in five discrete brain structures, namely the caudate putamen, hippocampus, cerebellum, occipital cortex and parietal cortex. As expected, diazepam injection produced a significant decrease in [(11)C]flumazenil binding, which was interpreted as benzodiazepine GABA-A receptor occupancy, whereas Etifoxine increased the binding of [(11)C]flumazenil. This first use of in vivo imaging after Etifoxine administration revealed the activated binding pattern of [(11)C]flumazenil and highlighted the pharmacological differences between Etifoxine and benzodiazepines. Using the same [(11)C]flumazenil radiotracer, PET neuroimaging could be applied to larger animals and, ultimately, to human subjects, thus providing new perspectives for better defining the molecular pharmacology of Etifoxine.
The Anxiolytic Etifoxine Binds to TSPO Ro5-4864 Binding Site with Long Residence Time Showing a High Neurosteroidogenic Activity.[Pubmed:28362078]
ACS Chem Neurosci. 2017 Jul 19;8(7):1448-1454.
The low binding affinity of the approved anxiolytic drug Etifoxine (Stresam) at the steroidogenic 18 kDa translocator protein (TSPO) has questioned the specific contribution of this protein in mediating the Etifoxine neurosteroidogenic efficacy. Residence time (RT) at the binding site of the classical TSPO ligand PK11195 is emerging as a relevant neurosteroidogenic efficacy measure rather than the binding affinity. Here Etifoxine was evaluated for (i) the in vitro neurosteroidogenic activity in comparison to poorly neurosteroidogenic reference TSPO ligands (PK11195 and Ro5-4864) and (ii) the affinity and RT at [(3)H]PK11195 and [(3)H]Ro5-4864 binding sites in rat kidney membranes. Etifoxine shows (i) high neurosteroidogenic efficacy and (ii) low affinity/short RT at the [(3)H]PK11195 site and low affinity/long RT at the [(3)H]Ro5-4864 site, at which Etifoxine competitively bound. These findings suggest that the long RT of Etifoxine at the Ro5-4864 binding site could account for its high neurosteroidogenic efficacy.
Etifoxine improves sensorimotor deficits and reduces glial activation, neuronal degeneration, and neuroinflammation in a rat model of traumatic brain injury.[Pubmed:27565146]
J Neuroinflammation. 2016 Aug 26;13(1):203.
BACKGROUND: Traumatic brain injury (TBI) results in important neurological impairments which occur through a cascade of deleterious physiological events over time. There are currently no effective treatments to prevent these consequences. TBI is followed not only by an inflammatory response but also by a profound reorganization of the GABAergic system and a dysregulation of translocator protein 18 kDa (TSPO). Etifoxine is an anxiolytic compound that belongs to the benzoxazine family. It potentiates GABAergic neurotransmission, either through a positive allosteric effect or indirectly, involving the activation of TSPO that leads to an increase in neurosteroids synthesis. In several models of peripheral nerve injury, Etifoxine has been demonstrated to display potent regenerative and anti-inflammatory properties and to promote functional recovery. Prior study also showed Etifoxine efficacy in reducing brain edema in rats. In light of these positive results, we used a rat model of TBI to explore Etifoxine treatment effects in a central nervous system injury, from functional outcomes to the underlying mechanisms. METHODS: Male Sprague-Dawley rats received contusion (n = 18) or sham (n = 19) injuries centered laterally to bregma over the left sensorimotor cortex. They were treated with Etifoxine (50 mg/kg, i.p.) or its vehicle 30 min following injury and every day during 7 days. Rats underwent behavioral testing to assess sensorimotor function. In another experiment, injured rats (n = 10) or sham rats (n = 10) received Etifoxine (EFX) (50 mg/kg, i.p.) or its vehicle 30 min post-surgery. Brains were then dissected for analysis of neuroinflammation markers, glial activation, and neuronal degeneration. RESULTS: Brain-injured rats exhibited significant sensorimotor function deficits compared to sham-injured rats in the bilateral tactile adhesive removal test, the beam walking test, and the limb-use asymmetry test. After 2 days of Etifoxine treatment, behavioral impairments were significantly reduced. Etifoxine treatment reduced pro-inflammatory cytokines levels without affecting anti-inflammatory cytokines levels in injured rats, reduced macrophages and glial activation, and reduced neuronal degeneration. CONCLUSIONS: Our results showed that post-injury treatment with Etifoxine improved functional recovery and reduced neuroinflammation in a rat model of TBI. These findings suggest that Etifoxine may have a therapeutic potential in the treatment of TBI.