S 32212 hydrochlorideCAS# 847871-78-7 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 847871-78-7 | SDF | Download SDF |
PubChem ID | 11487816 | Appearance | Powder |
Formula | C25H29ClN4O2 | M.Wt | 452.98 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 25 mM in water and to 25 mM in DMSO | ||
Chemical Name | N-[4-methoxy-3-(4-methylpiperazin-1-yl)phenyl]-1,2-dihydrobenzo[e]indole-3-carboxamide;hydrochloride | ||
SMILES | CN1CCN(CC1)C2=C(C=CC(=C2)NC(=O)N3CCC4=C3C=CC5=CC=CC=C45)OC.Cl | ||
Standard InChIKey | RAKGNVNONBJBSW-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C25H28N4O2.ClH/c1-27-13-15-28(16-14-27)23-17-19(8-10-24(23)31-2)26-25(30)29-12-11-21-20-6-4-3-5-18(20)7-9-22(21)29;/h3-10,17H,11-16H2,1-2H3,(H,26,30);1H | ||
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 | Inverse agonist of 5-HT2C receptors (pKi = 8.18 at human 5-HT2C INI receptors). Also an antagonist of human α2-adrenoceptors. Displays negligible affinity for α1A-adrenoceptors, histamine H1 receptors and muscarinic M1 receptors. |
S 32212 hydrochloride Dilution Calculator
S 32212 hydrochloride Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.2076 mL | 11.038 mL | 22.076 mL | 44.1521 mL | 55.1901 mL |
5 mM | 0.4415 mL | 2.2076 mL | 4.4152 mL | 8.8304 mL | 11.038 mL |
10 mM | 0.2208 mL | 1.1038 mL | 2.2076 mL | 4.4152 mL | 5.519 mL |
50 mM | 0.0442 mL | 0.2208 mL | 0.4415 mL | 0.883 mL | 1.1038 mL |
100 mM | 0.0221 mL | 0.1104 mL | 0.2208 mL | 0.4415 mL | 0.5519 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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Racemic R,S-venlafaxine hydrochloride-DNA interaction: experimental and computational evidence.[Pubmed:25801443]
Spectrochim Acta A Mol Biomol Spectrosc. 2015 Jun 15;145:540-552.
The interaction of racemic R,S-venlafaxine hydrochloride (rac-VEN) drug with calf thymus deoxyribonucleic acid (ct-DNA) was studied using various physico-chemical techniques and molecular docking at simulated physiological conditions (pH=7.4). The fluorescence study shows that ct-DNA interacted with rac-VEN and quenched its intrinsic fluorescence in a static quenching process. These results are further supported by UV-Vis spectra. The binding constant of rac-VEN with ct-DNA (0.57 x 10(4)) obtained from the spectroscopic techniques, which is more in keeping with the groove binding with DNA. Furthermore, the competition experiment using Hoechst33258 indicated that rac-VEN may bind to ct-DNA by a minor groove binding mode. In addition, iodide quenching effect on the fluorescence of rac-VEN before and after the interaction with ct-DNA is another evidence to groove binding. The thermodynamic parameters are calculated by van't Hoff equation, which demonstrated that hydrogen bonds and van der Waals interactions played major roles in the binding reaction. Molecular simulation studies carried out by using the AutoDock4 and Spartan 10 programs. From the best docking map, we found that R and S-isomers fit in the A6T7T8/T19A18A17 region in minor groove of B-DNA. Finally, these results indicated that the docking of S-VEN-B-DNA is more stable than R-VEN-B-DNA.
Efficient synthesis of alpha-fluoromethylhistidine di-hydrochloride and demonstration of its efficacy as a glutathione S-transferase inhibitor.[Pubmed:28228363]
Bioorg Med Chem Lett. 2017 Mar 15;27(6):1335-1340.
Histidine decarboxylase (HDC) is an enzyme that converts histidine to histamine. Inhibition of HDC has several medical applications, and HDC inhibitors are of considerable interest for the study of histidine metabolism. (S)-alpha-Fluoromethylhistidine di-hydrochloride (alpha-FMH) is a potent HDC inhibitor that is commercially available at high cost in small amounts only. Here we report a novel, inexpensive, and efficient method for synthesis of alpha-FMH using methyl 2-aziridinyl-3-(N-triphenylmethyl-4-imidazolyl) propionate and HF/pyridine, with experimental yield of 57%. To identify novel targets for alpha-FMH, we developed a three step in silico work-flow for identifying physically plausible protein targets. The work-flow resulted in 21 protein target hits, including several enzymes involved in glutathione metabolism, and notably, two isozymes of the glutathione S-transferase (GST) superfamily, which plays a central role in drug metabolism. In view of this predictive data, the efficacy of alpha-FMH as a GST inhibitor was investigated in vitro. alpha-FMH was demonstrated to be an effective inhibitor of GST at micromolar concentration, suggesting that off-target effects of alpha-FMH may limit physiological drug metabolism and elimination by GST-dependent mechanisms. The present study therefore provides new avenues for obtaining alpha-FMH and for studying its biochemical effects, with potential implications for drug development.
The hydrochloride and hydrobromide salt forms of (S)-amphetamine.[Pubmed:26422209]
Acta Crystallogr C Struct Chem. 2015 Oct;71(Pt 10):844-9.
Despite the high profile of amphetamine, there have been relatively few structural studies of its salt forms. The lack of any halide salt forms is surprising as the typical synthetic route for amphetamine initially produces the chloride salt. (S)-Amphetamine hydrochloride [systematic name: (2S)-1-phenylpropan-2-aminium chloride], C9H14N(+).Cl(-), has a Z' = 6 structure with six independent cation-anion pairs. That these are indeed crystallographically independent is supported by different packing orientations of the cations and by the observation of a wide range of cation conformations generated by rotation about the phenyl-CH2 bond. The supramolecular contacts about the anions also differ, such that both a wide variation in the geometry of the three N-H...Cl hydrogen bonds formed by each chloride anion and differences in C-H...Cl contacts are apparent. (S)-Amphetamine hydrobromide [systematic name: (2S)-1-phenylpropan-2-aminium bromide], C9H14N(+).Br(-), is broadly similar to the hydrochloride in terms of cation conformation, the existence of three N-H...X hydrogen-bond contacts per anion and the overall two-dimensional hydrogen-bonded sheet motif. However, only the chloride structure features organic bilayers and Z' > 1.
Antibacterial, cyto and genotoxic activities of A22 compound ((S-3, 4 -dichlorobenzyl) isothiourea hydrochloride).[Pubmed:27427089]
Microb Pathog. 2016 Oct;99:14-18.
The A22 is a chemical compound that acts as a reversible inhibitor of a bacterial cell wall protein MreB leading the rods to the coccoid form. Thus, by changing the bacterial form, many properties can be affected, as the acquisition of nutrients, cell division, the clamping surfaces, motility and pathogenesis. Infections caused by strains of Pseudomonas aeruginosa have great clinical importance because these microorganisms can include more than one resistance mechanism acting together, limiting treatment options. Thus, it is important to investigate the action of A22 against P. aeruginosa, once there are urgent needs for new antimicrobial compounds for increase the arsenal therapeutic to treat diseases caused by this microrganism. Therefore, this study investigated for the first time the antimicrobial activity of A22 against seve standards strains of Gram negative microorganisms and twenty-eight clinical isolates of P. aeruginosa. This study performed an additional investigation to analyze the cyto and genotoxic potential effects from A22 on human peripheral blood mononuclear cells (PBMCs). The antibacterial activity of A22 was studied by broth microdilution method and time-kill assay. The cytotoxicity was evaluated by MTT assay at 24, 48 and 72 h of exposure to A22 and the genotoxicity was evaluated by the Comet assay. The susceptibility tests showed A22 has a relevant antibacterial activity against P. aeruginosa, including multidrug-resistant (MDR) clinical isolates. The A22 treatment not showed genotoxic effects against PBMCs in almost all concentrations tested at 24 and 48 h of exposure. Only for concentration of 32 mug/mL (highest tested) the damage index was significantly higher in all moments. The MTT assay demonstrated that A22 was able to maintain cell viability in all exposure times. In summary, the A22 demonstrated important anti-Pseudomonas activity and showed no cyto and genotoxic significant effect. These results need to be considered in future in vitro and in vivo studies in order to introduce the A22 as a possible therapeutic option.
S32212, a novel serotonin type 2C receptor inverse agonist/alpha2-adrenoceptor antagonist and potential antidepressant: II. A behavioral, neurochemical, and electrophysiological characterization.[Pubmed:22178753]
J Pharmacol Exp Ther. 2012 Mar;340(3):765-80.
The present studies characterized the functional profile of N-[4-methoxy-3-(4-methylpiperazin-1-yl)phenyl]-1,2-dihydro-3-H-benzo[e]indole-3-c arboxamide) (S32212), a combined serotonin (5-HT)(2C) receptor inverse agonist and alpha(2)-adrenoceptor antagonist that also possesses 5-HT(2A) antagonist properties (J Pharmacol Exp Ther 340:750-764, 2012). Upon parenteral and/or oral administration, dose-dependent (0.63-40.0 mg/kg) actions were observed in diverse procedures. Both acute and subchronic administration of S32212 reduced immobility time in a forced-swim test in rats. Acutely, it also suppressed marble burying and aggressive behavior in mice. Long-term administration of S32212 was associated with rapid (1 week) and sustained (5 weeks) normalization of sucrose intake in rats exposed to chronic mild stress and with elevated levels of mRNA encoding brain-derived neurotrophic factor in hippocampus and amygdala (2 weeks). S32212 accelerated the firing rate of adrenergic perikarya in the locus coeruleus and elevated dialysis levels of noradrenaline in the frontal cortex and hippocampus of freely moving rats. S32212 also elevated the frontocortical levels of dopamine and acetylcholine, whereas 5-HT, amino acids, and histamine were unaffected. These neurochemical actions were paralleled by "promnemonic" properties: blockade of scopolamine-induced deficits in radial maze performance and social recognition and reversal of delay-induced impairments in social recognition, social novelty discrimination, and novel object recognition. It also showed anxiolytic actions in a Vogel conflict procedure. Furthermore, in an electroencephalographic study of sleep architecture, S32212 enhanced slow-wave and rapid eye movement sleep, while decreasing waking. Finally, chronic administration of S32212 neither elevated body weight nor perturbed sexual behavior in male rats. In conclusion, S32212 displays a functional profile consistent with improved mood and cognitive performance, together with satisfactory tolerance.
S32212, a novel serotonin type 2C receptor inverse agonist/alpha2-adrenoceptor antagonist and potential antidepressant: I. A mechanistic characterization.[Pubmed:22178752]
J Pharmacol Exp Ther. 2012 Mar;340(3):750-64.
Although most antidepressants suppress serotonin (5-HT) and/or noradrenaline reuptake, blockade of 5-HT(2C) receptors and alpha(2)-adrenoceptors likewise enhances monoaminergic transmission. These sites are targeted by the urea derivative N- [4-methoxy-3-(4-methylpiperazin-1-yl)phenyl]-1,2-dihydro-3-H-benzo[e]indole-3-car boxamide (S32212). S32212 was devoid of affinity for monoamine reuptake sites, yet displayed pronounced affinity (pK(i), 8.2) for constitutively active human 5-HT(2CINI) (h5-HT(2CINI)) receptors, behaving as an inverse agonist in reducing basal Galpha(q) activation, [(3)H]inositol-phosphate production, and the spontaneous association of h5-HT(2CINI)-Renilla luciferase receptors with beta-arrestin2-yellow fluorescent protein. Furthermore, upon 18-h pretreatment, S32212 enhanced the plasma membrane expression of h5-HT(2CINI) receptors as visualized by confocal microscopy and quantified by enzyme-linked immunosorbent assay. Its actions were prevented by the neutral antagonist 6-chloro-5-methyl-N-[6-(2-methylpyridin-3-yloxy)pyridin-3-yl]indoline-1-carboxami de (SB242,084), which also impeded the induction by long-term exposure to S32212 of otherwise absent Ca(2+) mobilization in mouse cortical neurones. In vivo, S32212 blunted the inhibitory influence of the 5-HT(2C) agonist 2-(3-chlorobenzyloxy)-6-(1-piperazinyl)pyrazine (CP809,101) on ventrotegmental dopaminergic neurones. S32212 also blocked 5-HT-induced Galpha(q) and phospholipase C activation at the h5-HT(2A) and, less potently, h5-HT(2B) receptors and suppressed the discriminative stimulus properties of the 5-HT(2A) agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane in rats. S32212 manifested marked affinity for human alpha(2A)- (pK(i) 7.2), alpha(2B)- (pK(i) 8.2), and alpha(2C)- (pK(i) 7.4) adrenoceptors, at which it abolished noradrenaline-induced recruitment of Galpha(i3), Galpha(o), adenylyl cyclase, and extracellular-regulated kinase1/2. Moreover, S32212 dose-dependently abolished the discriminative stimulus effects of the alpha(2)-adrenoceptor agonist (S)-spiro[(1-oxa-2-amino-3-azacyclopent-2-ene)-4,2'-(1',2',3',4'-tetrahydronaphth alene)] (S18616). Finally, S32212 displayed negligible affinity for alpha(1A)-adrenoceptors, histamine H(1) receptors, and muscarinic M(1) receptors. In conclusion, S32212 behaves as an inverse agonist at h5-HT(2C) receptors and as an antagonist at human alpha(2)-adrenoceptors (and h5-HT(2A) receptors). Its promising profile in preclinical models potentially relevant to the treatment of depression is described in J Pharmacol Exp Ther 340:765-780, 2012.