Citalopram hydrobromideHighly potent and selective 5-HT uptake inhibitor CAS# 59729-32-7 |
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Quality Control & MSDS
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Chemical structure
3D structure
| Cas No. | 59729-32-7 | SDF | Download SDF |
| PubChem ID | 77995 | Appearance | Powder |
| Formula | C20H22BrFN2O | M.Wt | 405.31 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | (±)-Citalopram hydrobromide; Lu 10-171 | ||
| Solubility | DMSO : ≥ 38 mg/mL (93.76 mM) H2O : 10 mg/mL (24.67 mM; Need ultrasonic) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-3H-2-benzofuran-5-carbonitrile;hydrobromide | ||
| SMILES | CN(C)CCCC1(C2=C(CO1)C=C(C=C2)C#N)C3=CC=C(C=C3)F.Br | ||
| Standard InChIKey | WIHMBLDNRMIGDW-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C20H21FN2O.BrH/c1-23(2)11-3-10-20(17-5-7-18(21)8-6-17)19-9-4-15(13-22)12-16(19)14-24-20;/h4-9,12H,3,10-11,14H2,1-2H3;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 | Highly selective and potent 5-HT uptake inhibitor with no effect on noradrenalin or dopamine uptake (IC50 values are 1.8, 8800 and 41000 nM respectively). Has negligible activity at a wide range of receptors. |
Citalopram hydrobromide Dilution Calculator
Citalopram hydrobromide Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.4672 mL | 12.3362 mL | 24.6725 mL | 49.3449 mL | 61.6812 mL |
| 5 mM | 0.4934 mL | 2.4672 mL | 4.9345 mL | 9.869 mL | 12.3362 mL |
| 10 mM | 0.2467 mL | 1.2336 mL | 2.4672 mL | 4.9345 mL | 6.1681 mL |
| 50 mM | 0.0493 mL | 0.2467 mL | 0.4934 mL | 0.9869 mL | 1.2336 mL |
| 100 mM | 0.0247 mL | 0.1234 mL | 0.2467 mL | 0.4934 mL | 0.6168 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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Citalopram hydrobromide is an antidepressant drug of the selective serotonin reuptake inhibitor (SSRI) class. It has US FDA approval to treat major depression.
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Utility of eosin Y as a complexing reagent for the determination of citalopram hydrobromide in commercial dosage forms by fluorescence spectrophotometry.[Pubmed:25829234]
Luminescence. 2015 Dec;30(8):1352-9.
An accurate, selective and sensitive spectrofluorimetric method was developed for the determination of Citalopram hydrobromide in commercial dosage forms. The method was based on the formation of a fluorescent ion-pair complex between Citalopram hydrobromide and eosin Y in the presence of a disodium hydrogen phosphate/citric acid buffer solution of pH 3.4 that was extractable in dichloromethane. The extracted complex showed fluorescence intensity at lambdaem = 554 nm after excitation at 259 nm. The calibration curve was linear over at concentrations of 2.0-26.0 microg/mL. Under optimized experimental conditions, the proposed method was validated as per ICH guidelines. The effect of common excipients used as additives was tested and the tolerance limit calculated. The limit of detection for the proposed method was 0.121 mug/mL. The proposed method was successfully applied to the determination of Citalopram hydrobromide in commercial dosage forms. The results were compared with the reference RP-HPLC method.
Spectrophotometric determination of citalopram hydrobromide in tablet dosage form using chloranil.[Pubmed:24577911]
Pak J Pharm Sci. 2014 Mar;27(2):255-60.
A fast, sensitive and extraction free spectrophotometric method for the quantitative determination of Citalopram hydrobromide in pharmaceutical raw and tablet formulations has been proposed. The newly proposed method is based on the charge transfer reaction between citalopram as electron donor and chloranil as electron acceptor. The charge transfer complex of citalopram and chloranil shows lambda(max) at 550 nm in methanol. The experimental conditions such as reaction time, temperature, stoichiometry of the colored complex have been optimized. The developed method allows the determination of Citalopram hydrobromide over a concentration range of 1-25 mg/ ml. The proposed method is used to determine the citalopram in tablet dosage forms. The results of proposed method are compared to the official USP method. The newly developed method is accurate, reproducible and easy to perform. It does not require stringent experimental conditions. No interference has been observed for excipients and additives in tablet formulations.
Development and application of spectrophotometric methods for the determination of citalopram hydrobromide in dosage forms.[Pubmed:16595940]
Chem Pharm Bull (Tokyo). 2006 Apr;54(4):432-4.
Study was carried out to develop two simple, fast, accurate and sensitive spectrophotometric methods (A and B) for the determination of Citalopram hydrobromide in commercial tablet formulations. In method A, UV spectrophotometer determined the contents of Citalopram hydrobromide in tablets at 240 nm in methanol solvent. The linear range was 5-40 microg ml-1 with molar absorptivity 1.4x10(4) l mol-1 cm-1. While the method B based on the reaction of citalopram base as n-electron donor with 2,3-dichloro-5,6-dicyano-1,4-benzoquinone as pi-acceptors to give highly colored complex species that absorb maximally at 590 nm. Beer's law was obeyed in the concentration limit of 10-250 microg ml-1 with molar absorptivity 3.3x10(3) l mol-1 cm-1 for Citalopram hydrobromide. The limits of detection and limit of quantification was calculated and found to be 5.2 microg ml-1 and 17.4 microg ml-1 respectively. The proposed methods were found to be rapid, accurate, precise and sensitive for the determination of Citalopram hydrobromide in commercial tablet formulations with out interferences from common additives encountered.
The effect of citalopram hydrobromide on 5-HT2A receptors in the impulsive-aggressive dog, as measured with 123I-5-I-R91150 SPECT.[Pubmed:15739093]
Eur J Nucl Med Mol Imaging. 2005 Jun;32(6):708-16.
PURPOSE: Involvement of the serotonergic system in impulsive aggression has been demonstrated in both human and animal studies. The purpose of the present study was to investigate the effect of Citalopram hydrobromide (a selective serotonin re-uptake inhibitor) on the 5-HT(2A) receptor and brain perfusion in impulsive-aggressive dogs by means of single-photon emission computed tomography. METHODS: The binding index of the radioligand (123)I-5-I-R91150 was measured before and after treatment with Citalopram hydrobromide in nine impulsive-aggressive dogs. Regional perfusion was measured with (99m)Tc-ethyl cysteinate dimer (ECD). Behaviour was assessed before treatment and again after 6 weeks of treatment. RESULTS: A correlation was found between decreased binding and behavioural improvement in eight out of nine dogs. The 5-HT(2A) receptor binding index was significantly reduced after Citalopram hydrobromide treatment in all cortical regions but not in the subcortical area. None of the dogs displayed alterations in perfusion on the post-treatment scans. CONCLUSION: This study supports previous findings regarding the involvement of the serotonergic system in impulsive aggression in dogs in general. More specifically, the effect of treatment on the 5-HT(2A) receptor binding index could be demonstrated and the decreased binding index correlated with behavioural improvement.
Inhibition of 5-hydroxytryptamine reuptake by the antidepressant citalopram in the locus coeruleus modulates the rat brain noradrenergic transmission in vivo.[Pubmed:10963747]
Neuropharmacology. 2000 Aug 23;39(11):2036-43.
The in vivo effect of the serotonin (5-HT) reuptake inhibitor antidepressant citalopram, administered in the locus coeruleus (LC), on noradrenergic transmission was evaluated in the rat brain. In dual-probe microdialysis assays, citalopram (0.1-100 microM), in a concentration-dependent manner, increased extracellular noradrenaline (NA) in the LC and simultaneously decreased extracellular NA in the cingulate cortex (Cg). These effects of citalopram were abolished by pretreatment with the 5-HT synthesis inhibitor p-chlorophenylalanine (400 mg/kg, i.p.). When the alpha(2)-adrenoceptor antagonist RS79948 (1 microM) was perfused in the LC, local citalopram increased NA dialysate in the LC but no longer modified NA dialysate in the Cg. In electrophysiological experiments, the administration of citalopram (100 microM) in the LC by reversal dialysis, decreased the firing rate of LC neurones. The results demonstrate in vivo that local administration of citalopram in the LC leads to a decreased release of NA in the Cg. This modulation seems to be the result of an increase in NA concentration in the LC and the subsequent inhibition of LC neurones via alpha(2)-adrenoceptors. The effects of citalopram are dependent on the presence of endogenous 5-HT in the LC.
Effect of chronic administration of the selective serotonin (5-HT) uptake inhibitor citalopram on extracellular 5-HT and apparent autoreceptor sensitivity in rat forebrain in vivo.[Pubmed:9053730]
Naunyn Schmiedebergs Arch Pharmacol. 1995 Dec;352(6):597-606.
Rats were administered the selective serotonin (5-HT) uptake blocker citalopram or saline for 14 days to determine if prolonged treatment would lead to changes in extracellular 5-HT or autoreceptor sensitivity. One day after drug withdrawal, dialysis probes were implanted in the frontal cortex and dorsal hippocampus. Dialysis experiments were carried out using chloral hydrate anesthetized rats. The experimental protocol comprised the administration of three consecutive drug challenges: (1) After stable baseline levels were obtained, citalopram was infused through the dialysis probes to locally block uptake in the forebrain. (2) Subsequently, a 5-HT1B receptor agonist (RU24969 or CP93,129) was infused through the probe to test for changes in terminal autoreceptor sensitivity. (3) Last, citalopram was administered systemically to test the effect of indirect activation of somatodendritic autoreceptors. Under these conditions, with uptake already blocked locally in the forebrain, systemic citalopram produces a decrease in extracellular 5-HT, an effect that can be inhibited by pretreatment with antagonists of 5-HT1A receptors. The results indicate that during local infusion of citalopram extracellular 5-HT was significantly higher in the dorsal hippocampus of the chronic citalopram as compared to saline treatment group. This difference persisted throughout the full time course of the experiment. However, the decreases in 5-HT levels produced by local infusion of a 5-HT1B receptor agonist or after systemic citalopram administration were not significantly different between the chronic citalopram and saline treated groups. There were no significant differences between chronic citalopram and saline treated animals in frontal cortex. These results suggest that prolonged inhibition of 5-HT uptake may produce a selective change in the regulation of release from median raphe 5-HT neurons, but this change could not be clearly linked to a change in nerve terminal or somatodendritic autoreceptor sensitivity.
