Cetirizine DiHClH1 receptor inverse agonist CAS# 83881-52-1 |
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Quality Control & MSDS
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Chemical structure
3D structure
Cas No. | 83881-52-1 | SDF | Download SDF |
PubChem ID | 55182 | Appearance | Powder |
Formula | C21H27Cl3N2O3 | M.Wt | 461.81 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | P 071 | ||
Solubility | DMSO : 100 mg/mL (216.54 mM; Need ultrasonic) H2O : 100 mg/mL (216.54 mM; Need ultrasonic) | ||
Chemical Name | [2-[4-[(4-Chlorophenyl)phenylmethyl | ||
SMILES | [H+].[H+].[Cl-].[Cl-].OC(=O)COCCN1CCN(CC1)C(c2ccccc2)c3ccc(Cl)cc3 | ||
Standard InChIKey | PGLIUCLTXOYQMV-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C21H25ClN2O3.2ClH/c22-19-8-6-18(7-9-19)21(17-4-2-1-3-5-17)24-12-10-23(11-13-24)14-15-27-16-20(25)26;;/h1-9,21H,10-16H2,(H,25,26);2*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 | Histamine H1 receptor antagonist that displays selectivity over other receptors at concentrations up to 10 μM. A non-sedating antihistamine that inhibits histamine release and eosinophil chemotaxis during secondary phase allergic response. Inhibits activation of eosinophils, neutrophils and monocytes in vivo. |
Cetirizine DiHCl Dilution Calculator
Cetirizine DiHCl Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.1654 mL | 10.827 mL | 21.6539 mL | 43.3079 mL | 54.1348 mL |
5 mM | 0.4331 mL | 2.1654 mL | 4.3308 mL | 8.6616 mL | 10.827 mL |
10 mM | 0.2165 mL | 1.0827 mL | 2.1654 mL | 4.3308 mL | 5.4135 mL |
50 mM | 0.0433 mL | 0.2165 mL | 0.4331 mL | 0.8662 mL | 1.0827 mL |
100 mM | 0.0217 mL | 0.1083 mL | 0.2165 mL | 0.4331 mL | 0.5413 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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Cetirizine 2Hcl, a second-generation antihistamine, is a major metabolite of hydroxyzine, and a racemic selective H1 receptor inverse agonist used in the treatment of allergies, hay fever, angioedema, and urticaria.
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Suppression of histamine-induced skin reactions by loratadine and cetirizine diHCl.[Pubmed:2570701]
Eur J Clin Pharmacol. 1989;36(6):617-9.
The skin reactivity to histamine was measured in 10 healthy and 10 atopic subjects after the ingestion of single doses of loratadine 10 mg, Cetirizine DiHCl 10 mg and placebo, in a double-blind cross-over randomized study. The anti-H1 effect of Cetirizine DiHCl proved to be significantly more rapid, more pronounced and longer lasting than that of loratadine.
Effects of cetirizine on human eosinophil and neutrophil activation in vitro.[Pubmed:1682275]
Int Arch Allergy Appl Immunol. 1991;95(2-3):158-62.
The ability of cetirizine, a novel antihistamine agent, to inhibit the in vivo activation of human eosinophils, neutrophils and monocytes has been investigated using C3b- and IgG-dependent rosette formation, cytotoxicity against opsonised parasitic larvae and adherence to plasma-coated glass (PCG). The drug inhibited platelet-activating factor (PAF)-induced enhancement of eosinophil and neutrophil IgG (Fc) and complement (C3b) rosettes with an IC50 of 2 x 10(-5) M. There was also comparable inhibition of PAF-dependent enhancement of eosinophil cytotoxicity (for complement-coated schistosomula of Schistosoma mansoni). Cetirizine inhibited PAF-induced eosinophil, but not neutrophil, hyperadherence to PCG. These data support the view that cetirizine may exert some of its anti-allergic effects by inhibiting the activation of human granulocytes and that it may also selectively inhibit PAF-induced eosinophil hyperadherence.
Cetirizine. A review of its pharmacological properties and clinical potential in allergic rhinitis, pollen-induced asthma, and chronic urticaria.[Pubmed:1981354]
Drugs. 1990 Nov;40(5):762-81.
Cetirizine, a piperazine derivative and carboxylated metabolite of hydroxyzine, is a potent histamine H1-receptor antagonist with antiallergic properties. It has marked affinity for peripheral histamine H1-receptors and, at the standard dose of 10mg daily, lacks the CNS depressant effects of standard antihistamines. In addition, it inhibits histamine release and eosinophil chemotaxis during the secondary phase of the allergic response. Results from controlled clinical trials indicate that cetirizine is an effective and well tolerated treatment of seasonal and perennial allergic rhinitis and chronic idiopathic urticaria. Cetirizine appears to be as effective as conventional dosages of terfenadine, chlorpheniramine and hydroxyzine in relieving symptoms associated with these disorders and produces a markedly lower incidence of sedation than chlorpheniramine, hydroxyzine and several other standard antihistamines. Thus, cetirizine appears to provide a useful alternative to other 'nonsedating' antihistamines; cetirizine may also have a future role in the treatment of allergic asthma and certain forms of physical urticaria.
Cetirizine: actions on neurotransmitter receptors.[Pubmed:1979798]
J Allergy Clin Immunol. 1990 Dec;86(6 Pt 2):1025-8.
First-generation H1-antagonist antihistamines, such as hydroxyzine, have the ability to cross the blood-brain barrier and cause sedation, which limits their usefulness in the treatment of allergic disorders. Cetirizine, a carboxylated metabolite of hydroxyzine, possesses the parent compound's antihistaminic activity but causes less sedation. We compared the activity of cetirizine at central H1 sites with that of hydroxyzine and terfenadine. We also compared the ability of cetirizine and three antihistamines to cross the blood-brain barrier. In each case we found that the drug's potency at H1 receptors in the central nervous system was similar to its activity in displacing H1 receptors in the lung. However, the selectivity for H1 receptors varied widely from drug to drug. Cetirizine did not bind at any of the receptors investigated, except H1 sites, even at concentrations as high as 10 mumol/L. Hydroxyzine and dexchlorpheniramine and, to a lesser extent, terfenadine crossed the blood-brain barrier in significant amounts. Cetirizine passed into the central nervous system only half as readily as terfenadine. These findings suggest that cetirizine's low incidence of sedative effects is most likely caused by its diminished potential to cross the blood-brain barrier and also may be partly the result of its greater selectivity for H1 receptors, compared with its effect at other receptors that may be involved in sedation.