NedocromilCAS# 69049-73-6 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 69049-73-6 | SDF | Download SDF |
| PubChem ID | 50294 | Appearance | Powder |
| Formula | C19H17NO7 | M.Wt | 371.34 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | FPL 59002 | ||
| Solubility | DMSO : 16.67 mg/mL (44.89 mM; Need ultrasonic) | ||
| Chemical Name | 9-ethyl-4,6-dioxo-10-propylpyrano[3,2-g]quinoline-2,8-dicarboxylic acid | ||
| SMILES | CCCC1=C2C(=CC3=C1OC(=CC3=O)C(=O)O)C(=O)C=C(N2CC)C(=O)O | ||
| Standard InChIKey | RQTOOFIXOKYGAN-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C19H17NO7/c1-3-5-9-16-10(13(21)7-12(18(23)24)20(16)4-2)6-11-14(22)8-15(19(25)26)27-17(9)11/h6-8H,3-5H2,1-2H3,(H,23,24)(H,25,26) | ||
| 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. | ||
Nedocromil Dilution Calculator
Nedocromil Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.6929 mL | 13.4647 mL | 26.9295 mL | 53.859 mL | 67.3237 mL |
| 5 mM | 0.5386 mL | 2.6929 mL | 5.3859 mL | 10.7718 mL | 13.4647 mL |
| 10 mM | 0.2693 mL | 1.3465 mL | 2.6929 mL | 5.3859 mL | 6.7324 mL |
| 50 mM | 0.0539 mL | 0.2693 mL | 0.5386 mL | 1.0772 mL | 1.3465 mL |
| 100 mM | 0.0269 mL | 0.1346 mL | 0.2693 mL | 0.5386 mL | 0.6732 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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Nedocromil suppresses the action or formation of multiple mediators, including histamine, leukotriene C4 (LTC4), and prostaglandin D2 (PGD2).
In Vitro:Nedocromil inhibits the release of histamine, LTC4, and PGD2 from mast cells challenged with antigen (with IC30 values of 2.1 μM, 2.3 μM, and 1.9 μM, respectively) and with anti-human IgE (IC30 values of 4.7 μM, 1.3 μM, and 1.3 μM, respectively)[1].
In Vivo:Nedocromil-treated diabetic mice show significantly improved heart function compared with controls. The contractility and relaxation forces show similar improvements. However, the cardiac function of Nedocromil-treated diabetic mice remains significantly impaired when compared with normal mice. Nedocromil can significantly improve cardiac function in mice with diabetic cardiomyopathy, but the treatment cannot restore normal function[2].
References:
[1]. Wells E, et al. Characterization of primate bronchoalveolar mast cells. II. Inhibition of histamine, LTC4, and PGD2 release from primate bronchoalveolar mast cells and a comparison with rat peritoneal mastcells. J Immunol. 1986 Dec 15;137(12):3941-5.
[2]. Myocardial remodeling in diabetic cardiomyopathy associated with cardiac mast cell activation. Huang ZG, et al. PLoS One. 2013;8(3):e60827.
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G-protein-coupled receptor 35 is a target of the asthma drugs cromolyn disodium and nedocromil sodium.[Pubmed:20559017]
Pharmacology. 2010;86(1):1-5.
We report that the asthma drugs cromolyn disodium and Nedocromil sodium are potent G-protein-coupled receptor 35 (GPR35) agonists. We utilized calcium flux and inositol phosphate accumulation assays to examine the pharmacology of these asthma drugs on the human, mouse and rat GPR35. The compounds were more potent on the human GPR35 than on mouse and rat receptors. In contrast, zaprinast, a known GPR35 agonist, was more potent on mouse and rat GPR35 than the human ortholog. We show by quantitative PCR that GPR35 is expressed in human mast cells, human basophils and human eosinophils. We also demonstrate that GPR35 mRNA is upregulated upon challenge with IgE antibodies. We show that, unlike zaprinast, a potent phosphodiesterase 5 (PDE5) inhibitor, cromolyn disodium and Nedocromil sodium lack inhibitory activity towards PDE5. These findings suggest that GPR35 may play an important role in mast cell biology and be a potential target for the treatment of asthma.
The role of the Annexin-A1/FPR2 system in the regulation of mast cell degranulation provoked by compound 48/80 and in the inhibitory action of nedocromil.[Pubmed:26803520]
Int Immunopharmacol. 2016 Mar;32:87-95.
1.We investigated the role of Annexin (ANX)-A1 and its receptor, ALX/FPR2, in the regulation of mast cell degranulation produced by compound 48/80. 2.Both human cord-blood derived mast cells (CBDMCs) and murine bone marrow derived mast cells (BMDMCs) release phosphorylated ANX-A1 during treatment with glucocorticoids or the mast cell 'stabilising' drugs ketotifen and Nedocromil. 3.Compound 48/80 also stimulated ANX-A1 phosphorylation and release and this was also potentiated by Nedocromil. Anti-ANX-A1 neutralising monoclonal antibodies (Mabs) enhanced the release of pro-inflammatory mediators in response to compound 48/80. 4.Nedocromil and ketotifen potently inhibited the release of histamine, PGD2, tryptase and beta-hexosaminidase from mast cells challenged with compound 48/80. Anti-ANX-A1 neutralising Mabs prevented the inhibitory effect of these drugs. 5.BMDMCs derived from Anx-A1-/- mice were insensitive to the inhibitory effects of Nedocromil or ketotifen but cells retained their sensitivity to the inhibitory action of hu-r-ANX-A1. 6.The fpr2/3 antagonist WRW4 blocked the action of Nedocromil on PGD2, but not histamine, release. BMDMCs derived from fpr2/3-/- mice were insensitive to the inhibitory effects of Nedocromil on PGD2, but not histamine release. 7.Compound 48/80 stimulated both p38 and JNK phosphorylation in CBDMCs and this was inhibited by Nedocromil. Inhibition of p38 phosphorylation was ANX-A1 dependent. 8.We conclude that ANX-A1 is an important regulator of mast cell reactivity to compound 48/80 exerting a negative feedback effect through a mechanism that depends at least partly on the FPR receptor.
