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Nedocromil (sodium salt) Sale

(Synonyms: 奈多罗米钠,FPL 59002KP; Nedocromil disodium salt) 目录号 : GC44360

A mast cell stabilizer

Nedocromil (sodium salt) Chemical Structure

Cas No.:69049-74-7

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实验参考方法

Animal experiment:

Mice[2]8-12 weeks old C57/BL6 male mice between 23-25 g receive intraperitoneal (i.p.) injections of 50 mg/kg Streptozotocin (STZ), dissolved in 100 mM citrate buffer pH 4.5, for five consecutive days. Diabetic mice (13-week-old) are randomly divided into three groups: 1) untreated group; 2) Nedocromil group, with Nedocromil released at the rate of 30 mg/kg per day from a subcutaneous (s.c.) pellet implantation; and vehicle group, with an inactive pellet implanted. Normal mice (non-diabetic) and normal mice that receive Nedocromil (30 mg/kg per day) are also included in this study for comparison. All sample groups included 15 mice (n=15)[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.

产品描述

Nedocromil sodium suppresses the action or formation of multiple mediators, including histamine, leukotriene C4 (LTC4), and prostaglandin D2 (PGD2).

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].

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.

Chemical Properties

Cas No. 69049-74-7 SDF
别名 奈多罗米钠,FPL 59002KP; Nedocromil disodium salt
Canonical SMILES O=C(C=C(C([O-])=O)O1)C(C1=C2CCC)=CC3=C2N(CC)C(C([O-])=O)=CC3=O.[Na+].[Na+]
分子式 C19H15NO7•2Na 分子量 415.3
溶解度 DMSO: 20 mg/ml,Ethanol: 30 mg/ml,PBS (pH 7.2): 1 mg/ml 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.4079 mL 12.0395 mL 24.079 mL
5 mM 0.4816 mL 2.4079 mL 4.8158 mL
10 mM 0.2408 mL 1.2039 mL 2.4079 mL
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Research Update

Nedocromil sodium. An updated review of its pharmacological properties and therapeutic efficacy in asthma

Drugs 1993 May;45(5):693-715.PMID:7686465DOI:10.2165/00003495-199345050-00007.

Nedocromil sodium, the disodium salt of a pyranoquinoline dicarboxylic acid, has anti-inflammatory properties in vitro, in animal models of asthma, and in humans, as evidenced by inhibition of inflammatory cell activation and mediator release, early and late allergen-induced bronchoconstriction and airway hyperresponsiveness. Recent therapeutic trials confirm the safety and efficacy of inhaled Nedocromil sodium as adjunctive therapy in adult patients whose asthma is not adequately controlled by beta-agonists alone. Nedocromil sodium has also been shown to improve symptoms when added to existing treatment with methylxanthines and corticosteroids. Some studies show Nedocromil sodium to be successful replacement therapy for methylxanthines, in addition to enabling a modest reduction in inhaled corticosteroids in some patients. Thus, Nedocromil sodium may be suitable in patients with asthma as an adjunct to existing therapy, as an alternative to regularly administered oral and inhaled beta-agonists and oral methyl-xanthines, and potentially, to low dose inhaled corticosteroids as maintenance therapy in patients with mild to moderate asthma being considered for corticosteroid therapy.

Chloride transport and the actions of Nedocromil sodium and cromolyn sodium in asthma

J Allergy Clin Immunol 1996 Nov;98(5 Pt 2):S102-5; discussion S105-6.PMID:8939184doi

Nedocromil sodium has been shown to be capable of inhibiting chloride ion flux in mast cells, epithelial cells, and neurons. This feature may explain how it can prevent responses such as mast-cell degranulation, the effects of osmolarity changes in the airways, and neuronal activation. This mechanism may also provide a unifying hypothesis to explain the effects of Nedocromil sodium on a range of cell types involved in asthma, such as sensory and efferent neurons and cells involved in inflammation.

The effect of Nedocromil sodium on childhood asthma during the viral season

Am J Respir Crit Care Med 1995 Dec;152(6 Pt 1):1879-86.PMID:8520750DOI:10.1164/ajrccm.152.6.8520750.

Viral-induced symptomatic respiratory infections (SRI) frequently cause exacerbations of asthma in children. This study investigated the protective effects of 0.5% Nedocromil sodium nebulizer solution given three times a day in preventing asthma exacerbations associated with SRI. Ninety-three mild-moderate asthmatic children (6 to 12 yr of age) received either 0.5% Nedocromil sodium or placebo for 24 wk during the viral season. The Nedocromil sodium group was symptom-free 58% of the days, and the placebo-treated patients were symptom-free 45% of the days (p = 0.027). During Weeks 1-12, significant differences favored Nedocromil sodium for asthma summary score (means: Nedocromil sodium = 0.61, placebo = 0.92; p = 0.026), and daytime asthma (Nedocromil sodium = 0.78, placebo = 1.22; p = 0.03). Significant differences were noted during monthly intervals for cough (Weeks 1-4: Nedocromil sodium = 0.61, placebo = 0.92, p = 0.027) and peak expiratory flow rate (PEFR) (Nedocromil sodium 262, placebo = 254 L/min, p = 0.041 Weeks 9-12). Patients in the active treatment group reduced their need for rescue inhaled beta 2-agonist by 10%, whereas patients treated with placebo demonstrated a 24% increase. There was a strong correlation between asthma symptoms and SRI symptoms (r = 0.47; p < 0.001). During SRIs, patients in the Nedocromil sodium group demonstrated more rapid resolution of asthma symptoms immediately following infection (p = 0.033 summary score, p = 0.039 sleep difficulty). No serious adverse events were noted. Nedocromil sodium did not prevent the infection or exacerbation of asthma symptoms during SRI.(ABSTRACT TRUNCATED AT 250 WORDS)

Nedocromil sodium: a new drug for the management of bronchial asthma

Thorax 1984 Nov;39(11):809-12.PMID:6150563DOI:10.1136/thx.39.11.809.

Nedocromil sodium (FPL 59002) is a pyranoquinoline dicarboxylic acid that has been developed for the management of bronchial asthma. We report the results of a double blind group comparative trial in which the disodium salt of Nedocromil delivered by pressurised aerosol and a placebo were compared in the management of patients with a diagnosis of bronchial asthma who entered the double blind period on a minimum dose of beclomethasone dipropionate. In almost all the assessments of clinical activity Nedocromil sodium was shown to be more effective than placebo. These include improvements in diary card symptom scores, reduction in concomitant use of a bronchodilator aerosol, and patients' and investigators' assessments of efficacy. Unwanted effects were few and mild. No patients were withdrawn from the trial.

Nedocromil sodium inhibits the increase in airway reactivity induced by platelet activating factor in humans

Chest 1992 Jul;102(1):123-8.PMID:1320563DOI:10.1378/chest.102.1.123.

To investigate the effect of Nedocromil sodium on changes in airway reactivity to methacholine induced by platelet activating factor, we studied 12 nonasthmatic, nonatopic subjects (24 to 41 years) in a double-blind trial. The FEV1 and airflow at 30 percent of vital capacity from a partial forced expiration (V30p) were used to assess changes in airway caliber. Two concentration-response curves to doubling concentrations of MCh (from 0.3 mg/ml) were performed 48 h apart. The concentrations of MCh causing a 20 percent fall in FEV1 (PC20FEV1) or a 40 percent fall in V30p (PC40V30p) were calculated. After the first MCh challenge, subjects were matched by airway reactivity and randomly assigned to Nedocromil sodium (two puffs qid 2 mg/puff) or placebo treatment. Two days after the second MCh challenge, PAF was inhaled, and changes in airway caliber were recorded. Administration of either Nedocromil sodium or placebo was ended at this time and airway response to MCh was assessed two days after PAF. The two concentration-response curves to MCh obtained before PAF exposure were superimposable. The PAF caused a dose-related bronchoconstriction in both groups; the maximal fall in V30p was 27.6 +/- 6.6 percent (mean +/- SE) in the Nedocromil sodium group and 37.4 +/- 4.6 percent in the placebo group. Two days after PAF, the PC20FEV1 did not change in subjects who received Nedocromil sodium (4.86 vs 4.32 mg/ml; geometric mean), but it fell from 6.59 to 1.12 mg/ml (p less than 0.05) in placebo-treated subjects. These results indicate that Nedocromil sodium inhibits PAF-induced increase in airway reactivity.