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CAS 151767-02-1 Montelukast Sodium Leukotriene Receptor Antagonist Montelukast Sodium API

CAS 151767-02-1 Montelukast Sodium Leukotriene Receptor Antagonist Montelukast Sodium API

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    CAS 151767-02-1 Montelukast Sodium


    Montelukast Sodium Leukotriene Receptor


    151767-02-1 Antagonist Montelukast Sodium

  • Product Name
    Montelukast Sodium
  • Boiling Point
    750.5ºC At 760mmHg
  • CAS No
  • Point Of Flammability
  • Appearance
    White To Tan
  • Place Of Origin
  • Molecular Formula
  • Molecular Weight
  • Shelf Life
    2 Years
  • Storage
    Cool Dry Place
  • Place of Origin
  • Brand Name
    Kan Ying
  • Minimum Order Quantity
  • Price
    To discuss
  • Packaging Details
  • Delivery Time
  • Payment Terms
    L/C, D/A, D/P, T/T, Western Union, MoneyGram,Dollars
  • Supply Ability

CAS 151767-02-1 Montelukast Sodium Leukotriene Receptor Antagonist Montelukast Sodium API

Montelukast sodium leukotriene receptor antagonist Montelukast sodium API quality assurance CAS 151767-02-1 

1. Product name:Montelukast sodium
[R - (E)] - 1 - [[[1 - [3 - (2 - (7 - chloro - 2 - quinoline) vinyl] phenyl - 3 - [2 - (1 - hydroxy - 1 - methyl ethyl) phenyl] propyl] sulfur) methyl] cyclopropane sodium acetate | | LuSi meng meng sodium, sodium reference substance
2. Montelukast sodium basic information


product name Montelukast sodium
CAS no 151767-02-1
Boiling point 750.5ºC at 760mmHg
Molecular formula C35H35ClNNaO3S
Molecular weight 608.165
Flash point 407.7ºC
Precise quality 607.192383
PSA 98.55000
LogP 7.61330
Appearance white to tan
Storage conditions -20°C Freezer, Under Inert Atmosphere
Water solubility DMSO: ≥8mg/mL at 60°C


3. Montelukast sodium Usage And Synthesis:

Pharmacological effect Cysteinyl leukotrienes (LTC4, LTD4, LTE4) is a eicosane-type substance released by various kinds of cells including mast cells and eosinophils with strong inflammatory effect. These important asthma pre-inflammatory mediators can bind to the Cysteinyl leukotriene receptors (CysLT) identified in the human airways, resulting in a variety of airway responses including bronchoconstriction, mucus secretion, increased vascular permeability, and eosinophil accumulation.
Montelukast sodium is an orally active selective leukotriene receptor antagonist that can specifically inhibit the cysteinyl leukotriene receptor. It was successfully developed by the Merck Company (German) and had entered into market in Canada, Finland, and Mexican in 1997. It is suitable for the prevention and long-term treatment of adults and children asthma, including the prevention of daytime and nighttime asthma symptoms, the treatment of asthma patients who are aspirin-sensitive and prevention of exercise-induced bronchial contraction, it can also be used to relieve the seasonal allergic rhinitis symptoms of 15 year-old or over 15 year-old patients whose symptoms are invalid and intolerant to other treatment.


Montelukast is a selective leukotriene receptor antagonist and has been approved for the oral administration treatment of asthma and allergic rhinitis. It is also a potent oral preparation that can significantly improve the inflammatory indicators. Biological determination of biochemistry and pharmacology has showed that montelukast sodium has a high affinity and selectivity to the CysLT1 receptors (compared with other kinds of pharmacologically important airway receptors such as prostanoid, cholinergic and β-adrenergic receptors). Montelukast can effectively suppress the physiological effects caused by the binding between LTC4, LTD4 and LTE4 receptor and CysLT1 receptor without any receptor agonistic activity. There is the secondary type of cysteinyl leukotriene receptor (CysLT2) presented in the lungs cysteinyl leukotriene receptor but may be limited to the blood vessels. So far, researchers haven’t cloned two receptors so the situation of CysLT receptor is illustrated through binding assay and pharmacological analysis. It has been now thought that montelukast does not antagonize CysLT2 receptors.

Uses It can be applied to alleviate the symptoms caused by allergic rhinitis.
Description Montelukast was launched as Singulair in Mexico and Finland for the management of mild to moderate asthma inadequately controlled by inhaled corticosteroids and short-acting beta2-agonists. Montelukast can be obtained by an seven-step synthesis from 3-[2(E)-(7-chloroquinolin-2-yl)vinyl] benzaldehyde. Montelukast is a potent, selective and orally active antagonist of the CysLT1 (formerly called LTD4) receptor, thus blocking the effects of the cysteinyl leukotrienes LTC4, LTD4 and LTE4 on microvascular permeability and the activation of eosinophils. Montelukast represents the third molecule of this class which has been approved in asthma after pranlukast (1995) and zafirlukast (1996). Montelukast has been studied extensively in placebo-controlled clinical trials, in mildly or severe asthmatic patients challenged with LTD4 or exercise. A variety of acute bronchoconstricting challenges were inhibited or attenuated with all doses used. Montelukast demonstrated clinically significant improvements in the parameters of asthma control associated with an appreciable improvement in quality of life., reducing days with asthma exacerbations and allowing significant tapering of corticosteroids. Montelukast is well-tolerated and only needs to be administered once a day.


Uses A selective leukotriene D4-receptor antagonist. Used as an antiasthmatic
Uses antiinfective
Uses A potent and highly selective CysLT1 receptor antagonist, without demonstrated CysLT2 activity


4. Montelukast sodium indications:

It is indicated for the prevention and long-term treatment of asthma in adults and children, including the prevention of daytime and nighttime asthma symptoms, the treatment of asthmatic patients who are sensitive to aspirin, and the prevention of exercise-induced bronchoconstriction.


5.Matters needing attention:

1. It is forbidden for those who are allergic to any ingredients of this product.
2. The efficacy of oral administration of this drug in the treatment of acute asthma attacks has not been established. Therefore, oral administration of this drug should not be used in the treatment of acute asthma attacks, and patients should be advised to prepare necessary first aid medicines.
3. Although concomitant doses of inhaled corticosteroids may be reduced gradually under the supervision of a physician, they should not be taken abruptly in place of inhaled or oral corticosteroids.
4. Effects on pregnancy and lactation: the application of this drug in pregnant women has not been studied yet, and it is only used during pregnancy when it is very necessary. It is not known whether the drug is excreted in the human breast. Because many drugs are excreted in the body through milk, they should be used with caution in lactating women.
5. Effect on children: Safe and effective dose and usage of children under 6 years old have not been studied.
6, medication for the elderly: the efficacy or safety of this drug has nothing to do with age


6. In vitro studies:

Montelukast may help reduce eosinophil inflammation in upper airway inflammatory diseases such as rhinitis and nasal polyps. Montelukast significantly inhibited FBS induced secretion of GM-CSF, IL-6 and IL-8 in nasal mucosa and polyp epithelial cells, but not sicAM-1. Montelukast also showed inhibition of ECM-induced eosinophil survival in nasal mucosa and polyp epithelial cells (P & LT; 0.05) [1].

7.In vivo study

Montelukast significantly reduced mild, moderate, and partial severe exacerbations of chronic mild to moderate asthma, but was less effective for ICS or ICS plus LABA [2]. Airway NK1R expression was up-regulated in asthma-induced rats, and montelukast could down-regulate the expression of NK1R during airway remodeling [3]. Repeated treatment with Montelukast (1 or 2 mg/kg, ig, 4 weeks) to block CysLT1R decreased the expression of CysLT1R induced by Aβ1-42, and inhibited the increase of NF-κBp65, TNF-α, IL- induced by Aβ1-42, 1β and caspase-3 activation. Bcl-2 is down-regulated in the hippocampus and cortex. Correspondingly, montelukast treatment significantly improved memory impairment in mice induced by Aβ1-42, but had little effect on normal mice [4].

8. Cell experiment

Nasal mucosa and polyp epithelial cells were stimulated by fetal bovine serum (FBS) with or without MK for 24 h. Cytokine concentrations in epithelial secretions were measured by ELISA. Peripheral blood eosinophils were incubated with epithelial conditioned medium (ECM) with or without montelukast for up to 3 days, and the survival of eosinophils was assessed by trypan blue dye removal [1].
CAS 151767-02-1 Montelukast Sodium Leukotriene Receptor Antagonist Montelukast Sodium API 0

9. Experiments on animals

Rats: 24 Sprague Dawley rats were randomly divided into control group, asthma group and Montelukast group. A rat model of asthma was induced by ovalbumin (OVA) inhalation. Saline was used instead of sensitizing solution and 1% OVA in the control group. Each rat in the montelukast group was given montelukast (15mg/kg) in tube feeding 2 hours before OVA inhalation. All rats were treated for 8 weeks [3]. Mice: Montelukast was dissolved in 0.5% sodium carboxymethyl cellulose (CMC-NA). Mice were randomly divided into four groups :(1) vector plus vector, (2) Aβ1-42 vector plus vector, (3) Aβ1-42 gammontelukast (1.0mg/kg), (4) Aβ1-42 gammontelukast (2.0mg/kg). The solution was injected bilaterally into the ventricle through a micropipette [4].

CAS 151767-02-1 Montelukast Sodium Leukotriene Receptor Antagonist Montelukast Sodium API 1