Montelukast Dicyclohexylamine Salt

Modify Date: 2024-01-09 10:02:20

Montelukast Dicyclohexylamine Salt structure	Common Name	Montelukast Dicyclohexylamine Salt
	CAS Number	577953-88-9	Molecular Weight	767.501
	Density	N/A	Boiling Point	N/A
	Molecular Formula	C47H59ClN2O3S	Melting Point	65-67°C (lit.)
	MSDS	N/A	Flash Point	N/A

Purity		Quantity		Budget		Inquiry

Use of Montelukast Dicyclohexylamine Salt Montelukast (MK0476) dicyclohexylamine is a potent, selective and orally active antagonist of cysteinyl leukotriene receptor 1 (CysLT1). Montelukast dicyclohexylamine can be used for the reseach of asthma and liver injury. Montelukast dicyclohexylamine also has an antioxidant effect in intestinal ischemia-reperfusion injury, and could reduce cardiac damage. Montelukast dicyclohexylamine decreases eosinophil infiltration into the asthmatic airways. Montelukast dicyclohexylamine can also be used for COVID-19 research[1][2][3][4].

• Properties

• Spectrum

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 Names

Name	1-(((1(R)-(3-(2-(7-chloro-2-quinolinil)ethenyl)phenyl)-3-(2-(1-hydroxy-1-methylethyl)phenyl)propyl)thio)methyl)cyclopropane acetic acid dicyclohexylamine salt
Synonym	More Synonyms

 Montelukast Dicyclohexylamine Salt Biological Activity

Description	Montelukast (MK0476) dicyclohexylamine is a potent, selective and orally active antagonist of cysteinyl leukotriene receptor 1 (CysLT1). Montelukast dicyclohexylamine can be used for the reseach of asthma and liver injury. Montelukast dicyclohexylamine also has an antioxidant effect in intestinal ischemia-reperfusion injury, and could reduce cardiac damage. Montelukast dicyclohexylamine decreases eosinophil infiltration into the asthmatic airways. Montelukast dicyclohexylamine can also be used for COVID-19 research[1][2][3][4].
Related Catalog	Signaling Pathways >> GPCR/G Protein >> Leukotriene Receptor Research Areas >> Inflammation/Immunology
Target	CysLT1
In Vitro	Montelukast (5 μM; 1 h) inhibits APAP (Acetaminophen) (HY-66005)-induced cell damage[1]. Montelukast (0.01-10 μM, 30 min) diminishes the 5-oxo-ETE–induced cell migration and modulates the activation of the plasmin-plasminogen system[3]. Montelukast (10 μM, 18 h) modulates the activation of MMP-9[3]. Cell Migration Assay [3] Cell Line: Eosinophils Concentration: 0.01-10 μM Incubation Time: 30 min Result: Diminished the 5-oxo-ETE–induced cell migration. Western Blot Analysis[3] Cell Line: Eosinophils Concentration: 10 μM Incubation Time: 18 h Result: Reduced the 5-oxo-ETE–boosted MMP-9 secretion.
In Vivo	Montelukast (3 mg/kg; oral gavage) protects against APAP-induced hepatotoxicity in mice[1]. Montelukast (1 mg/kg; miniosmotic pump administration) reduces the airway remodeling changes observed in OVA-treated mice and blocks the actions of cysteinyl leukotrienes (LT) C4, D4, and E4 mediated by the CysLT1 receptor[2]. Montelukast (1 mg/kg; miniosmotic pump administration) reduces the elevated levels of IL-4 and IL-13 found in the BAL fluid of OVA-treated mice[2]. Animal Model: C57BL/6J mice (8-week-old; 22-25 g) are induced acute hepatic injury[1] Dosage: 3 mg/kg Administration: Oral gavage 1 h after saline or APAP administration Result: Decreased serum levels of alanine transaminase (ALT) and aspartate aminotransferase (AST), and alleviated liver damage.
References	[1]. Pu S, et, al. Montelukast Prevents Mice Against Acetaminophen-Induced Liver Injury. Front Pharmacol. 2019 Sep 18; 10:1070. [2]. William RHJ, et, al. A role for cysteinyl leukotrienes in airway remodeling in a mouse asthma model. Am J Respir Crit Care Med. 2002 Jan 1; 165(1): 108-16. [3]. Langlois A, et al. Montelukast regulates eosinophil protease activity through a leukotriene-independent mechanism. J Allergy Clin Immunol. 2006;118(1):113-119. [4]. Khan AR, et al. Montelukast in hospitalized patients diagnosed with COVID-19. J Asthma. 2022 Apr;59(4):780-786.

 Chemical & Physical Properties

Melting Point	65-67°C (lit.)
Molecular Formula	C47H59ClN2O3S
Molecular Weight	767.501
Exact Mass	766.393494
PSA	107.75000
LogP	12.58030
Storage condition	2-8°C

 Safety Information

Hazard Codes	Xi
RIDADR	NONH for all modes of transport

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