Disease relevance of Cinalukast

• Studies of the combination of Ro 24-5913, a peptidoleukotriene antagonist, and Ro 24-4736, a PAF antagonist, in guinea pig and rat models of lung inflammation [1].

High impact information on Cinalukast

• CONCLUSION: Orally administered cinalukast provides at least 8 hours of protection against exercise-induced bronchoconstriction [2].
• In vitro, Ro 24-5913 competes with [3H]LTD4 for its binding site on guinea pig lung membranes with an IC50 of 6.4 +/- 2.2 nM [3].
• In summary, Ro 24-5913 is representative of a novel chemical class of LTD4 receptor antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)[3]
• In comparison with other LTD4 antagonists evaluated in this guinea pig model, Ro 24-5913 is markedly superior in terms of oral potency, bioavailability and oral duration of action [3].
• The host-guest complexation processes between cinalukast and alpha-CyD or heptakis-(2,6-di-O-methyl)-beta-cyclodextrin (DIMEB) and between montelukast and DIMEB have been investigated by fluorescence spectroscopy [4].

Biological context of Cinalukast

• In vivo, Ro 24-5913 dose-dependently inhibits LTD4-induced bronchoconstriction in guinea pigs by the i.v. (ID50 0.13 mg/kg), oral (ID50 0.12 mg/kg) and aerosol (IC50 0.008%) routes of administration [3].

Associations of Cinalukast with other chemical compounds

• OBJECTIVES: The degree and duration of protection against exercise-induced bronchoconstriction afforded by three doses of a specific leukotriene D4 receptor antagonist, cinalukast, were assessed after an initial dosing and after 1 week of therapy [2].
• This in vivo activity is specific as evidenced by the inability of Ro 24-5913 to inhibit bronchoconstriction induced by LTB4, PAF or histamine [3].

References