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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

The mechanism by which epinastine stops an adenosine analog from contracting BDE rat airways.

Epinastine is an antihistamine and antiallergic drug. The object of this work was to use a rat model of noncholinergic bronchospasm to identify novel nonantihistamine mechanisms that might contribute to the efficacy of this drug in asthma. Oral epinastine blocked bronchospasm (increase in RL) in BDE rats induced by the adenosine A3 receptor agonist N6-2-(4-aminophenyl)ethyladenosine with an ED50 of only 0.47 mg/kg. An intravenous dose of 10 microg/kg epinastine was also effective. In vitro, epinastine bound 5-HT2a, 5-HT7, and 5-HT3 receptors (Ki values, respectively, 21, 33, and 159 nM). In the in vivo rat model, 5-HT2a antagonist ketanserin, 5-HT7 agonist 5-carboxamidotryptamine, and (to a limited extent) 5-HT3 antagonist ondansetron could all, like epinastine, block bronchospasm, but the "classic" antihistamine chlorpheniramine was ineffective. Epinastine could not block bronchospasm in the presence of 1 mg/kg NK2 receptor antagonist L 659877 or 20 microg/kg potassium channel blocker iberiotoxin, suggesting the epinastine was acting on a neurokinin- and potassium channel-mediated mechanism. Epinastine has other modes of action apart from its antihistamine activity that may be relevant to its use in asthma.[1]


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