Cyclodextrins against asthma?

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A recently reported finding of Canadian researchers proved the specific effect of lysophosphatidic acid (LPA, see the structure below) by activation of carotid bodies in asthmatic bronchoconstriction [1]. Bronchoconstriction is the leading cause of hospitalization and asthmatic sudden death. LPA is an important biomarker of the immune response in the murine house dust model of asthma and is found in human bronchiolar lavage fluid following asthmatic challenge. The Canadian group proved that LPA released from asthmatic lung in response to allergen activates transient receptor potential cation channel vanilloid 1 receptors (TRPV1) in the carotid body causing acute bronchoconstriction.

Wilson’s group showed that blocking LPA receptors by antagonists reduces acute bronchoconstriction.

Looking at the structure of LPA the question arises:

if complexation of LPA by alpha-CDs (HPACD or RAMEA) would hinder LPA binding to the receptors causing similarly reduced bronchoconstriction.


LPA structure


  1. G. Jendzjowsky, A. Roy, N. O. Barioni, M. M. Kelly, F. H. Y. Green, C. N. Wyatt, R. L. Pye, L. Tenorio-Lopes & R. J. A. Wilson Preventing acute asthmatic symptoms by targeting a neuronal mechanism involving carotid body lysophosphatidic acid receptors. Nature Communication 2018, 9, 4030

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