Prostanoid receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

Richard M. Breyer; Lucie Clapp; Robert A. Coleman; Mark Giembycz; Akos Heinemann; Rebecca Hills; Robert L. Jones; Shuh Narumiya; Xavier Norel; Roy Pettipher; Yukihiko Sugimoto; David F. Woodward; Chengcan Yao

doi:10.2218/gtopdb/F58/2019.4

Authors

Richard M. Breyer Vanderbilt University
Lucie Clapp University College London https://orcid.org/0000-0001-7802-4481
Robert A. Coleman Pharmagene Laboratories
Mark Giembycz University of Calgary
Akos Heinemann Otto Loewi Research Center (for Vascular Biology, Immunology and Inflammation) https://orcid.org/0000-0002-8554-2372
Rebecca Hills University of Edinburgh
Robert L. Jones University of Strathclyde
Shuh Narumiya Kyoto University Faculty of Medicine
Xavier Norel Laboratory for Vascular Translational Science https://orcid.org/0000-0003-0734-3359
Roy Pettipher Atopix Therapeutics Ltd
Yukihiko Sugimoto Kumamoto University
David F. Woodward Allergan plc
Chengcan Yao University of Edinburgh https://orcid.org/0000-0003-3754-2842

DOI:

https://doi.org/10.2218/gtopdb/F58/2019.4

Abstract

Prostanoid receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Prostanoid Receptors [644]) are activated by the endogenous ligands prostaglandins PGD₂, PGE₁, PGE₂ , PGF_2α, PGH₂, prostacyclin [PGI₂] and thromboxane A₂. Measurement of the potency of PGI₂ and thromboxane A₂ is hampered by their instability in physiological salt solution; they are often replaced by cicaprost and U46619, respectively, in receptor characterization studies.

Prostanoid receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

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