IUPHAR/BPS Guide to Pharmacology CITE

Prostanoid receptors (version 2019.5) in the IUPHAR/BPS Guide to Pharmacology Database

Richard M. Breyer1, Lucie Clapp2, Robert A. Coleman3, Mark Giembycz4, Akos Heinemann5, Rebecca Hills6, Robert L. Jones7, Shuh Narumiya8, Xavier Norel9, Roy Pettipher10, Yukihiko Sugimoto11, Mohib Uddin12, David F. Woodward13 and Chengcan Yao6
  1. Vanderbilt University, USA
  2. University College London, UK
  3. Pharmagene Laboratories, UK
  4. University of Calgary, Canada
  5. Otto Loewi Research Center (for Vascular Biology, Immunology and Inflammation), Austria
  6. University of Edinburgh, UK
  7. University of Strathclyde, UK
  8. Kyoto University Faculty of Medicine, Japan
  9. Laboratory for Vascular Translational Science, France
  10. Atopix Therapeutics Ltd, UK
  11. Kumamoto University, Japan
  12. AstraZeneca, Sweden
  13. Allergan plc, USA


Prostanoid receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Prostanoid Receptors [659]) are activated by the endogenous ligands prostaglandins PGD2, PGE1, PGE2 , PGF, 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.


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Prostanoid receptors
Introduction to Prostanoid receptors
            DP1 receptor
            DP2 receptor
            EP1 receptor
            EP2 receptor
            EP3 receptor
            EP4 receptor
            FP receptor
            IP receptor
            TP receptor


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