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P2Y receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database
Author(s) -
Maria P. Abbracchio,
JeanMarie Boeynaems,
José L. Boyer,
Geoffrey Burnstock,
Stefania Ceruti,
Marta Fumagalli,
Christian Gachet,
Rebecca Hills,
Robert G. Humphries,
Kazu Inoue,
Kenneth A. Jacobson,
Charles Kennedy,
Brian F. King,
Davide Lecca,
Christa E. Müller,
María Teresa MirasPortugal,
Vera Ralevic,
Gary A. Weisman
Publication year - 2019
Publication title -
iuphar/bps guide to pharmacology cite
Language(s) - English
Resource type - Journals
ISSN - 2633-1020
DOI - 10.2218/gtopdb/f52/2019.4
Subject(s) - receptor , p2y receptor , prasugrel , p2y12 , pharmacology , cangrelor , uridine triphosphate , chemistry , agonist , platelet , medicine , biochemistry , nucleotide , platelet aggregation , aspirin , clopidogrel , gene
P2Y receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on P2Y Receptors [3, 5]) are activated by the endogenous ligands ATP, ADP, uridine triphosphate, uridine diphosphate and UDP-glucose. The relationship of many of the cloned receptors to endogenously expressed receptors is not yet established and so it might be appropriate to use wording such as 'uridine triphosphate-preferring (or ATP-, etc.) P2Y receptor' or 'P2Y1-like', etc., until further, as yet undefined, corroborative criteria can be applied [46, 109, 187, 375, 388].Clinically used drugs acting on these receptors include the dinucleoside polyphosphate diquafosol, agonist of the P2Y2 receptor subtype, approved in Japan for the management of dry eye disease [236], and the P2Y12 receptor antagonists prasugrel, ticagrelor and cangrelor, all approved as antiplatelet drugs [52, 316].

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