par Boeynaems, Jean-Marie 
;Robaye, Bernard ;Janssens, Rodolphe ;Suarez Gonzalez, Nathalie ;Communi, Didier
Référence Drug development research, 52, 1-2, page (187-189)
Publication Publié, 2001-02
;Robaye, Bernard ;Janssens, Rodolphe ;Suarez Gonzalez, Nathalie ;Communi, Didier Référence Drug development research, 52, 1-2, page (187-189)
Publication Publié, 2001-02
Article révisé par les pairs
| Résumé : | Currently the only P2Y receptor subtype targeted by drugs in clinical use is the P2TAC (or P2Y12) receptor, which has been recently cloned and is only distantly related to other P2Y subtypes. It is believed that the active metabolites of thienopyridine antithrombotic agents (ticlopidine, clopidogrel) bind covalently to that receptor and inactivate it in an irreversible way. The same receptor is also the target of competitive antagonists derived from ATP, such as AR-C69931MX. Other subtypes also have potential as pharmacotherapeutic targets. The demonstration that P2Y1–/– mice have a defective platelet aggregation and increased resistance to thromboembolism suggests that P2Y1 antagonists could constitute a new class of antithrombotic agents. Activation of the P2Y2 receptor by aerosolized UTP and derivatives constitutes one strategy for the symptomatic treatment of cystic fibrosis and other obstructive airway diseases. The study of P2Y2–/– mice suggests that P2Y4 and P2Y6 receptors might constitute additional targets in that framework. P2Y6 receptor antagonists might be useful in inflammatory bowel disease in view of their expression on activated T lymphocytes infiltrating the lesions in patients. The P2Y11 receptor mediates the stimulatory effect of ATP on the granulocytic differentiation of HL-60 promyelocytic leukemia cells, suggesting that P2Y11 agonists might be useful in the treatment of some forms of neutropenia and leukemia. Drug Dev. Res. 52:187–189, 2001. © 2001 Wiley-Liss, Inc. |
