Ticagrelor

A potent, selective, reversible and oral P2Y12 receptor antagonist with pKi of 8.7; effectively inhibits platelet aggregation without significant increases in bleeding time in vivo; is used for the prevention of thrombotic events (for example stroke or heart attack) in people with acute coronary syndrome or myocardial infarction with ST elevation.Thrombosis Approved (In Vitro) :Ticagrelor promotes a greater inhibition of adenosine 5′-diphosphate (ADP) –induced Ca2+ release in ished platelets vs other P2Y12R antagonists. This additional effect of ticagrelor beyond P2Y12R antagonism is in part as a consequence of ticagrelor inhibiting the equilibrative nucleoside transporter 1 (ENT1) on platelets, leading to accumulation of extracellular adenosine and activation of Gs-coupled adenosine A2A receptors. B16-F10 cells exhibit decreased interaction with platelets from ticagrelor-treated mice compared to saline-treated mice. (In Vivo) :In B16-F10 melanoma intravenous and intrasplenic metastasis models, mice treated with a clinical dose of ticagrelor (10 mg/kg) exhibits marked reductions in lung (84%) and liver (86%) metastases. Furthermore, ticagrelor treatment improves survival compared to saline-treated animals. A similar effect is observed in a 4T1 breast cancer model, with reductions in lung (55%) and bone marrow (87%) metastases following ticagrelor treatment. Single oral administration of ticagrelor (1-10 mg/kg) causes dose-related inhibitory effect on platelet aggregation. Ticagrelor, at the highest dose (10 mg/kg) significantly inhibits platelet aggregation at 1 h after dosing and the peak inhibition is observed at 4 h after dosing.

274693-27-5

AR-C 126532XX | AZD 6140 | AZD6140 | AZD-6140

Pharmacology & Drug Discovery

>98% (HPLC)

10 mM in DMSO

O[C@H]1[C@@H] (O) [C@H] (N2N=NC3=C (N[C@H]4[C@H] (C5=CC=C (F) C (F) =C5) C4) N=C (SCCC) N=C32) C[C@@H]1OCCO

C23H28F2N6O4S

522.5681

Storage temperature: -20°C. Stability: ≥ 2 years

For research use only.