Ticagrelor

Research use only, not for human use.

A potent, selective, reversible and oral P2Y12 receptor antagonist with pKi of 8.7.

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.

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 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.

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

GPCR/G Protein

P2Y Receptor

CYP2C9|Midazolam4-hydroxylation|P2Y12

Cardiovascular Disease

Thrombosis

274693-27-5

522.5681

C23H28F2N6O4S

>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

1,2-Cyclopentanediol, 3-[7-[[(1R,2S)-2-(3,4-difluorophenyl)cyclopropyl]amino]-5-(propylthio)-3H-1,2,3-triazolo[4,5-d]pyrimidin-3-yl]-5-(2-hydroxyethoxy)-, (1S,2S,3R,5S)-

(-20℃)

With Ice Pack

≥ 2 years