Тикагрелор

In December 2010, the P2Y₁₂ receptor antagonist ticagrelor (also known as AZD6140) was approved in Europe for the treatment of acute coronary syndrome (ACS), a condition that covers several clinical symptoms with the potential to cause acute myocardial ischemia (MI). ADP binds to two purinergic receptors, the P2Y1 and P2Y₁₂ receptors. The action of ADP binding to the P2Y₁₂ receptor results in activation of the GP Ⅱb/Ⅲa (integrin) receptor.GP Ⅱb/Ⅲa initiates and prolongs platelet aggregation, which in turn results in the cross-linking of platelets through fibrin and finally thrombus formation. Inhibition of ADP stimulation of the P2Y₁₂ receptor has been found to be an effective strategy for managing the atherothrombotic events associated with ACS and potentially resulting from percutaneous coronary intervention (PCI, stent implantation) .

White Solid

ChEBI: A triazolopyrimidine that is an adenosine isostere; the cyclopentane ring is similar to ribose and the nitrogen-rich [1,2,3]triazolo[4,5-d]pyrimidine moiety resembles the nucleobase adenine. A platelet aggregation inhibitor which is used for p evention of thromboembolic events in patients with acute coronary syndrome.

Ticagrelor, discovered and developed by AstraZeneca, is a platelet adenosine diphosphate (ADP) P2Y12 (P2T) reversible receptor antagonist approved in the E.U. in 2010 and launched in Germany and the UK in 2011 for the treatment of patients with acute coronary syndromes (ACS). It was approved in the U.S. and Canada in 2011 following successful clinical trial results in patients with ACS which showed it to be superior to preexisting drugs for reducing death due to vascular causes. Ticagrelor is an oral drug indicated for use in combination with acetylsalicylic acid (aspirin) for the prevention of atherothrombotic events in adult patients with ACS (unstable angina, non-ST elevation myocardial infarction (NSTEMI), or ST elevation myocardial infarction (STEMI)). Unlike its competitors prasugrel and clopidogrel, which require bioactivation, ticagrelor is not a prodrug and does not require in vivo activation. It has a rapid onset of action, relatively rapid reversibility, greater potency, and exhibits consistency in platelet inhibition. Following dosing, ticagrelor reaches Cmax in about 1.5 h, with formation of a major metabolite with equipotent intrinsic activity to the parent compound.