ticagrelor

Ticagrelor (AR-C 126532XX), produced by AstraZeneca, is an inhibitor of platelet aggregation. Unlike clopidogrel, ticagrelor is not a prodrug required metabolic activation. The drug was approved for use in the European Union by the European Commission on December 3, 2010, and by the US FDA on July 20, 2011. Its trade names are Brilinta (US), Brilique(EU) and Possia(EU).

Ticagrelor metabolite M5 (T437700) is a metabolite of Ticagrelor, the first reversible oral antagonist of P2Y12 receptor. Compared to Clopidogrel, Ticagrelor has faster and more consistent inhibition on ADP-receptors. Ticagrelor is used in the treatment of acute coronary syndromes (ACS).

Deshydroxyethoxy ticagrelor (AR-C124910) is a metabolite of Ticagrelor that exhibits antibacterial activity against MRSA and possesses antiplatelet effects.

Ticagrelor-d7 is a deuterated compound of Ticagrelor. Ticagrelor has a CAS number of 274693-27-5. Ticagrelor, produced by AstraZeneca, is an inhibitor of platelet aggregation. Unlike clopidogrel, ticagrelor is not a prodrug required metabolic activation. The drug was approved for use in the European Union by the European Commission on December 3, 2010, and by the US FDA on July 20, 2011. Its trade names are Brilinta (US), Brilique(EU) and Possia(EU).

Antiplatelet agent 1 is a ticagrelor analogue that exhibits anti-platelet effects and can be used in platelet agglutination studies.

Antiplatelet agent 2 is a ticagrelor analogue that exhibits anti-platelet effects and can be used in platelet agglutination studies.

Bivalirudin TFA, a synthetic 20-residue peptide, serves as a reversible inhibitor of thrombin. Its IC50 value highlights its target specificity in vitro, where, combined with Eptifibatide (8 mg mL) at a low concentration (70 ng mL), it significantly reduces platelet aggregation induced by thrombin (0.2 U mL) by approximately 90% [1]. The compound demonstrates no effect on thrombin generation assay (TGA) parameters up to 10 μmol L [2]. Additionally, it facilitates the binding of MPO to BAEC, leading to functional alterations such as increased NO consumption and enhanced MPO-mediated redox modifications [3]. In vivo studies reveal its efficacy in preventing the rise of antiheparin PF4 antibody IgG levels in rats, with significant findings from the toxicokinetic assessment signaling its safety profile at tested doses, although higher doses resulted in fatalities [4][5]. In clinical trials, its antithrombotic effects were explored, comparing it with alternatives like Ticagrelor and Clopidogrel in a Phase 4 study.

Bentracimab (PB 2452) is a monoclonal antibody that neutralizes Ticagrelor and its primary active metabolite by binding with high affinity, rapidly reversing Ticagrelor's antiplatelet effects [1].