Akkaif Mohammed Ahmed, Ng Mei Li, Sk Abdul Kader Muhamad Ali, Daud Nur Aizati Athirah, Sha'aban Abubakar, Ibrahim Baharudin
School of Pharmaceutical Sciences, Universiti Sains Malaysia, 11800, Gelugor, Penang, Malaysia.
Advanced Medical and Dental Institute, Universiti Sains Malaysia, 13200, Gelugor, Penang, Malaysia.
Pharmacol Rep. 2021 Dec;73(6):1551-1564. doi: 10.1007/s43440-021-00309-0. Epub 2021 Jul 20.
Ticagrelor is an oral antiplatelet drug that can reversibly bind to the platelet P2Y12 receptor. Ticagrelor is metabolized mainly by CYP3A4 and produces a rapid blood concentration-dependent platelet inhibitory effect. Unlike other P2Y12 receptor antagonists, many clinical features of ticagrelor are not related to P2Y12 receptor antagonism.
This review aims to gather existing literature on the clinical effects of ticagrelor after inhibiting adenosine uptake.
The current study reviewed literature related to the effects of ticagrelor on adenosine metabolism. The review also examined the drug's biological effects and clinical characteristics to see how it could be used in a clinical setting.
Many studies have shown that ticagrelor can inhibit equilibrative nucleoside transporter 1 (ENT1). This inhibition leads to intracellular adenosine uptake, increased adenosine half-life and plasma concentration levels and an enhanced adenosine-mediated biological effect.
Based on the studies reviewed, it was found that ticagrelor essentially inhibits adenosine absorption of adenosine into cells through ENT1, which increases the concentration in the blood and subsequently increases the protection of the heart muscle by adenosine. It also prevents platelet aggregation, and extends the biological effects of coronary arteries. Moreover, it leads to a lower mortality rate in acute coronary syndrome (ACS) patients.
替格瑞洛是一种口服抗血小板药物,可与血小板P2Y12受体可逆性结合。替格瑞洛主要通过CYP3A4代谢,产生快速的血药浓度依赖性血小板抑制作用。与其他P2Y12受体拮抗剂不同,替格瑞洛的许多临床特征与P2Y12受体拮抗作用无关。
本综述旨在收集有关替格瑞洛抑制腺苷摄取后临床效果的现有文献。
本研究回顾了与替格瑞洛对腺苷代谢影响相关的文献。该综述还研究了该药物的生物学效应和临床特征,以了解其在临床环境中的应用方式。
许多研究表明,替格瑞洛可抑制平衡核苷转运体1(ENT1)。这种抑制导致细胞内腺苷摄取、腺苷半衰期延长和血浆浓度水平升高,以及腺苷介导的生物学效应增强。
基于所回顾的研究,发现替格瑞洛本质上通过ENT1抑制腺苷进入细胞的吸收,这增加了血液中的浓度,随后增加了腺苷对心肌的保护作用。它还可防止血小板聚集,并延长冠状动脉的生物学效应。此外,它可降低急性冠状动脉综合征(ACS)患者的死亡率。