Ticagrelor: Pharmacokinetics, Pharmacodynamics, Clinical Efficacy, and Safety

Dobesh, Paul P.; Oestreich, Julie H.

doi:10.1002/phar.1477

Cited by 175 publications

(159 citation statements)

References 64 publications

Supporting

Mentioning

154

Contrasting

Unclassified

Order By: Relevance

“…Ticagrelor, like cangrelor, is a derivative of adenosine triphosphate in which the purine was replaced by a triazolopyrimidine heterocycle [13]. This oral agent binds reversibly to the platelet P2Y 12 receptor.…”

Section: Pharmacologic Characteristics Of P2y 12 Antagonistsmentioning

confidence: 99%

Transition strategies from cangrelor to oral platelet P2Y12 receptor antagonists

Schneider

2016

Coronary Artery Disease

View full text Add to dashboard Cite

Cangrelor is the first parenteral antagonist of the platelet P2Y12 receptor. This direct-acting antagonist of the platelet P2Y12 receptor should be considered an adjunct to a percutaneous coronary intervention in patients who have not been adequately pretreated with platelet P2Y12 receptor antagonists at the time of the procedure. The use of cangrelor requires transition to an oral platelet P2Y12 receptor antagonist. Transition strategies have been developed on the basis of pharmacologic characteristics of platelet P2Y12 receptor antagonists, results of pharmacodynamic studies, and results from clinical trials. Cangrelor blocks the binding to the platelet P2Y12 receptor of the active metabolite of the thienopyridines, clopidogrel and prasugrel. The active metabolite of thienopyridines is present in blood for a short interval after administration. For this reason, clopidogrel should be administered after cangrelor is stopped. Prasugrel can be administered at the end of the cangrelor infusion or up to 30 min before cangrelor is stopped. Ticagrelor is also a reversible direct-acting antagonist of the platelet P2Y12 receptor. Because there is no interaction between ticagrelor and cangrelor, ticagrelor can be administered before or during the infusion of cangrelor.

show abstract

Section: Pharmacologic Characteristics Of P2y 12 Antagonistsmentioning

confidence: 99%

Transition strategies from cangrelor to oral platelet P2Y12 receptor antagonists

Schneider

2016

Coronary Artery Disease

View full text Add to dashboard Cite

show abstract

“…The active metabolite works by forming an irreversible covalent bond with receptors P2Y12. Along these covalent bonds, ADP cannot bind to receptors P2Y12 [23]. Clopidogrel has different responses that lead to inhibition of platelet aggregation be affected [24].…”

Section: Discussionmentioning

confidence: 99%

Effectiveness of Ticagrelor Compared to Clopidogrel in Reducing the Risk of Major Adverse Cardiovascular Events in Patients With Coronary Heart Disease After Percutaneous Coronary Intervention

Nur’amin

Dwiprahasto

Kristin

2017

Int J Pharm Pharm Sci

View full text Add to dashboard Cite

Objective: Antiplatelet therapy is recommended in patients with coronary heart disease (CHD) who had the percutaneous coronary intervention (PCI) procedure to reduce major adverse cardiovascular events (MACE). There has been a lack of population-based studies that showed the superior effectiveness of ticagrelor over clopidogrel and similar studies have not been conducted in Indonesia yet. The aim of the study was to investigate the effectiveness of ticagrelor compared to clopidogrel in reducing the risk of MACE in patients with CHD after PCI. Methods:A retrospective cohort study with 1-year follow-up was conducted. 361 patients consisted of 111 patients with ticagrelor exposure and 250 patients with clopidogrel exposure. The primary outcome was MACE, defined as a composite of repeat revascularization, myocardial infarction, or all-cause death. The association between antiplatelet exposure and the MACE was analyzed with Cox proportional hazard regression, adjusted for sex, age, comorbid, PCI procedures and concomitant therapy.Results: MACE occurred in 22.7% of the subjects. Clopidogrel had a significantly higher risk of MACE compared with ticagrelor (28.8%, vs 9.0%, hazard ratio (HR): 1.96 (95% CI 1.01 to 3.81, p=0.047). There were no significant differences in risk of repeat revascularization (20.40% vs 5.40%, HR: 2.32, 95% CI 0.99 to 5.42, p = 0.05), myocardial infarction (11.60% vs 3.60%, HR: 2.08, 95% CI, 0.73 to 5.93, p = 0.17), and death (1.60% vs 1.80%, HR: 0.77, 95% CI, 0.14 to 4.25, p = 0.77). Conclusion:Clopidogrel had a higher risk of MACE compared to clopidogrel in patients with CHD after PCI, but there were no significant differences in the risk of repeat revascularization, myocardial infarction, and all-cause death.

show abstract

“…The great advantage is the rapid decline of antiplatelets effect after last intake. It has been reported that 24 hours after the last intake, the antiplatelet effect of ticagrelor declines by 50% [60].…”

Section: Antiplatelet Agentsmentioning

confidence: 99%

The Two Faces of Thrombosis: Coagulation Cascade and Platelet Aggregation. Are Platelets the Main Therapeutic Target?

Cimmino¹,

Fischetti²,

Golino³

2017

J Thrombo Cir

View full text Add to dashboard Cite

Acute thrombus formation is the pathophysiological substrate underlying several clinical conditions, such as acute coronary syndrome (ACS) and stroke. Activation of coagulation cascade is a key step of the thrombotic process: vessel injury results in exposure of the glycoprotein tissue factor (TF) to the flowing blood. Once exposed, TF binds factor VII/VIIa (FVII/FVIIa) and in presence of calcium ions, it forms a tertiary complex able to activate FX to FXa, FIX to FIXa, and FVIIa itself. The final step is thrombin formation at the site of vessel injury with subsequent platelet activation, fibrinogen to fibrin conversion and ultimately thrombus formation.Platelets are the key cells in primary hemostasis. For years they have been considered only as cell fragments participating to primary hemostasis and onto which coagulation factors are assembled in the process of thrombus formation. However, recent advances in platelets pathophysiology have shown that these cells are able to regulate their gene and protein expression, make de novo protein synthesis, and release different mediators with paracrine effects that may interfere with different cell functions.Pharmacological modulation of both side of thrombosis, coagulation cascade and platelet activation, is of great clinical importance. Several clinical trials have clearly shown the efficacy of anticoagulation and/or anti platelet aggregation in different thrombotic disorders. This article aims at reviewing the recent advancements on the two faces of thrombosis focusing on the emerging role of platelets not only as clot-forming components, but highlighting their involvement in the inflammatory-immune system, as well as in modulation of different cell functions.

show abstract

Ticagrelor: Pharmacokinetics, Pharmacodynamics, Clinical Efficacy, and Safety

Cited by 175 publications

References 64 publications

Transition strategies from cangrelor to oral platelet P2Y12 receptor antagonists

Transition strategies from cangrelor to oral platelet P2Y12 receptor antagonists

Effectiveness of Ticagrelor Compared to Clopidogrel in Reducing the Risk of Major Adverse Cardiovascular Events in Patients With Coronary Heart Disease After Percutaneous Coronary Intervention

The Two Faces of Thrombosis: Coagulation Cascade and Platelet Aggregation. Are Platelets the Main Therapeutic Target?

Contact Info

Product

Resources

About