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Ticagrelor (Monograph)

Brand name: Brilinta
Drug class: Platelet-aggregation Inhibitors
Chemical name: (1S,2S,3R,5S)-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)-1,2-cyclopentanediol
Molecular formula: C23H28F2N6O4S
CAS number: 274693-27-5

Medically reviewed by Drugs.com on Sep 25, 2023. Written by ASHP.

Warning

    Bleeding

  • Potential risk of bleeding; may be serious, sometimes fatal.1 2 13 41 42 (See Bleeding under Cautions.)

  • Avoid use in patients with active pathologic bleeding or history of intracranial hemorrhage.1 Do not initiate in patients undergoing urgent CABG.1

  • If bleeding occurs, attempt to manage without discontinuing ticagrelor; increased risk of subsequent cardiovascular events possible with premature discontinuance.1 45 (See Discontinuance of Therapy in Patients with Coronary Artery Disease under Cautions.)

    Reduced Efficacy with Higher Aspirin Dosages in Patients with Acute Coronary Syndrome

  • Avoid use of aspirin maintenance dosages >100 mg daily in patients with acute coronary syndrome (ACS).1 15 16 36 (See Reduced Response with Higher Aspirin Dosages in Patients with ACS under Cautions.)

Introduction

Platelet-activation and -aggregation inhibitor; nonthienopyridine, reversible, P2Y12 platelet adenosine diphosphate (ADP)-receptor antagonist.1 13 16 18 33 41 42 991 992 994

Uses for Ticagrelor

Acute Coronary Syndrome or History of MI

Used in conjunction with aspirin to reduce the risk of cardiovascular death, MI, and stroke in patients with ACS.1 2 4 5 8 9 32 33 35 36 60 991 992 994 1005

Dual antiplatelet therapy (DAPT) with a P2Y12 inhibitor (e.g., clopidogrel, prasugrel, ticagrelor) and aspirin is considered the current standard of care in patients with ACS.33 991 992 994 1005

ACC/AHA has issued guidelines for treatment options and duration of DAPT.991 992 994 1005 Aspirin should almost always be continued indefinitely; decisions about specific P2Y12 inhibitor and duration of therapy should be based on risks of bleeding versus benefits of ischemic reduction, clinical judgment, and patient preference.1005

ACC/AHA generally recommends a shorter duration of DAPT for patients at reduced ischemic, but high bleeding, risk and a longer duration for patients at high ischemic, but reduced bleeding, risk.1005

In ACS patients managed medically (without revascularization or reperfusion therapy) or with PCI and stent implantation (bare-metal or drug-eluting), P2Y12 inhibitor therapy should be given for at least 12 months; in patients who have tolerated DAPT without bleeding complications and do not have a high risk of bleeding, continuation of such therapy for longer than 12 months may be reasonable.1005

With regard to the specific P2Y12 inhibitor, evidence supports use of clopidogrel or ticagrelor in medically-managed ACS patients; clopidogrel, prasugrel, or ticagrelor may be used in ACS patients treated with PCI.991 992 994 1005

In patients undergoing CABG, P2Y12 inhibitor therapy should be resumed after surgery to complete 12 months of therapy.1005

Unlike clopidogrel, genetic polymorphism of the CYP2C19 isoenzyme does not appear to affect the pharmacodynamic or clinical response to ticagrelor.1 The Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines recommend ticagrelor as an alternative antiplatelet agent to clopidogrel in patients who are poor or intermediate metabolizers of CYP2C19.1000

When selecting an appropriate antiplatelet regimen, consider individual patient (e.g., ischemic and bleeding risk) and drug-related (e.g., adverse effects, drug interaction potential) factors.13 14 41 43 49

Also used to reduce the risk of cardiovascular death, MI, and stroke in patients with a history of MI; in the principal study establishing efficacy for this indication, patients had a history of MI 1–3 years prior to study entry.31 60

AHA/ACC states that in patients with stable ischemic heart disease (SIHD) being treated with DAPT for previous (1–3 years prior) MI, continuation of such therapy may be reasonable if tolerated without any bleeding complications.1005

Coronary Artery Disease but No Prior Stroke or MI

Used to reduce the risk of an initial MI or stroke in patients with established CAD who are at high risk for these thrombotic cardiovascular events.1 62

Use in conjunction with aspirin therapy.1

There is evidence supporting use of ticagrelor in reducing risk of a first MI and stroke in patients with CAD and type 2 diabetes mellitus, although treatment effect is small.32 62 Reduction in ischemic events is accompanied by increased risk of bleeding.1 62

Acute Ischemic Stroke or Transient Ischemic Attack

Used to reduce the risk of stroke in patients with acute ischemic stroke (National Institutes of Health Stroke Scale [NIHSS] ≤5) or high-risk TIA.1 63

Use in conjunction with aspirin therapy.1

Not studied in patients with more severe stroke or cardioembolic stroke; those undergoing thrombectomy or thrombolysis; and those in whom treatment was administered >24 hours after symptom onset.63

Ticagrelor Dosage and Administration

Administration

Administer orally without regard to meals.1 48

For patients unable to swallow tablets whole, may crush and mix with water.1 Also can administer crushed tablet in water mixture via a nasogastric tube (CH8 or greater).1

If a dose is missed, take next dose at the regularly scheduled time.1

Dosage

Adults

Acute Coronary Syndrome or History of MI
Oral

180-mg loading dose followed by maintenance dosage of 90 mg twice daily during the first year.1 35 36 After first year, maintenance dosage of 60 mg twice daily recommended.1

Adjunctive aspirin therapy: Administer maintenance dosage of 75–100 mg daily.1 (See Reduced Response with Higher Aspirin Dosages in Patients with ACS under Cautions.)

Manufacturer makes no specific recommendation regarding duration of maintenance therapy; however, ticagrelor was administered for up to 12 months in the pivotal efficacy study (PLATO).1 2 13 Recommendations for duration of dual antiplatelet therapy can be found in ACC/AHA guidelines.1005 (See Acute Coronary Syndrome or History of MI under Uses.)

Coronary Artery Disease but No Prior Stroke or MI
Oral

60 mg twice daily.1

Adjunctive aspirin therapy: Administer maintenance dosage of 75–100 mg daily.1

Acute Ischemic Stroke or Transient Ischemic Attack
Oral

180-mg loading dose followed by maintenance dosage of 90 mg twice daily for up to 30 days.1

Adjunctive aspirin therapy: After initial loading dose (300–325 mg), administer maintenance dosage of 75–100 mg daily.1

Transitioning from Clopidogrel to Ticagrelor Therapy
Oral

May transition patients directly from clopidogrel to ticagrelor therapy without interruption in antiplatelet effects.1 26 In clinical trials, patients who switched from clopidogrel to ticagrelor received an initial loading dose of ticagrelor regardless of whether a previous loading dose of clopidogrel had been given.2 26

Special Populations

Renal Impairment

No dosage adjustment required in patients with renal impairment.1 31

Hepatic Impairment

No dosage adjustment required in patients with mild hepatic impairment (Child-Pugh class A).1 29 (See Hepatic Impairment under Cautions.)

Geriatric Patients

Dosage adjustment based on age not required.1

Detailed Ticagrelor dosage information

Cautions for Ticagrelor

Contraindications

Warnings/Precautions

Warnings

Bleeding

Risk of bleeding, including serious, sometimes fatal bleeding.1 2 13 41 42 50 (See Boxed Warning.)

Overall risk of major and minor bleeding somewhat greater with ticagrelor than with clopidogrel in the PLATO trial.1 4 9 42 Increased risk principally involved non-CABG-related major bleeding, including fatal intracranial hemorrhage.1 2 4 6 8 9 13 41 994 Rates of major CABG-related bleeding were similar between ticagrelor and clopidogrel.1 2 4 5 16

Bleeding was reported more frequently with ticagrelor compared with placebo in other preapproval studies.1 60 62 63

In general, risk factors for bleeding include advanced age, history of bleeding disorders, female gender, renal dysfunction, performance of PCI, and concurrent use of other drugs that affect hemostasis (e.g., anticoagulants, thrombolytic agents, high dosages of aspirin, long-term use of NSAIAs).65

Contraindicated in patients who are actively bleeding or who have a history of intracranial hemorrhage.1 Also not recommended in patients likely to undergo urgent CABG.1 Temporarily discontinue drug at least 5 days prior to surgery (e.g., CABG) whenever possible.1 70

If possible, manage bleeding without discontinuing ticagrelor; premature discontinuance may increase risk of subsequent cardiovascular events.1 (See Discontinuance of Therapy in Patients with Coronary Artery Disease under Cautions.)

Reduced Response with Higher Aspirin Dosages in Patients with ACS

In the PLATO study, a reduced response to ticagrelor was observed when used with aspirin maintenance dosages >100 mg daily in patients with ACS.1 15 16 Avoid aspirin dosages >100 mg daily.1 (See Boxed Warning.)

Other Warnings and Precautions

Dyspnea

Risk of dyspnea,1 2 4 8 13 16 20 22 24 26 30 36 generally mild to moderate and self-limiting.1 2 20 22 Adverse effects on pulmonary function not observed.1 16 22 Mechanism of dyspnea unknown, but thought to be related to an adenosine-mediated response.13 16 20 22

If any new, prolonged, or worsening dyspnea related to ticagrelor occurs, no specific treatment required; may continue therapy without interruption if possible.1 If dyspnea is intolerable and results in discontinuance of ticagrelor, consider another antiplatelet agent.1

Discontinuance of Therapy in Patients with Coronary Artery Disease

In general, avoid premature discontinuance of antiplatelet therapy (e.g., P2Y12-receptor antagonists, aspirin) in patients with CAD because of subsequent increased risk of ischemic complications.1 45 51 52 53 54 55 56 57 Stent thrombosis, MI, and/or death observed in patients with coronary stents who prematurely discontinued antiplatelet therapy.45 50 51 52 53 54 55 56 57

If temporary discontinuance of ticagrelor required (e.g., prior to significant surgery or for bleeding), reinstitute therapy as soon as possible.1 45 Interrupt therapy for 5 days prior to surgical procedures with a major bleeding risk if possible; resume therapy when hemostasis is achieved.1

Bradyarrhythmias

Ventricular pauses ≥3 seconds, usually occurring during first week of therapy, reported.1 2 16 21 30 36 Mostly asymptomatic and not associated with any clinically important effects (e.g., syncope, need for pacemaker insertion).1 2 21

Because patients with baseline increased risk of bradycardia (e.g., those with sick sinus syndrome, second- or third-degree AV block, or syncope due to bradycardia without a pacemaker) were excluded from clinical studies,1 some clinicians recommend caution when used in such patients.21

Laboratory Test Interference

May cause false negative results in platelet function tests for heparin-induced thrombocytopenia (e.g., heparin-induced platelet aggregation [HIPA] assay).1 However, not expected to affect PF4 antibody testing for heparin-induced thrombocytopenia.1

Specific Populations

Pregnancy

No drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes identified.1

Lactation

Distributed into milk in rats; not known whether distributed into human milk.1 Breast-feeding not recommended during ticagrelor therapy.1

Pediatric Use

Safety and efficacy not established in pediatric patients.1 2

Geriatric Use

No overall differences in efficacy or safety between geriatric and younger patients.1

Ticagrelor pharmacokinetics not substantially affected by age.1 27

Hepatic Impairment

Possible increased exposure and risk of bleeding.1 (See Absorption: Special Populations under Pharmacokinetics.)

Avoid use in patients with severe hepatic impairment.1 Carefully consider use in those with moderate hepatic impairment after weighing risks versus benefits.1 May be used in patients with mild hepatic impairment without dosage adjustment.1 29

Renal Impairment

Pharmacokinetics and clinical efficacy not substantially altered in patients with renal impairment.1 24 31 (See Renal Impairment under Dosage and Administration.)

Not studied in patients with end-stage renal disease (ESRD) on dialysis; however, clinically important differences not expected in such patients receiving intermittent hemodialysis.1

Ticagrelor is not dialyzable.1

Common Adverse Effects

Bleeding, dyspnea.1

Drug Interactions

Metabolized principally by CYP isoenzyme 3A4.1 Weak inhibitor of CYP3A4/5 and potential activator of CYP3A5.1 Does not inhibit CYP 1A2, 2C19, or 2E1.1

P-glycoprotein substrate and inhibitor.1

Drugs Affecting Hemostasis

Possible increased risk of bleeding.1 (See Bleeding under Cautions and see Specific Drugs under Interactions.)

Drugs Affecting or Metabolized by Hepatic Microsomal Enzymes

Potent CYP3A inhibitors: Potential pharmacokinetic interaction (substantially increased exposure to ticagrelor); possible increased risk of bleeding.1 36 Avoid concomitant use.1

Moderate CYP3A inhibitors: Possible increased ticagrelor exposure; dosage adjustment not necessary.1

Potent CYP3A inducers: Potential pharmacokinetic interaction (substantially decreased plasma ticagrelor concentrations); possible reduced efficacy.1 36 Avoid concomitant use.1

CYP3A substrates: Potential pharmacokinetic interaction (increased plasma concentrations of substrate drug).1 36

Drugs Affecting or Affected by P-glycoprotein Transport

P-glycoprotein substrates: Potential pharmacokinetic interaction (increased plasma concentrations of substrate drug).1 36

Specific Drugs

Drug

Interaction

Comments

Anticoagulants

Possible increased risk of bleeding1

Anticonvulsants (carbamazepine, phenobarbital, phenytoin)

Substantially reduced plasma ticagrelor concentrations due to CYP3A induction1

Avoid concomitant use1

Antifungals, azole (itraconazole, ketoconazole, voriconazole)

Substantially increased exposure to ticagrelor due to potent CYP3A inhibition1

Avoid concomitant use1

Aspirin

Possible reduced efficacy of ticagrelor when used with aspirin dosages >100 mg daily1 15 16

Increased risk of bleeding possible with high dosages of aspirin1

Pharmacokinetics of ticagrelor not altered1

Limit concomitant aspirin maintenance dosage to 75–100 mg daily1

Atazanavir

Substantially increased exposure to ticagrelor due to potent CYP3A inhibition1

Avoid concomitant use1

Clarithromycin

Substantially increased exposure to ticagrelor due to potent CYP3A inhibition1

Avoid concomitant use1

Cyclosporine

Possible increased exposure to ticagrelor1

Desmopressin

Pharmacokinetics of ticagrelor not affected1

No dosage adjustment necessary1

Digoxin

Pharmacokinetics of digoxin not substantially altered1

No dosage adjustment necessary; monitor serum digoxin concentrations prior to and following any change in ticagrelor therapy1

Diltiazem

Possible decreased exposure to ticagrelor due to moderate CYP3A inhibition1

No dosage adjustment necessary1

Enoxaparin

Pharmacokinetics of ticagrelor not affected1

Possible increased risk of bleeding1

No dosage adjustment necessary1

Heparin

Pharmacokinetics of ticagrelor not affected1

Possible increased risk of bleeding1

No dosage adjustment necessary1

HMG-CoA reductase inhibitors (statins)

Lovastatin, simvastatin: Possible increased serum concentrations of the statin1

Atorvastatin: Pharmacokinetics of atorvastatin not substantially altered1

Lovastatin, simvastatin: Do not exceed dosage of 40 mg daily1

Atorvastatin: No dosage adjustment necessary1

Hormonal contraceptives (ethinyl estradiol/levonorgestrel)

Increased peak plasma concentrations of and systemic exposure to ethinyl estradiol; pharmacokinetics of levonorgestrel not altered 1 46

Ticagrelor not expected to affect contraceptive efficacy42 46

No dosage adjustment necessary1

Nefazodone

Substantially increased exposure to ticagrelor due to potent CYP3A inhibition1

Avoid concomitant use1

Nelfinavir

Substantially increased exposure to ticagrelor due to potent CYP3A inhibition1

Avoid concomitant use1

NSAIAs

Possible increased risk of bleeding with chronic NSAIA use1

Opiate agonists (e.g., morphine)

May delay and reduce absorption of ticagrelor and its active metabolite1

Ticagrelor exposure was decreased and time to peak plasma concentration was delayed when coadministered with IV fentanyl or IV morphine; platelet aggregation was higher up to 3 hours post-loading dose in ACS patients who received these drugs concomitantly1

Consider use of a parenteral antiplatelet agent in ACS patients who require treatment with morphine or other opiate agonist1

Proton-pump inhibitors

Platelet response to ticagrelor not affected7

May be used concomitantly1 7

Rifampin

Substantially decreased peak plasma concentrations of and systemic exposure to ticagrelor due to potent CYP3A induction1

Avoid concomitant use1

Ritonavir

Substantially increased exposure to ticagrelor due to potent CYP3A inhibition1

Avoid concomitant use1

Saquinavir

Substantially increased exposure to ticagrelor due to potent CYP3A inhibition1

Avoid concomitant use1

Thrombolytics

Possible increased risk of bleeding1

Tolbutamide

Pharmacokinetics of tolbutamide not substantially altered1

Dosage adjustment not necessary1
Ticagrelor drug interactions (more detail)

Ticagrelor Pharmacokinetics

Absorption

Bioavailability

Rapidly but incompletely absorbed after oral administration;13 25 27 28 29 mean absolute oral bioavailability about 36%.1

Plasma concentrations of ticagrelor and its major metabolite increase in a dose-dependent manner; peak concentrations achieved within approximately 1.5 and 2.5 hours, respectively.1 18 25 27 28 29

Onset

Maximum inhibition of platelet aggregation observed approximately 2 hours after a dose.1 19 25 26 27 28

Additional inhibition of platelet aggregation (absolute increase of 26.4%) observed in patients who transition from clopidogrel to ticagrelor therapy.1 26

Duration

Maximum inhibition of platelet aggregation maintained for ≥8 hours after a dose.1 Following discontinuance, platelet activity returns to baseline after 5 days.1 19

Food

High-fat meal increased systemic exposure to ticagrelor by 21% and decreased peak plasma concentrations of the active metabolite by 22%; no effect on plasma concentrations of ticagrelor or systemic exposure to active metabolite.1 48

Special Populations

Individuals with mild (Child-Pugh class A) hepatic impairment had slightly higher systemic exposure to ticagrelor than those with normal hepatic function; however, no clinically important effects observed.1 29

Individuals with severe (Clcr <30 mL/minute) renal impairment had slightly higher systemic exposure to ticagrelor than those with normal renal function; however, no effect on platelet inhibition or tolerability.31

Distribution

Plasma Protein Binding

>99% for both ticagrelor and active metabolite.1

Elimination

Metabolism

Metabolized principally by CYP3A4 to active metabolite.1 13 27

Elimination Route

Primarily eliminated in feces; <1% of a dose is recovered in urine (as parent drug and active metabolite).1 13

Half-life

Ticagrelor: Approximately 7 hours.1 25 28

Active metabolite: Approximately 9 hours.1 25 28

Stability

Storage

Oral

Tablets

25°C (may be exposed to 15–30°C).1

Actions

Advice to Patients

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

Ticagrelor

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Tablets, film-coated

60 mg

Brilinta

AstraZeneca

90 mg*

Brilinta

AstraZeneca

Ticagrelor Tablets

AHFS DI Essentials™. © Copyright 2024, Selected Revisions October 4, 2021. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

References

1. AstraZeneca. Brilinta, (ticagrelor) tablets prescribing information. Wilmington, DE; 2021 Feb.

2. Wallentin L, Becker RC, Budaj A et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2009; 361:1045-57. http://www.ncbi.nlm.nih.gov/pubmed/19717846?dopt=AbstractPlus

3. James S, Akerblom A, Cannon CP et al. Comparison of ticagrelor, the first reversible oral P2Y(12) receptor antagonist, with clopidogrel in patients with acute coronary syndromes: Rationale, design, and baseline characteristics of the PLATelet inhibition and patient Outcomes (PLATO) trial. Am Heart J. 2009; 157:599-605. http://www.ncbi.nlm.nih.gov/pubmed/19332184?dopt=AbstractPlus

4. Steg PG, James S, Harrington RA et al. Ticagrelor versus clopidogrel in patients with ST-elevation acute coronary syndromes intended for reperfusion with primary percutaneous coronary intervention: A Platelet Inhibition and Patient Outcomes (PLATO) trial subgroup analysis. Circulation. 2010; 122:2131-41. http://www.ncbi.nlm.nih.gov/pubmed/21060072?dopt=AbstractPlus

5. Held C, Asenblad N, Bassand JP et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes undergoing coronary artery bypass surgery: results from the PLATO (Platelet Inhibition and Patient Outcomes) trial. J Am Coll Cardiol. 2011; 57:672-84. http://www.ncbi.nlm.nih.gov/pubmed/21194870?dopt=AbstractPlus

6. Becker RC, Bassand JP, Budaj A et al. Bleeding complications with the P2Y12 receptor antagonists clopidogrel and ticagrelor in the PLATelet inhibition and patient Outcomes (PLATO) trial. Eur Heart J. 2011; 32:2933-44. http://www.ncbi.nlm.nih.gov/pubmed/22090660?dopt=AbstractPlus

7. Storey RF, Angiolillo DJ, Patil SB et al. Inhibitory effects of ticagrelor compared with clopidogrel on platelet function in patients with acute coronary syndromes: the PLATO (PLATelet inhibition and patient Outcomes) PLATELET substudy. J Am Coll Cardiol. 2010; 56:1456-62. http://www.ncbi.nlm.nih.gov/pubmed/20832963?dopt=AbstractPlus

8. Cannon CP, Harrington RA, James S et al. Comparison of ticagrelor with clopidogrel in patients with a planned invasive strategy for acute coronary syndromes (PLATO): a randomised double-blind study. Lancet. 2010; 375:283-93. http://www.ncbi.nlm.nih.gov/pubmed/20079528?dopt=AbstractPlus

9. James SK, Roe MT, Cannon CP et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes intended for non-invasive management: substudy from prospective randomised PLATelet inhibition and patient Outcomes (PLATO) trial. BMJ. 2011; 342:d3527. http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=3117310&blobtype=pdf http://www.ncbi.nlm.nih.gov/pubmed/21685437?dopt=AbstractPlus

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12. Serebruany VL, Atar D. The PLATO trial: do you believe in magic?. Eur Heart J. 2010; 31:764-7. http://www.ncbi.nlm.nih.gov/pubmed/20007979?dopt=AbstractPlus

13. Anderson SD, Shah NK, Yim J et al. Efficacy and safety of ticagrelor: a reversible P2Y12 receptor antagonist. Ann Pharmacother. 2010; 44:524-37. http://www.ncbi.nlm.nih.gov/pubmed/20124464?dopt=AbstractPlus

14. Tapp L, Shantsila E, Lip GY. Role of ticagrelor in clopidogrel nonresponders: resistance is futile?. Circulation. 2010; 121:1169-71. http://www.ncbi.nlm.nih.gov/pubmed/20194888?dopt=AbstractPlus

15. Mahaffey KW, Wojdyla DM, Carroll K et al. Ticagrelor compared with clopidogrel by geographic region in the Platelet Inhibition and Patient Outcomes (PLATO) trial. Circulation. 2011; 124:544-54. http://www.ncbi.nlm.nih.gov/pubmed/21709065?dopt=AbstractPlus

16. Gaglia MA, Waksman R. Overview of the 2010 Food and Drug Administration Cardiovascular and Renal Drugs Advisory Committee meeting regarding ticagrelor. Circulation. 2011; 123:451-6. http://www.ncbi.nlm.nih.gov/pubmed/21242480?dopt=AbstractPlus

17. Schömig A. Ticagrelor--is there need for a new player in the antiplatelet-therapy field?. N Engl J Med. 2009; 361:1108-11. http://www.ncbi.nlm.nih.gov/pubmed/19717845?dopt=AbstractPlus

18. Storey RF, Husted S, Harrington RA et al. Inhibition of platelet aggregation by AZD6140, a reversible oral P2Y12 receptor antagonist, compared with clopidogrel in patients with acute coronary syndromes. J Am Coll Cardiol. 2007; 50:1852-6. http://www.ncbi.nlm.nih.gov/pubmed/17980251?dopt=AbstractPlus

19. Gurbel PA, Bliden KP, Butler K et al. Randomized double-blind assessment of the ONSET and OFFSET of the antiplatelet effects of ticagrelor versus clopidogrel in patients with stable coronary artery disease: the ONSET/OFFSET study. Circulation. 2009; 120:2577-85. http://www.ncbi.nlm.nih.gov/pubmed/19923168?dopt=AbstractPlus

20. Storey RF, Becker RC, Harrington RA et al. Characterization of dyspnoea in PLATO study patients treated with ticagrelor or clopidogrel and its association with clinical outcomes. Eur Heart J. 2011; 32:2945-53. http://www.ncbi.nlm.nih.gov/pubmed/21804104?dopt=AbstractPlus

21. Scirica BM, Cannon CP, Emanuelsson H et al. The incidence of bradyarrhythmias and clinical bradyarrhythmic events in patients with acute coronary syndromes treated with ticagrelor or clopidogrel in the PLATO (Platelet Inhibition and Patient Outcomes) trial: results of the continuous electrocardiographic assessment substudy. J Am Coll Cardiol. 2011; 57:1908-16. http://www.ncbi.nlm.nih.gov/pubmed/21545948?dopt=AbstractPlus

22. Storey RF, Bliden KP, Patil SB et al. Incidence of dyspnea and assessment of cardiac and pulmonary function in patients with stable coronary artery disease receiving ticagrelor, clopidogrel, or placebo in the ONSET/OFFSET study. J Am Coll Cardiol. 2010; 56:185-93. http://www.ncbi.nlm.nih.gov/pubmed/20620737?dopt=AbstractPlus

23. Wallentin L, James S, Storey RF et al. Effect of CYP2C19 and ABCB1 single nucleotide polymorphisms on outcomes of treatment with ticagrelor versus clopidogrel for acute coronary syndromes: a genetic substudy of the PLATO trial. Lancet. 2010; 376:1320-8. http://www.ncbi.nlm.nih.gov/pubmed/20801498?dopt=AbstractPlus

24. James S, Budaj A, Aylward P et al. Ticagrelor versus clopidogrel in acute coronary syndromes in relation to renal function: results from the Platelet Inhibition and Patient Outcomes (PLATO) trial. Circulation. 2010; 122:1056-67. http://www.ncbi.nlm.nih.gov/pubmed/20805430?dopt=AbstractPlus

25. Teng R, Butler K. Pharmacokinetics, pharmacodynamics, tolerability and safety of single ascending doses of ticagrelor, a reversibly binding oral P2Y(12) receptor antagonist, in healthy subjects. Eur J Clin Pharmacol. 2010; 66:487-96. http://www.ncbi.nlm.nih.gov/pubmed/20091161?dopt=AbstractPlus

26. Gurbel PA, Bliden KP, Butler K et al. Response to ticagrelor in clopidogrel nonresponders and responders and effect of switching therapies: the RESPOND study. Circulation. 2010; 121:1188-99. http://www.ncbi.nlm.nih.gov/pubmed/20194878?dopt=AbstractPlus

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28. Butler K, Teng R. Pharmacokinetics, pharmacodynamics, safety and tolerability of multiple ascending doses of ticagrelor in healthy volunteers. Br J Clin Pharmacol. 2010; 70:65-77. http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=2909809&blobtype=pdf http://www.ncbi.nlm.nih.gov/pubmed/20642549?dopt=AbstractPlus

29. Butler K, Teng R. Pharmacokinetics, pharmacodynamics, and safety of ticagrelor in volunteers with mild hepatic impairment. J Clin Pharmacol. 2011; 51:978-87. http://www.ncbi.nlm.nih.gov/pubmed/20926753?dopt=AbstractPlus

30. Cannon CP, Husted S, Harrington RA et al. Safety, tolerability, and initial efficacy of AZD6140, the first reversible oral adenosine diphosphate receptor antagonist, compared with clopidogrel, in patients with non-ST-segment elevation acute coronary syndrome: primary results of the DISPERSE-2 trial. J Am Coll Cardiol. 2007; 50:1844-51. http://www.ncbi.nlm.nih.gov/pubmed/17980250?dopt=AbstractPlus

31. Bonaca MP, Bhatt DL, Steg PG et al. Ischaemic risk and efficacy of ticagrelor in relation to time from P2Y12 inhibitor withdrawal in patients with prior myocardial infarction: insights from PEGASUS-TIMI 54. Eur Heart J. 2016; 37:1133-42. http://www.ncbi.nlm.nih.gov/pubmed/26491109?dopt=AbstractPlus

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33. Collet JP, Thiele H, Barbato E et al. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J. 2021; 42:1289-1367. http://www.ncbi.nlm.nih.gov/pubmed/32860058?dopt=AbstractPlus

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