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Ticagrelor: Drug information

Ticagrelor: Drug information
2024© UpToDate, Inc. and its affiliates and/or licensors. All Rights Reserved.
For additional information see "Ticagrelor: Patient drug information"

For abbreviations, symbols, and age group definitions show table
ALERT: US Boxed Warning
Bleeding risk:

Ticagrelor, like other antiplatelet agents, can cause significant, sometimes fatal, bleeding.

Do not use ticagrelor in patients with active pathological bleeding or a history of intracranial hemorrhage.

Do not start ticagrelor in patients undergoing urgent coronary artery bypass graft surgery.

If possible, manage bleeding without discontinuing ticagrelor. Stopping ticagrelor increases the risk of subsequent cardiovascular events.

Aspirin dose and ticagrelor effectiveness in patients with acute coronary syndrome:

Maintenance doses of aspirin >100 mg daily reduce the effectiveness of ticagrelor and should be avoided.

Brand Names: US
  • Brilinta
Brand Names: Canada
  • AG-Ticagrelor;
  • APO-Ticagrelor;
  • Brilinta;
  • JAMP-Ticagrelor;
  • M-Ticagrelor;
  • TARO-Ticagrelor
Pharmacologic Category
  • Antiplatelet Agent;
  • Antiplatelet Agent, Non-thienopyridine;
  • P2Y12 Antagonist
Dosing: Adult

Dosage guidance:

Safety: Use with caution or avoid use in patients at increased risk for bradycardic events.

Clinical considerations: In patients who require concomitant therapeutic anticoagulation, antiplatelet selection and/or duration of therapy may differ in order to balance risks for thrombosis and bleeding (Ref). Concurrent aspirin maintenance dose should not exceed 100 mg/day.

Acute coronary syndrome

Acute coronary syndrome:

ST-elevation myocardial infarction:

Percutaneous coronary intervention, primary:

Loading dose: Oral: 180 mg once as early as possible after diagnosis in combination with aspirin and a parenteral anticoagulant; followed by maintenance dose (Ref).

Maintenance dose: Oral:

First 12 months after diagnosis: 90 mg twice daily beginning ~6 to 12 hours after the initial loading dose in combination with aspirin (Ref).

After 12 months from diagnosis: Reduce maintenance dose to 60 mg twice daily in combination with aspirin; in selected patients with ongoing high ischemic risk, may continue 90 mg twice daily in combination with aspirin. Also see "Duration of Therapy" below (Ref).

Post-fibrinolysis:

Note: If fibrinolysis is chosen for reperfusion, it is recommended to administer clopidogrel (instead of ticagrelor) in combination with the fibrinolytic, aspirin, and a parenteral anticoagulant as soon as possible after diagnosis; subsequently, in patients <75 years of age, may transition from clopidogrel to ticagrelor (Ref).

Loading dose: Oral: 180 mg once ≥12 hours after administration of fibrinolytic therapy (regardless of whether clopidogrel was co-administered at the time of diagnosis); followed by maintenance dose (Ref).

Maintenance dose: Oral:

First 12 months after diagnosis: 90 mg twice daily beginning ~6 to 12 hours after the initial loading dose in combination with aspirin (Ref).

After 12 months from diagnosis: Reduce maintenance dose to 60 mg twice daily in combination with aspirin; in selected patients with ongoing high ischemic risk, may continue 90 mg twice daily in combination with aspirin. Also see "Duration of Therapy" below (Ref).

No reperfusion:

Loading dose: Oral: 180 mg once as early as possible after diagnosis in combination with aspirin and a parenteral anticoagulant; followed by maintenance dose (Ref).

Maintenance dose: Oral:

First 12 months after diagnosis: 90 mg twice daily beginning ~6 to 12 hours after the initial loading dose in combination with aspirin (Ref).

After 12 months from diagnosis: Reduce maintenance dose to 60 mg twice daily in combination with aspirin; in selected patients with ongoing high ischemic risk, may continue 90 mg twice daily in combination with aspirin. Also see "Duration of Therapy" below (Ref).

Duration of therapy:

Preferred approach: Continue ticagrelor plus aspirin (dual antiplatelet therapy [DAPT]) for ≥12 months unless major bleeding is a concern. For patients at high risk of bleeding or who experience overt bleeding, DAPT for 6 months may be reasonable. If there have been no major bleeding complications within initial 12 months, continuation of DAPT may be considered. Reevaluate the need for DAPT at regular intervals based on bleeding and thrombotic risks. When DAPT is complete, discontinue ticagrelor and continue aspirin indefinitely for secondary prevention (Ref).

Alternative approach in select patients to minimize bleeding events: Ticagrelor in combination with aspirin (DAPT) should be continued for 1 to 3 months after PCI, then discontinue aspirin and continue ticagrelor monotherapy. When ticagrelor is discontinued, restart aspirin for secondary prevention (Ref).

Non-ST-elevation acute coronary syndromes:

Note: The following dosing recommendations are the same whether reperfusion with percutaneous coronary intervention (PCI) is planned or no reperfusion is planned.

Loading dose: Oral: 180 mg once as early as possible after diagnosis in combination with aspirin and a parenteral anticoagulant; followed by maintenance dose. If coronary angiography is planned soon after diagnosis, it is reasonable to delay the initial loading dose until after coronary anatomy is known (Ref).

Maintenance dose: Oral:

First 12 months after diagnosis: 90 mg twice daily beginning ~6 to 12 hours after the initial loading dose in combination with aspirin (Ref).

After 12 months from diagnosis: Reduce maintenance dose to 60 mg twice daily in combination with aspirin. In selected patients with ongoing high ischemic risk, may continue 90 mg twice daily in combination with aspirin. Also see “Duration of Therapy” below (Ref).

Duration of therapy:

Preferred approach: Continue ticagrelor plus aspirin (DAPT) for ≥12 months unless major bleeding is a concern. For patients at high risk of bleeding or who experience overt bleeding, DAPT for 6 months may be reasonable. If there have been no major bleeding complications within initial 12 months, continuation of DAPT may be considered. Reevaluate the need for DAPT at regular intervals based on bleeding and thrombotic risks. When DAPT is complete, discontinue ticagrelor and continue aspirin indefinitely for secondary prevention (Ref).

Alternative approach in select patients to minimize bleeding events: Ticagrelor in combination with aspirin (DAPT) should be continued for 1 to 3 months after PCI, then discontinue aspirin and continue ticagrelor monotherapy. When ticagrelor is discontinued, restart aspirin for secondary prevention (Ref).

Coronary artery disease and high risk for ischemic cardiovascular events, primary prevention

Coronary artery disease (stable) and high risk for ischemic cardiovascular events, primary prevention:

Note: Evaluate bleeding and thrombotic risks as well as patient preferences when considering dual antiplatelet therapy versus monotherapy with aspirin for primary prevention. Some experts recommend limiting use of dual antiplatelet therapy to patients with coronary artery disease and diabetes mellitus, at high risk for ischemic cardiovascular events, and at low risk for bleeding (Ref).

Oral: 60 mg twice daily in combination with aspirin; continue ticagrelor and aspirin indefinitely (Ref).

Minor ischemic stroke or high-risk transient ischemic attack

Minor ischemic stroke (based on National Institutes of Health Stroke Scale score) or high-risk transient ischemic attack (TIA; based on ABCD2 score):

Note: May consider short-term dual antiplatelet therapy (DAPT) with ticagrelor in combination with aspirin in patients with recent (≤24 hours) minor ischemic stroke or high risk TIA and ipsilateral >30% stenosis of a major intracranial artery. Initiate antiplatelet therapy as soon as possible in the absence of contraindications. If an IV thrombolytic was administered, delay starting antiplatelet therapy for at least 24 hours, but administer as soon as possible thereafter (Ref). Avoid DAPT in patients with hemorrhagic transformation (Ref).

Oral: Initial: 180 mg once in combination with aspirin, followed by 90 mg twice daily, beginning ~6 to 12 hours after initial loading dose, in combination with aspirin for 21 to 30 days. After completion of DAPT, continue long-term single-agent antiplatelet therapy with aspirin (Ref).

Percutaneous coronary intervention for stable ischemic heart disease

Percutaneous coronary intervention for stable ischemic heart disease (off-label use):

Loading dose: Oral: 180 mg once prior to percutaneous coronary intervention in combination with aspirin and a parenteral anticoagulant; followed by a maintenance dose (Ref).

Maintenance dose: Oral: 90 mg twice daily beginning ~12 hours after the initial loading dose in combination with aspirin (Ref).

Duration of therapy: Continue ticagrelor plus aspirin for 1 to 3 months; then discontinue aspirin and continue ticagrelor monotherapy for up to 1 to 2 years. When ticagrelor is discontinued, switch to aspirin for treatment of stable ischemic heart disease (Ref).

Transitioning between P2Y12 inhibitors:

Note: This provides general guidance on transitioning between P2Y12 inhibitors.

Transitioning from another P2Y12 inhibitor to ticagrelor:

Transitioning from clopidogrel:

≤30 days after acute coronary syndrome (ACS) or PCI: Administer ticagrelor 180 mg loading dose once within 24 hours after the last dose of clopidogrel (irrespective of timing of previous clopidogrel dose), followed by 90 mg twice daily beginning 12 hours later (Ref).

>30 days after ACS or PCI: Administer ticagrelor 90 mg twice daily beginning 24 hours after the last dose of clopidogrel (Ref). Note: Some experts administer a ticagrelor 180 mg loading dose once within 24 hours after the last dose of clopidogrel (irrespective of timing of previous clopidogrel dose), followed by 90 mg twice daily beginning 12 hours later (Ref).

Transitioning from prasugrel:

≤30 days after ACS or PCI: Administer ticagrelor 180 mg loading dose once within 24 hours after the last dose of prasugrel (irrespective of timing of previous prasugrel dose), followed by 90 mg twice daily beginning 12 hours later (Ref).

>30 days after ACS or PCI: Administer ticagrelor 90 mg twice daily beginning 24 hours after the last dose of prasugrel (Ref). Note: Some experts administer a ticagrelor 180 mg loading dose once within 24 hours after the last dose of prasugrel (irrespective of timing of previous prasugrel dose), followed by 90 mg twice daily beginning 12 hours later (Ref).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Adult

The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.

Altered kidney function: No dosage adjustment necessary for any degree of kidney dysfunction (Ref).

Hemodialysis, intermittent (thrice weekly): Not dialyzed: No supplemental dose or dosage adjustment necessary (Ref). A retrospective analysis of dialysis patients who had undergone percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) showed no difference in cardiovascular end points or bleeding for ticagrelor compared to clopidogrel (Ref); however, patients with end-stage kidney disease (ESKD) are at increased risk for bleeding, with or without antiplatelet therapy (Ref); monitor closely.

Peritoneal dialysis: Unlikely to be dialyzed (highly protein bound): No dosage adjustment necessary (Ref). A retrospective analysis of dialysis patients who had undergone PCI for AMI showed no difference in cardiovascular end points or bleeding for ticagrelor compared to clopidogrel (Ref); however, patients with ESKD are at increased risk for bleeding, with or without antiplatelet therapy (Ref); monitor closely.

CRRT: No dosage adjustment necessary (Ref).

PIRRT (eg, sustained, low-efficiency diafiltration): No dosage adjustment necessary (Ref).

Dosing: Hepatic Impairment: Adult

Mild impairment: No dosage adjustment necessary.

Moderate impairment: There are no dosage adjustments provided in the manufacturer's labeling (has not been studied); however, undergoes hepatic metabolism; use caution.

Severe impairment: Avoid use.

Dosing: Older Adult

Refer to adult dosing.

Adverse Reactions (Significant): Considerations
Bleeding

Ticagrelor may cause hemorrhage, including major hemorrhage. In the PLATO trial, ticagrelor was associated with an increased rate of non-procedure related bleeding, but there was no difference in the rate of overall major bleeding compared with clopidogrel (Ref). In the EUCLID trial, bleeding risk was also similar between patients who received ticagrelor versus patients who received clopidogrel (Ref). In the ISAR-REACT 5 trial, there was no difference in the rate of major bleeding between patients who received ticagrelor versus patients who received prasugrel (Ref). In the THATO trial, ticagrelor in combination with aspirin was associated with an increased risk of severe bleeding and intracranial hemorrhage compared to aspirin monotherapy in those with an acute ischemic stroke or transient ischemic attack (Ref). Reports of fatal or severe bleeding, including fatal and nonfatal intracranial bleeding, were rare (Ref). Bleeding should be suspected if the patient becomes hypotensive following recent coronary angiography, percutaneous coronary intervention, coronary artery bypass graft (CABG), or other surgical procedure, even in the absence of overt signs of bleeding. Studies suggest that platelet transfusions are ineffective in reversing the antiplatelet effect of ticagrelor, possibly due to reversible binding to the P2Y12 receptor (Ref).

Onset: Varied; bleeding events occurred at all time points, up to 12 months of follow-up, with bleeding in some instances within 30 days of treatment (Ref).

Risk factors:

• Low body weight (≤65 kg) (Ref)

• Hemoglobin ≤12 g/dL (Ref)

• Chronic kidney disease (CrCl <60 mL/minute) (Ref)

• Moderate to severe hepatic impairment

• Concurrent use of other medications that increase bleeding risk (eg, anticoagulants, aspirin, nonsteroidal anti-inflammatory drugs) (Ref)

• Older age (≥80 years) (Ref)

• Recent trauma or surgery (eg, CABG)

• Recent or recurrent GI bleeding

• Active peptic ulcer disease

Bradyarrhythmias

Ventricular pause and bradyarrhythmias, including atrioventricular (AV) block, have been reported with the use of ticagrelor (Ref). In the PLATO trial, a non-statistically significant higher incidence of bradyarrhythmias was found, and statistical significance was confirmed in a substudy of patients enrolled in the PLATO trial (Ref). Bradyarrhythmias consisted primarily of asymptomatic and nocturnal ventricular pause originating from the sinoatrial node (SA) (Ref). These bradyarrhythmias have rarely been associated with syncope which are reversible upon discontinuation of ticagrelor (Ref).

Mechanism: Not fully established; one potential mechanism includes direct effects on cardiac automaticity or conduction by P2Y12 inhibition. Another potential mechanism includes inhibition of adenosine uptake by erythrocytes, increasing systemic adenosine concentrations, exacerbating vagal-mediated nocturnal bradycardia, and/or directly inhibiting SA node conduction (Ref).

Onset: Varied; ventricular pauses ≥3 seconds were noted more frequently with ticagrelor than with clopidogrel during the first week following hospitalization for an acute coronary syndrome (Ref). In some case studies, bradycardia occurred within hours after ticagrelor administration (Ref).

Risk factors:

• Concurrent use of AV nodal blocking agents (Ref)

• Underlying conduction disorder (sick sinus syndrome, AV nodal block, left or right bundle branch block, bradycardia-related syncope not protected by a pacemaker) (Ref)

Respiratory effects

Respiratory effects, including dyspnea (most common) and sleep apnea, including Cheyne-Stokes respiration, have been reported with ticagrelor (Ref). Multiple trials have reported an increased incidence of dyspnea in patients receiving ticagrelor compared to clopidogrel or aspirin alone (Ref). One study reported central sleep apnea hypopnea syndrome and obstructive sleep apnea hypopnea syndrome more frequently in patients taking ticagrelor; however, other studies have not found this association (Ref). Although not fatal, dyspnea and sleep apnea may not be well tolerated, warranting discontinuation. In most cases, dyspnea is self-limiting and resolves within 1 week of treatment (Ref). Sleep apnea also appears to resolve upon discontinuation (Ref).

Mechanism: Non–­dose-related; inhibits sodium-independent equilibrative nucleoside transporter-1, increasing adenosine levels in plasma and affecting vagal fibers in the lungs, leading to dyspnea (Ref). Additionally, ticagrelor may have CNS P2Y12 receptor inhibitory effects, increasing chemo-sensitivity to hypercapnia (Ref).

Onset:

• Dyspnea: Rapid; typically develops within the first 24 hours of therapy; however, may occur later (Ref).

• Sleep apnea: Varied; sleep apnea events occurred from 7 days to up to 1 year following therapy initiation (Ref).

Risk factors:

• Females (Ref)

• Age >70 years (Ref)

• Chronic obstructive pulmonary disease (Ref)

Thrombotic thrombocytopenic purpura (TTP)

Cases of thrombotic thrombocytopenic purpura (TTP) associated with ticagrelor have been reported, and while rare, some have resulted in fatalities, particularly following rechallenge (Ref). The overall evidence of ticagrelor-associated TTP is limited to case reports. Early signs of TTP may include neurologic changes (eg, headache, fatigue, hemiparesis/stroke) (Ref). TTP is typically characterized by thrombocytopenia, hemolytic anemia, kidney or liver failure, and fever (Ref).

Mechanism: Possibly immunologic; production of autoantibodies against ADAMTS-13, inducing microvascular thrombosis and other symptoms of TTP may play a major role (Ref). In several cases, low ADAMTS-13 was found, supporting this mechanism (Ref).

Onset: Varied; patients presented from 2 weeks to 2 months following initiation of ticagrelor (Ref).

Adverse Reactions

The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.

>10%: Respiratory: Dyspnea (14% to 21%) (table 1)

Ticagrelor: Adverse Reaction: Dyspnea

Drug (Ticagrelor)

Comparator (Clopidogrel)

Number of Patients (Ticagrelor)

Number of Patients (Clopidogrel)

21%

N/A

9,619

N/A

14%

8%

9,235

9,186

14%

6%

6,958

6,996

1% to 10%:

Cardiovascular: ECG abnormality (ventricular pause: 2% to 6%) (table 2)

Ticagrelor: Adverse Reaction: ECG Abnormality

Drug (Ticagrelor)

Comparator (Clopidogrel)

Comments

6%

4%

Ventricular pauses; acute phase

2%

2%

Ventricular pauses; after 1 month

Gastrointestinal: Nausea (4%)

Hematologic & oncologic: Hemorrhage (4%; major hemorrhage: 4%) (table 3)

Ticagrelor: Adverse Reaction: Major Hemorrhage

Drug (Ticagrelor)

Comparator (Clopidogrel)

Number of Patients (Ticagrelor)

Number of Patients (Clopidogrel)

Comments

4%

3%

9,235

9,186

Noncoronary artery bypass graft surgery-related bleeding events

Nervous system: Dizziness (5%)

Neuromuscular & skeletal: Gout (≤2%)

Renal: Increased serum creatinine (4% to 7%; transient)

Frequency not defined: Endocrine & metabolic: Increased uric acid

Postmarketing:

Cardiovascular: Atrioventricular block (Waldmann 2018), bradycardia (Waldmann 2018)

Dermatologic: Skin rash

Hematologic & oncologic: Thrombotic thrombocytopenic purpura (Wang 2018)

Hypersensitivity: Angioedema (Piranavan 2018; Seecheran 2017)

Respiratory: Cheyne-Stokes respiration (Giannoni 2016), sleep apnea (central) (Paboeuf 2019)

Miscellaneous: Laboratory test abnormality (false negative platelet functional tests, including heparin-induced platelet aggregation [HIPA] assay)

Contraindications

Hypersensitivity (eg, angioedema) to ticagrelor or any component of the formulation; active pathological bleeding (eg, peptic ulcer, intracranial hemorrhage); history of intracranial hemorrhage

Canadian labeling: Additional contraindications (not in US labeling): Moderate to severe hepatic impairment; concomitant use of strong CYP3A4 inhibitors (eg, ketoconazole, clarithromycin, ritonavir, atazanavir, nefazodone)

Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Warnings/Precautions

Concerns related to adverse effects:

• Hyperuricemia: Use with caution in patients with a history of hyperuricemia or gouty arthritis. Renal uptake and transport of uric acid are inhibited by ticagrelor and its active metabolite and the risk of hyperuricemia may be increased (Butler 2012a; Zhang 2015). However, reports of gout did not differ between treatment groups in the PLATO trial.

Disease-related concerns:

• Bleeding disorders: Use with caution in patients with platelet disorders, bleeding disorders, and/or at increased risk for bleeding.

• Heparin-induced thrombocytopenia: False-negative results may occur for platelet activation functional assays, which are used to diagnose heparin-induced thrombocytopenia. This may be due to ticagrelor inhibition of P2Y12 receptors on healthy donor platelets, which are used for the assay, reducing platelet activation and interfering with results.

• Hepatic impairment: Use with caution in patients with moderate hepatic impairment (limited experience); avoid use in severe hepatic impairment (has not been studied).

• Renal impairment: Creatinine levels may rise during therapy (mechanism undetermined); monitor renal function.

Special populations:

• Acute ischemic stroke/transient ischemic attack patients: Use is not recommended in acute ischemic stroke or transient ischemic attack patients with an NIHSS score >5 or patients receiving thrombolysis; not studied.

• Lower GI bleed patients: An individualized and multidisciplinary approach should be utilized to determine therapy discontinuation and management in patients with acute lower GI bleed who are on antiplatelet medications; risk of ongoing bleeding should be weighed with risk of thromboembolic events. In patients receiving dual antiplatelet therapy (aspirin plus P2Y12 inhibitor [eg, clopidogrel, prasugrel, ticagrelor, ticlopidine]) or P2Y12 inhibitor monotherapy, the P2Y12 inhibitor should generally be resumed as soon as possible and at least within 7 days, taking into account control of bleeding and cardiovascular risk (aspirin should not be discontinued) (Strate 2016).

• Surgical patients: For elective coronary artery bypass graft (CABG) surgery, discontinue ticagrelor at least 3 days before surgery; when urgent CABG is necessary, discontinue ticagrelor for at least 24 hours prior to surgery (patient-specific situations should be discussed with a cardiologist, interventional cardiologist, and a cardiac surgeon) (ACC/AHA [Grines 2007]; ACC/AHA [Lawton 2022]). In patients undergoing noncardiac surgery, the risks and benefits of ticagrelor should be evaluated between the surgeon and the cardiology team. Elective noncardiac surgery should not be performed in patients in whom dual antiplatelet therapy (DAPT) will need to be discontinued perioperatively within 30 days following bare metal stent placement or within 3 months of drug-eluting stent placement. In patients undergoing urgent noncardiac surgery during the first 4 to 6 weeks after BMS or DES placement, continue DAPT. In patients undergoing noncardiac surgery that requires discontinuation of ticagrelor, hold for 3 to 5 days preoperatively, continue aspirin and restart ticagrelor as soon as possible (eg, ≤24 hours) after surgery based on bleeding and thrombotic risks (ACC/AHA [Fleisher 2014]; ACC/AHA [Lawton 2022]; ACC/AHA [Levine 2016]; ACCP [Douketis 2022]).

Other warnings/precautions:

• Discontinuation of therapy: For patients who undergo percutaneous coronary intervention with stenting, premature interruption of therapy may result in increased risk of myocardial infarction, stent thrombosis, stroke, or death. If therapy must be held temporarily (eg, bleeding, surgery), restart as soon as possible. Duration of therapy is determined by the type of stent placed (bare metal or drug eluting), whether an acute coronary syndrome event was ongoing at the time of placement, as well as risks for bleeding and thrombosis (ACC/AHA [Lawton 2022]).

Dosage Forms: US

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral:

Brilinta: 60 mg, 90 mg

Generic Equivalent Available: US

No

Pricing: US

Tablets (Brilinta Oral)

60 mg (per each): $9.02

90 mg (per each): $9.02

Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral:

Brilinta: 60 mg, 90 mg

Generic: 60 mg, 90 mg

Administration: Adult

Oral: Administer with or without food. Missed doses should be taken at their next regularly scheduled time. For patients unable to swallow whole, tablets may be crushed and mixed with water to create a suspension for oral or NG (CH8/Fr8 or greater according to the manufacturer) use. If suspension is administered orally, refill glass with water, stir and drink; if administered via NG tube, flush NG tube through with water after administration (Ref). Administration of crushed tablets, while bioequivalent to administration of whole tablets, may result in increased concentrations of ticagrelor and the major active metabolite at earlier time points (Ref).

Medication Guide and/or Vaccine Information Statement (VIS)

An FDA-approved patient medication guide, which is available with the product information and at https://www.accessdata.fda.gov/drugsatfda_docs/label/2022/022433s034lbl.pdf#page=35, must be dispensed with this medication.

Use: Labeled Indications

Acute coronary syndrome: To reduce the risk of cardiovascular death, myocardial infarction (MI), and stroke in patients with acute coronary syndrome (ACS) or a history of MI. Ticagrelor also reduces the risk of stent thrombosis in patients who have been stented for treatment of ACS.

Coronary artery disease (stable) and high risk for ischemic cardiovascular events, primary prevention: To reduce the risk of first MI or stroke in patients with coronary artery disease at high risk for such events. Note: Efficacy was established in patients with type 2 diabetes mellitus (Steg 2019), but the manufacturer does not limit use to this setting.

Minor ischemic stroke (based on National Institutes of Health Stroke Scale score) or high-risk transient ischemic attack (based on ABCD2 score): To reduce the risk of stroke in patients who meet these criteria.

Use: Off-Label: Adult

Percutaneous coronary intervention for stable ischemic heart disease

Medication Safety Issues
Sound-alike/look-alike issues:

Brilinta may be confused with Brintellix, Briviact.

High-Risk Medication:

Beers Criteria: Ticagrelor is identified in the Beers Criteria as a potentially inappropriate medication to be used with caution, especially in patients 75 years and older due to increased risk of bleeding compared with clopidogrel; however, cardiovascular benefit in certain older adults may offset risk (Beers Criteria [AGS 2023]).

Metabolism/Transport Effects

Substrate of CYP3A4 (major); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential; Inhibits BCRP/ABCG2

Drug Interactions

Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.

Abrocitinib: Agents with Antiplatelet Properties may enhance the antiplatelet effect of Abrocitinib. Management: Do not use antiplatelet drugs with abrocitinib during the first 3 months of abrocitinib therapy. The abrocitinib prescribing information lists this combination as contraindicated. This does not apply to low dose aspirin (81 mg/day or less). Risk X: Avoid combination

Acalabrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Agents with Antiplatelet Properties (e.g., P2Y12 inhibitors, NSAIDs, SSRIs, etc.): May enhance the antiplatelet effect of other Agents with Antiplatelet Properties. Risk C: Monitor therapy

Alpelisib: BCRP/ABCG2 Inhibitors may increase the serum concentration of Alpelisib. Management: Avoid coadministration of BCRP/ABCG2 inhibitors and alpelisib due to the potential for increased alpelisib concentrations and toxicities. If coadministration cannot be avoided, closely monitor for increased alpelisib adverse reactions. Risk D: Consider therapy modification

Anagrelide: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Anticoagulants: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants. Risk C: Monitor therapy

Antiplatelet Agents (P2Y12 Inhibitors): May enhance the antiplatelet effect of Ticagrelor. Risk X: Avoid combination

Apixaban: Antiplatelet Agents (P2Y12 Inhibitors) may enhance the adverse/toxic effect of Apixaban. Specifically, the risk for bleeding may be increased. Management: Carefully consider risks and benefits of this combination and monitor closely; Canadian labeling recommends avoiding prasugrel or ticagrelor. Risk D: Consider therapy modification

Aspirin: May enhance the antiplatelet effect of Ticagrelor. Aspirin may diminish the therapeutic effect of Ticagrelor. More specifically, the benefits of ticagrelor relative to clopidogrel may be diminished in adult patients receiving daily aspirin doses greater than 100-150 mg daily. Management: Avoid maintenance aspirin doses greater than 150 mg/day in patients receiving ticagrelor. After any initial dose, only low-dose aspirin (75 to 100 mg/day) is recommended. Risk D: Consider therapy modification

Atorvastatin: Ticagrelor may increase the serum concentration of Atorvastatin. Risk C: Monitor therapy

Bemiparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Bemiparin. Management: Avoid concomitant use of bemiparin with antiplatelet agents. If concomitant use is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification

Berotralstat: BCRP/ABCG2 Inhibitors may increase the serum concentration of Berotralstat. Management: Decrease the berotralstat dose to 110 mg daily when combined with BCRP inhibitors. Risk D: Consider therapy modification

Caplacizumab: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Caplacizumab. Specifically, the risk of bleeding may be increased. Management: Avoid coadministration of caplacizumab with antiplatelets if possible. If coadministration is required, monitor closely for signs and symptoms of bleeding. Interrupt use of caplacizumab if clinically significant bleeding occurs. Risk D: Consider therapy modification

Cephalothin: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Cephalothin. Specifically, the risk for bleeding may be increased. Risk C: Monitor therapy

Cladribine: BCRP/ABCG2 Inhibitors may increase the serum concentration of Cladribine. Management: Avoid concomitant use of BCRP inhibitors during the 4 to 5 day oral cladribine treatment cycles whenever possible. If combined, consider dose reduction of the BCRP inhibitor and separation in the timing of administration. Risk D: Consider therapy modification

Clofazimine: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

Collagenase (Systemic): Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Collagenase (Systemic). Specifically, the risk of injection site bruising and or bleeding may be increased. Risk C: Monitor therapy

CycloSPORINE (Systemic): May increase the serum concentration of Ticagrelor. Risk C: Monitor therapy

CYP3A4 Inducers (Moderate): May decrease serum concentrations of the active metabolite(s) of Ticagrelor. CYP3A4 Inducers (Moderate) may decrease the serum concentration of Ticagrelor. Risk C: Monitor therapy

CYP3A4 Inducers (Strong): May decrease serum concentrations of the active metabolite(s) of Ticagrelor. CYP3A4 Inducers (Strong) may decrease the serum concentration of Ticagrelor. Risk X: Avoid combination

CYP3A4 Inhibitors (Moderate): May decrease serum concentrations of the active metabolite(s) of Ticagrelor. CYP3A4 Inhibitors (Moderate) may increase the serum concentration of Ticagrelor. Risk C: Monitor therapy

CYP3A4 Inhibitors (Strong): May decrease serum concentrations of the active metabolite(s) of Ticagrelor. CYP3A4 Inhibitors (Strong) may increase the serum concentration of Ticagrelor. Risk X: Avoid combination

Dabigatran Etexilate: Ticagrelor may enhance the anticoagulant effect of Dabigatran Etexilate. Ticagrelor may increase the serum concentration of Dabigatran Etexilate. Management: Carefully consider the anticipated risks and benefits of this combination. Increase monitoring bleeding if these agents are combined and consider avoiding the use of this combination in the presence of reduced renal function. Risk D: Consider therapy modification

Dasatinib: May enhance the anticoagulant effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Deoxycholic Acid: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Deoxycholic Acid. Specifically, the risk for bleeding or bruising in the treatment area may be increased. Risk C: Monitor therapy

Diamorphine: May diminish the antiplatelet effect of Antiplatelet Agents (P2Y12 Inhibitors). Diamorphine may decrease the serum concentration of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor therapy

Digoxin: Ticagrelor may increase the serum concentration of Digoxin. Risk C: Monitor therapy

Edoxaban: Antiplatelet Agents (P2Y12 Inhibitors) may enhance the adverse/toxic effect of Edoxaban. Specifically, the risk of bleeding may be increased. Management: Carefully consider the anticipated risks and benefits of this combination. If combined, increased monitoring for bleeding is recommended. Risk D: Consider therapy modification

Enoxaparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Enoxaparin. Management: Discontinue antiplatelet agents prior to initiating enoxaparin whenever possible. If concomitant administration is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification

FentaNYL: May diminish the antiplatelet effect of Antiplatelet Agents (P2Y12 Inhibitors). FentaNYL may decrease the serum concentration of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor therapy

Fexinidazole: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk X: Avoid combination

Fusidic Acid (Systemic): May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Management: Consider avoiding this combination if possible. If required, monitor patients closely for increased adverse effects of the CYP3A4 substrate. Risk D: Consider therapy modification

Grapefruit Juice: May increase the serum concentration of Ticagrelor. Risk C: Monitor therapy

Heparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Heparin. Management: Decrease the dose of heparin or agents with antiplatelet properties if coadministration is required. Risk D: Consider therapy modification

Herbal Products with Anticoagulant/Antiplatelet Effects (eg, Alfalfa, Anise, Bilberry): May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Bleeding may occur. Risk C: Monitor therapy

Ibritumomab Tiuxetan: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Ibritumomab Tiuxetan. Both agents may contribute to impaired platelet function and an increased risk of bleeding. Risk C: Monitor therapy

Ibrutinib: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Icosapent Ethyl: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Inotersen: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Itraconazole: May increase the serum concentration of Ticagrelor. Risk X: Avoid combination

Lecanemab: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Specifically, the risk of hemorrhage may be increased. Risk C: Monitor therapy

Limaprost: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Lipid Emulsion (Fish Oil Based): May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Lomitapide: Ticagrelor may increase the serum concentration of Lomitapide. Management: Patients taking lomitapide 10 mg/day or more should decrease the lomitapide dose by half with concurrent ticagrelor; the lomitapide dose may then be increased to a max adult dose of 30 mg/day (patients on lomitapide 5 mg/day may continue that dose). Risk D: Consider therapy modification

Lovastatin: Ticagrelor may increase the serum concentration of Lovastatin. Management: Limit lovastatin doses to 40 mg/day if coadministered with ticagrelor. Risk D: Consider therapy modification

Morphine (Systemic): May diminish the antiplatelet effect of Antiplatelet Agents (P2Y12 Inhibitors). Morphine (Systemic) may decrease the serum concentration of Antiplatelet Agents (P2Y12 Inhibitors). Management: Consider alternative anti-ischemic/analgesic therapies (eg, beta-blockers, nitroglycerin) in patients with acute coronary syndromes treated with a P2Y12 inhibitor when possible. The risks associated with other opioids are unknown. Risk D: Consider therapy modification

Multivitamins/Fluoride (with ADE): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Multivitamins/Minerals (with ADEK, Folate, Iron): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Multivitamins/Minerals (with AE, No Iron): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Obinutuzumab: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Obinutuzumab. Specifically, the risk of serious bleeding-related events may be increased. Risk C: Monitor therapy

Omega-3 Fatty Acids: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

PAZOPanib: BCRP/ABCG2 Inhibitors may increase the serum concentration of PAZOPanib. Risk X: Avoid combination

Pentosan Polysulfate Sodium: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Specifically, the risk of bleeding may be increased by concurrent use of these agents. Risk C: Monitor therapy

Pentoxifylline: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Pirtobrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Prostacyclin Analogues: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Red Yeast Rice: Ticagrelor may increase the serum concentration of Red Yeast Rice. Management: Avoid using doses of red yeast rice greater than the equivalent of lovastatin 40 mg/day with ticagrelor. Monitor for increased systemic effects of lovastatin in patients receiving concurrent ticagrelor. Risk D: Consider therapy modification

Rivaroxaban: Antiplatelet Agents (P2Y12 Inhibitors) may enhance the adverse/toxic effect of Rivaroxaban. Specifically, the risk of bleeding may be increased. Management: Carefully consider risks and benefits of this combination and monitor closely; Canadian labeling recommends avoiding prasugrel or ticagrelor. Risk D: Consider therapy modification

Rosuvastatin: Ticagrelor may enhance the myopathic (rhabdomyolysis) effect of Rosuvastatin. Ticagrelor may increase the serum concentration of Rosuvastatin. Risk C: Monitor therapy

Selective Serotonin Reuptake Inhibitors: May enhance the antiplatelet effect of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor therapy

Selumetinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Serotonin/Norepinephrine Reuptake Inhibitors: May enhance the antiplatelet effect of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor therapy

Simvastatin: Ticagrelor may increase the serum concentration of Simvastatin. Management: Avoid using doses of simvastatin greater than 40 mg/day with ticagrelor. Monitor for increased systemic effects of simvastatin in patients receiving concurrent ticagrelor. Risk D: Consider therapy modification

Talazoparib: BCRP/ABCG2 Inhibitors may increase the serum concentration of Talazoparib. Risk C: Monitor therapy

Thrombolytic Agents: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents. Risk C: Monitor therapy

Tipranavir: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Topotecan: BCRP/ABCG2 Inhibitors may increase the serum concentration of Topotecan. Risk X: Avoid combination

Ubrogepant: BCRP/ABCG2 Inhibitors may increase the serum concentration of Ubrogepant. Management: Use an initial ubrogepant dose of 50 mg and second dose (at least 2 hours later if needed) of 50 mg when used with a BCRP inhibitor. Risk D: Consider therapy modification

Urokinase: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Urokinase. Risk X: Avoid combination

Vitamin E (Systemic): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Volanesorsen: May enhance the antiplatelet effect of Therapeutic Antiplatelets. Risk C: Monitor therapy

Zanubrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy

Pregnancy Considerations

Outcome data following the use of ticagrelor in pregnancy are limited (Antonijevic 2023, Serna Candel 2019, Verbruggen 2015).

Due to lack of data, use in pregnancy is not recommended (ESC [Regitz-Zagrosek 2018]).

Breastfeeding Considerations

It is not known if ticagrelor is present in breast milk.

Breastfeeding is not recommended by the manufacturer.

Monitoring Parameters

Signs of bleeding; hemoglobin and hematocrit periodically; sign/symptoms of bradycardia; renal function; uric acid levels (patients with gout or at risk of hyperuricemia); signs/symptoms of dyspnea.

Mechanism of Action

Reversibly and noncompetitively binds the adenosine diphosphate (ADP) P2Y12 receptor on the platelet surface which prevents ADP-mediated activation of the GPIIb/IIIa receptor complex thereby reducing platelet aggregation. Due to the reversible antagonism of the P2Y12 receptor, recovery of platelet function is likely to depend on serum concentrations of ticagrelor and its active metabolite.

Pharmacokinetics (Adult Data Unless Noted)

Onset of inhibition of platelet aggregation (IPA): 180 mg loading dose: ~41% within 30 minutes (similar to clopidogrel 600 mg at 8 hours)

Peak effect: Time to maximal IPA: 180 mg loading dose: IPA ~88% at 2 hours post administration

Duration of IPA: 180 mg loading dose: 87% to 89% maintained from 2 to 8 hours; 24 hours after the last maintenance dose, IPA is 58% (similar to maintenance dosing for clopidogrel)

Time after discontinuation when IPA is 30%: ~56 hours; IPA 10%: ~110 hours (Gurbel 2009). Mean IPA observed with ticagrelor at 3 days post-discontinuation was comparable to that observed with clopidogrel at 5 days post discontinuation.

Absorption: Rapid

Distribution: 88 L

Protein binding: >99% (parent drug and active metabolite)

Metabolism: Hepatic via CYP3A4/5 to active metabolite (AR-C124910XX)

Bioavailability: ~36% (range: 30% to 42%)

Half-life elimination: Parent drug: ~7 hours; active metabolite: ~9 hours

Time to peak:

Whole tablets: Parent drug: 1.5 hours (median; range: 1 to 4 hours); Active metabolite (AR-C124910XX): 2.5 hours (median; range: 1.5 to 5 hours)

Crushed tablets: Oral or nasogastric tube administration: Parent drug: ~1 hour (median; range: 1 to 4 hours); Active metabolite (AR-C124910XX): 2 hours (median; range: 1 to 8 hours). Note: Significantly higher concentrations of both ticagrelor and AR-C124910XX may appear at earlier time points (0.5 and 1 hour, respectively) when administered as crushed tablets (Teng 2015).

Excretion: Feces (58%); urine (26%); actual amount of parent drug and active metabolite excreted in urine was <1% of total dose administered

Pharmacokinetics: Additional Considerations (Adult Data Unless Noted)

Altered kidney function: AUC and Cmax were 38% and 51% higher, respectively, in patients with end-stage renal disease on hemodialysis compared to patients with normal renal function following a single 90 mg dose of ticagrelor administered on a nondialysis day; similar exposure was observed when administered immediately prior to dialysis. Inhibition of platelet aggregation was independent of dialysis and similar to healthy adults with normal renal function.

Cigarette smoking: Mean clearance was increased by ~22% in smokers.

Brand Names: International
International Brand Names by Country
For country code abbreviations (show table)

  • (AE) United Arab Emirates: Brilinta;
  • (AR) Argentina: Brilinta | Brilique | Ticazan;
  • (AT) Austria: Brilique;
  • (AU) Australia: Brilinta;
  • (BD) Bangladesh: Acora | Brilinta | Brirel | Plarit | Ticacard | Ticaflow | Ticalog | Tiga | Tigel;
  • (BE) Belgium: Brilique;
  • (BG) Bulgaria: Brilique;
  • (BR) Brazil: Brilinta | Coaly | Tiag;
  • (CH) Switzerland: Brilique;
  • (CL) Chile: Brilinta | Revagrel;
  • (CN) China: Brilinta;
  • (CO) Colombia: Brilinta | Tiare | Ticagrel | Vasogrelor;
  • (CZ) Czech Republic: Brilique;
  • (DE) Germany: Brilique;
  • (DO) Dominican Republic: Brilinta;
  • (EC) Ecuador: Brilinta | Timed;
  • (EE) Estonia: Brilique;
  • (EG) Egypt: Brilique | Lintaram | Thrombolinta;
  • (ES) Spain: Brilique;
  • (FI) Finland: Brilique;
  • (FR) France: Brilinta | Brilique;
  • (GB) United Kingdom: Brilique;
  • (GR) Greece: Brilique;
  • (HK) Hong Kong: Brilinta;
  • (HR) Croatia: Brilique;
  • (HU) Hungary: Brilique;
  • (ID) Indonesia: Brilinta;
  • (IE) Ireland: Brilique;
  • (IN) India: Axcer | Brigrel | Brilinta | Tackel | Tiare | Ticabest | Ticabid | Ticacip | Ticaflo | Ticagat | Ticagold | Ticahenz | Ticalor | Ticaplat | Ticasave | Ticasave plus | Ticaspan | Ticastro | Ticatroy | Ticavic | Ticus | Tigemac | Tikacad | Torplat | Vasoglor | Xygrel;
  • (IT) Italy: Brilique;
  • (JO) Jordan: Brilinta | Tagbro | Thincor;
  • (JP) Japan: Brilinta;
  • (KE) Kenya: Brilinta | Corolor | Tiglor;
  • (KR) Korea, Republic of: Austica | Boryung ticagrelor | Brelor | Brilcoron | Brilgrelor | Brilinta | Brilor | Britica | Btaon | Dongkoo ticagrelor | Glotica | Hutica | Inno.n ticagrelor | Samjin ticagrelor | Seoul ticagrelor | Tibrinta | Ticabrel | Ticabril | Ticada | Ticagen | Ticagle | Ticagrin | Ticaon | Ticarax | Tielinta | Tiglia | Tiglor | Tigrel | Tigrela | Tirinta | Trilinta | Unitica | Yooyoung tica;
  • (KW) Kuwait: Brilinta;
  • (LB) Lebanon: Brilinta | Klotego;
  • (LT) Lithuania: Brilique;
  • (LU) Luxembourg: Brilique;
  • (LV) Latvia: Brilique;
  • (MA) Morocco: Brilique;
  • (MX) Mexico: Brilinta;
  • (MY) Malaysia: Brilinta;
  • (NL) Netherlands: Brilique;
  • (NO) Norway: Brilique;
  • (NZ) New Zealand: Brilinta | Ticagrelor sandoz;
  • (PE) Peru: Brilinta | Supagrel;
  • (PH) Philippines: Brilinta;
  • (PK) Pakistan: Anplag | Bilinta | Grehil | Virata;
  • (PL) Poland: Brilique;
  • (PR) Puerto Rico: Brilinta;
  • (PT) Portugal: Brilique;
  • (QA) Qatar: Brilinta;
  • (RO) Romania: Brilique;
  • (RU) Russian Federation: Brilinta;
  • (SA) Saudi Arabia: Brilinta | Ticagrelor spc;
  • (SE) Sweden: Brilique;
  • (SG) Singapore: Brilinta;
  • (SI) Slovenia: Brilique;
  • (SK) Slovakia: Brilique;
  • (TH) Thailand: Brilinta;
  • (TN) Tunisia: Brilique | Theraglor;
  • (TR) Turkey: Agrilor | Brilinta | Camilla | Tilanta | Tixalor;
  • (TW) Taiwan: Brilinta;
  • (UA) Ukraine: Brilinta;
  • (UG) Uganda: Brilinta;
  • (UY) Uruguay: Brilinta;
  • (VE) Venezuela, Bolivarian Republic of: Brilinta | Clenosan;
  • (VN) Viet Nam: Platetica | Topogis;
  • (ZA) South Africa: Brilinta | Tiare | Ticagrel
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