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Ticagrelor ball-and-stick animation.gif
Clinical data
Trade names Brilinta, Brilique, others
Other namesAZD-6140
AHFS/Drugs.com Monograph
MedlinePlus a611050
License data
Routes of
By mouth
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability 36%
Protein binding >99.7%
Metabolism Liver (CYP3A4)
Elimination half-life 7 hrs (ticagrelor), 8.5 hrs (active metabolite AR-C124910XX)
Excretion Bile duct
  • (1S,2S,3R,5S)-3-[7-[(1R,2S)-2-(3,4-Difluorophenyl)cyclopropylamino]-5-(propylthio)- 3H-[1,2,3]triazolo[4,5-d]pyrimidin-3-yl]-5-(2-hydroxyethoxy)cyclopentane-1,2-diol
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard 100.114.746 OOjs UI icon edit-ltr-progressive.svg
Chemical and physical data
Formula C23H28F2N6O4S
Molar mass 522.57 g·mol−1
3D model (JSmol)
  • CCCSc1nc(N[C@@H]2C[C@H]2c2ccc(F)c(F)c2)c2nnn([C@@H]3C[C@H](OCCO)[C@@H](O)[C@H]3O)c2n1
  • InChI=1S/C23H28F2N6O4S/c1-2-7-36-23-27-21(26-15-9-12(15)11-3-4-13(24)14(25)8-11)18-22(28-23)31(30-29-18)16-10-17(35-6-5-32)20(34)19(16)33/h3-4,8,12,15-17,19-20,32-34H,2,5-7,9-10H2,1H3,(H,26,27,28)/t12-,15+,16+,17-,19-,20+/m0/s1 X mark.svgN
 X mark.svgNYes check.svgY  (what is this?)    (verify)

Ticagrelor, sold under the brand name Brilinta among others, is a medication used for the prevention of stroke, heart attack and other events in people with acute coronary syndrome, meaning problems with blood supply in the coronary arteries. It acts as a platelet aggregation inhibitor by antagonising the P2Y12 receptor. [5] The drug is produced by AstraZeneca.


90 mg tablet of Brilinta Brilinta.png
90 mg tablet of Brilinta

The most common side effects include dyspnea (difficulty breathing), bleeding and raised uric acid level in the blood. [4]

It was approved for medical use in the European Union in December 2010, [4] [6] [7] and in the United States in July 2011. [3] [8] [9] In 2020, it was the 247th most commonly prescribed medication in the United States, with more than 1 million prescriptions. [10] [11]

Medical uses

In the US, ticagrelor is indicated to reduce the risk of stroke in people with acute ischemic stroke or high-risk transient ischemic attack. [3]

In the EU, ticagrelor, co-administered with acetylsalicylic acid (aspirin), is indicated for the prevention of atherothrombotic events in adults with acute coronary syndromes or a history of myocardial infarction and a high risk of developing an atherothrombotic event; and for the prevention of atherothrombotic events in adults with a history of myocardial infarction and a high risk of developing an atherothrombotic event. [4]


Contraindications to ticagrelor are active bleeding, increased risk of bradycardia, concomitant therapy of ticagrelor and strong cytochrome P-450 3A (CYP3A4) inhibitors and moderate or severe hepatic impairment due to the risk of increased exposure to ticagrelor. [12] [13]

Adverse effects

The common adverse effects are increased risk of bleeding (which may be severe) [14] and shortness of breath (dyspnoea). [15] Dyspnoea is usually transient and mild-to-moderate in severity, with a higher risk at < 1 month, 1–6 months and >6 months of follow up compared to clopidogrel. [15] [16] [17] [18] Discontinuation of therapy is rare, although some people do not persist or switch therapies. [15] [16] [17] People who develop tolerable dyspnoea as a side effect of ticagrelor should be reassured to continue therapy, as it does not impact on the drug's cardiovascular benefit and bleeding risk in acute coronary syndrome (ACS). [15] Furthermore, two small subgroup analyses found no associations between ticagrelor and adverse changes in heart and lung function that may induce dyspnoea in stable coronary artery disease (CAD) and people with ACS without heart failure or significant lung disease. [16] [19]

Ventricular pauses ≥3 seconds may occur in people with ACS the first week of treatment, but are likely to be mostly asymptomatic and transient, without causing increased clinical bradycardic adverse events. [20] Caution is recommended when using ticagrelor in people with advanced sinoatrial node disease. [21] Allergic skin reactions such as rash and itching have been observed in less than 1% of people taking ticagrelor. [22]


Inhibitors of the liver enzyme CYP3A4, such as ketoconazole and possibly grapefruit juice, increase blood plasma levels of ticagrelor and consequently can lead to bleeding and other adverse effects. Ticagrelor is a weak CYP3A4 inhibitor [23] and is known to increase the concentrations of CYP3A4 metabolised medications; however, this interaction is unlikely to be clinically significant for atorvastatin and simvastatin [24] [23] [12] at recommended doses. CYP3A4 inducers, for example rifampicin and possibly St. John's wort, can reduce the effectiveness of ticagrelor. There is no evidence for interactions via CYP2C9.

The drug also inhibits P-glycoprotein (P-gp), leading to increased plasma levels of digoxin, ciclosporin and other P-gp substrates. Levels of ticagrelor and AR-C124910XX (the active metabolite of ticagrelor formed by O-deethylation [25] ) are not significantly influenced by P-gp inhibitors. [22]

It is recommended to use low-dose aspirin (75–100 mg per day) with ticagrelor as dual antiplatelet therapy (DAPT). [12] [26] [27] [28] [29] [30] The combination of ticagrelor with aspirin doses greater than 100 mg per day may be less effective. [31]


Mechanism of action

Like the thienopyridines prasugrel, clopidogrel and ticlopidine, ticagrelor blocks adenosine diphosphate (ADP) receptors of subtype P2Y12. In contrast to the other antiplatelet drugs, ticagrelor has a binding site different from ADP, making it an allosteric antagonist, and the blockage is reversible. [32] Moreover, the drug does not need hepatic activation, which might work better for people with genetic variants regarding the enzyme CYP2C19 (although it is not certain whether clopidogrel is significantly influenced by such variants). [33] [34] [35] Ticagrelor was found to result in a lower risk of stroke at 90 days than clopidogrel, which requires metabolic conversion, among Han Chinese CYP2C19 loss-of-function carriers with minor ischemic stroke or TIA. [36]


Ticagrelor is absorbed quickly from the gut, the bioavailability being 36%, and reaches its peak concentration after about 1.5 hours. The main metabolite, AR-C124910XX, is formed quickly via CYP3A4 by de-hydroxyethylation at position 5 of the cyclopentane ring. [25]

Plasma concentrations of ticagrelor are slightly increased (12–23%) in elderly people, women, people of Asian ethnicity, and people with mild hepatic impairment. They are decreased in people that self-identified as 'black' and those with severe renal impairment. These differences are not considered clinically relevant. In Japanese people, concentrations are 40% higher than in Caucasians, or 20% after body weight correction. The drug has not been tested in people with severe hepatic impairment. [22] [37]

Consistently with its reversible mode of action, ticagrelor is known to act faster and shorter than clopidogrel. [38] This means it has to be taken twice instead of once a day which is a disadvantage in respect of compliance, but its effects are more quickly reversible which can be useful before surgery or if side effects occur. [22] [39]


Ticagrelor is a nucleoside analogue: the cyclopentane ring is similar to the sugar ribose, and the nitrogen rich aromatic ring system resembles the nucleobase purine, giving the molecule an overall similarity to adenosine. The substance has low solubility and low permeability under the Biopharmaceutics Classification System. [6]

Ticagrelor as a nucleoside analogue Ticagrelor.svg
Ticagrelor as a nucleoside analogue
The nucleoside adenosine for comparison Adenosin.svg
The nucleoside adenosine for comparison


With clopidogrel

The PLATO trial concluded superiority of ticagrelor compared to clopidogrel in reducing the rate of death from vascular causes, MI, and stroke in people presenting with acute coronary syndromes. [12] A post-hoc subgroup analysis of the PLATO trial suggested a reduction in total mortality with ticagrelor compared to clopidogrel in people with non-ST elevation acute coronary syndrome. [40] However, this finding should only be considered exploratory as it was not a primary endpoint of the PLATO trial. [12] Subsequent studies have also been underpowered in evaluating total mortality benefits with ticagrelor. [41]

The PLATO trial [42] found that ticagrelor use, in conjunction with low-dose aspirin (where tolerated), had better all-cause mortality rates than the same treatment plan with clopidogrel (4.5% vs. 5.9%, p<0.001) in treating people with acute coronary syndrome. People given ticagrelor were less likely to die from vascular causes, heart attack, or stroke, regardless of whether the treatment plan was invasive. While the patient group on ticagrelor had more instances of fatal bleeding and intracranial bleeding, the difference in cases was not considered significant (p=0.70). Rates of major bleeding were not significantly different between the two groups (7.9% vs. 7.7%, p=0.57). However, dyspnoea was significantly more likely in the ticagrelor group (13.8% vs. 7.8%, p<0.001). Premature discontinuation of the study drug was far more common in the ticagrelor group (23.4% vs. 21.5%, p=0.002), which could be due to adverse events (7.4% vs. 6.0%, p<0.001) or the patient’s unwillingness to continue (10.1% vs. 9.2%, p = 0.04). [12]

The PLATO trial showed a statistically insignificant trend toward worse outcomes with ticagrelor versus clopidogrel among US participants in the study – who comprised 1627 of the total 13,326 participants. The hazard ratio actually reversed for the composite end point cardiovascular (death, MI, or stroke): 11.1% for participants given ticagrelor and 9.1% for participants given clopidogrel (HR = 1.27). [42] It is important to note that even though there was a trend to worse outcomes in the US patient population, this trend was still classed as insignificant, and therefore should not affect patient use in the US population. [42]

There is some conjecture in the safety and efficacy of ticagrelor within the Asian population, despite significant thrombotic benefits. [40] A meta-analysis of observational studies in several Asian countries proposed that ticagrelor did not increase the risk of considerable bleeding events in Asian individuals. [43] It is important to note that despite this being “real world” data, the study did not provide ethnic population demographics, leading to potential generalisation of data for Asian individuals. [43] There is evidence to suggest that East Asian individuals are at a higher risk of bleeding events when using ticagrelor. [44] [45] [46] Several recent meta-analyses of RCTs have been carried out in this population and although underpowered (more research is needed), the Asian Pacific Society of Cardiology Guidelines have taken these trials into account. [44] [45] [46] [47] The guidelines recommend that people of East Asian origin exercise caution and that treatment continuation after six months be based on net-clinical benefit. [47]

With prasugrel

In 2019, the results of the ISAR-REACT 5 trial was published, comparing ticagrelor and prasugrel in participants with acute coronary syndrome. [48]

An in vitro assay and mouse model study published in 2019, showed antibacterial activity against antibiotic-resistant Gram-positive bacteria including Methicillin Resistant Staphylococcus Aureus (MRSA) and Vancomycin Resistant Enterococcus (VRE). [49] This study used concentrations of ticagrelor for bactericidal activity that far exceeded those achieved by standard post Acute Coronary Syndrome (ACS) doses. [49] A single-center retrospective cohort study demonstrated a significant reduction in gram-positive infection in the first year of ticagrelor compared with clopidogrel post ACS. [50] Treatment with ticagrelor post PCI was also associated with a significantly lower absolute 1-year risk of S. aureus bacteraemia, sepsis, and pneumonia compared to clopidogrel in a nationwide observational study, however no causal inference can be drawn from the observational data. [51]

Related Research Articles

<span class="mw-page-title-main">Coronary artery disease</span> Reduction of blood flow to the heart muscle due to plaque buildup in the hearts arteries

Coronary artery disease (CAD), also called coronary heart disease (CHD), ischemic heart disease (IHD), myocardial ischemia, or simply heart disease, involves the reduction of blood flow to the heart muscle due to build-up of atherosclerotic plaque in the arteries of the heart. It is the most common of the cardiovascular diseases. Types include stable angina, unstable angina, and myocardial infarction. A common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw. Occasionally it may feel like heartburn. Usually symptoms occur with exercise or emotional stress, last less than a few minutes, and improve with rest. Shortness of breath may also occur and sometimes no symptoms are present. In many cases, the first sign is a heart attack. Other complications include heart failure or an abnormal heartbeat.

<span class="mw-page-title-main">Angioplasty</span> Procedure to widen narrow arteries or veins

Angioplasty, also known as balloon angioplasty and percutaneous transluminal angioplasty (PTA), is a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis. A deflated balloon attached to a catheter is passed over a guide-wire into the narrowed vessel and then inflated to a fixed size. The balloon forces expansion of the blood vessel and the surrounding muscular wall, allowing an improved blood flow. A stent may be inserted at the time of ballooning to ensure the vessel remains open, and the balloon is then deflated and withdrawn. Angioplasty has come to include all manner of vascular interventions that are typically performed percutaneously.

An antiplatelet drug (antiaggregant), also known as a platelet agglutination inhibitor or platelet aggregation inhibitor, is a member of a class of pharmaceuticals that decrease platelet aggregation and inhibit thrombus formation. They are effective in the arterial circulation where classical Vitamin K antagonist anticoagulants have minimal effect.

<span class="mw-page-title-main">Clopidogrel</span> Antiplatelet medication

Clopidogrel — sold under the brand name Plavix, among others — is an antiplatelet medication used to reduce the risk of heart disease and stroke in those at high risk. It is also used together with aspirin in heart attacks and following the placement of a coronary artery stent. It is taken by mouth. Its effect starts about two hours after intake and lasts for five days.

<span class="mw-page-title-main">Ticlopidine</span> Chemical compound

Ticlopidine, sold under the brand name Ticlid, is a medication used to reduce the risk of thrombotic strokes. It is an antiplatelet drug in the thienopyridine family which is an adenosine diphosphate (ADP) receptor inhibitor. Research initially showed that it was useful for preventing strokes and coronary stent occlusions. However, because of its rare but serious side effects of neutropenia and thrombotic thrombocytopenic purpura it was primarily used in patients in whom aspirin was not tolerated, or in whom dual antiplatelet therapy was desirable. With the advent of newer and safer antiplatelet drugs such as clopidogrel and ticagrelor, its use remained limited.

<span class="mw-page-title-main">Prasugrel</span> Medication used to prevent formation of blood clots

Prasugrel, sold under the brand name Effient in the US, Australia and India, and Efient in the EU) is a medication used to prevent formation of blood clots. It is a platelet inhibitor and an irreversible antagonist of P2Y12 ADP receptors and is of the thienopyridine drug class. It was developed by Daiichi Sankyo Co. and produced by Ube and marketed in the United States in cooperation with Eli Lilly and Company.

<span class="mw-page-title-main">Acute coronary syndrome</span> Medical condition

Acute coronary syndrome (ACS) is a syndrome due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. The most common symptom is centrally located pressure-like chest pain, often radiating to the left shoulder or angle of the jaw, and associated with nausea and sweating. Many people with acute coronary syndromes present with symptoms other than chest pain, particularly women, older people, and people with diabetes mellitus.

<span class="mw-page-title-main">Unstable angina</span> Medical condition

Unstable angina is a type of angina pectoris that is irregular or more easily provoked. It is classified as a type of acute coronary syndrome.

<span class="mw-page-title-main">Eptifibatide</span> Antiplatelet drug

Eptifibatide, is an antiplatelet drug of the glycoprotein IIb/IIIa inhibitor class. Eptifibatide is a cyclic heptapeptide derived from a disintegrin protein found in the venom of the southeastern pygmy rattlesnake. It belongs to the class of the arginin-glycin-aspartat-mimetics and reversibly binds to platelets. Eptifibatide has a short half-life. The drug is the third inhibitor of GPIIb/IIIa that has found broad acceptance after the specific antibody abciximab and the non-peptide tirofiban entered the global market.

P2Y<sub>12</sub> Protein-coding gene in the species Homo sapiens

P2Y12 is a chemoreceptor for adenosine diphosphate (ADP) that belongs to the Gi class of a group of G protein-coupled (GPCR) purinergic receptors. This P2Y receptor family has several receptor subtypes with different pharmacological selectivity, which overlaps in some cases, for various adenosine and uridine nucleotides. The P2Y12 receptor is involved in platelet aggregation and is thus a biological target for the treatment of thromboembolisms and other clotting disorders. Two transcript variants encoding the same isoform have been identified for this gene.

<span class="mw-page-title-main">Ivabradine</span> Heart medication

Ivabradine, sold under the brand name Procoralan among others, is a medication, which is a pacemaker current (If) inhibitor, used for the symptomatic management of heart-related chest pain and heart failure. Patients who qualify for use of Ivabradine for coronary heart failure are patients who have symptomatic heart failure, with reduced ejection volume, and heart rate at least 70 bpm, and the condition not able to be fully managed by beta blockers.

<span class="mw-page-title-main">Bivalirudin</span> Anticoagulant drug

Bivalirudin (Bivalitroban), sold under the brand names Angiomax and Angiox and manufactured by The Medicines Company, is a specific and reversible direct thrombin inhibitor (DTI).

<span class="mw-page-title-main">Coronary stent</span> Medical apparatus implanted into coronary arteries

A coronary stent is a tube-shaped device placed in the coronary arteries that supply blood to the heart, to keep the arteries open during the treatment of coronary heart disease. It is used in a procedure called percutaneous coronary intervention (PCI). Coronary stents are divided into two broad types - drug-eluting and bare metal, as of 2023 drug-eluting stents were used in more than 90% of all PCI procedures. Stents reduce angina and have been shown to improve survival and decrease adverse events after a patient has suffered a heart attack - acute myocardial infarction.

<span class="mw-page-title-main">Vorapaxar</span> Chemical compound

Vorapaxar is a thrombin receptor antagonist based on the natural product himbacine, discovered by Schering-Plough and developed by Merck & Co.

<span class="mw-page-title-main">Thienopyridine</span> Class of chemical compounds

Thienopyridines are a class of selective, irreversible ADP receptor/P2Y12 inhibitors used for their anti-platelet activity. They have a significant role in the management of cardiovascular disease.

<span class="mw-page-title-main">Myocardial infarction</span> Interruption of blood supply to a part of the heart

A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in one of the coronary arteries of the heart, causing infarction to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck or jaw. Often it occurs in the center or left side of the chest and lasts for more than a few minutes. The discomfort may occasionally feel like heartburn. Other symptoms may include shortness of breath, nausea, feeling faint, a cold sweat, feeling tired, and decreased level of consciousness. About 30% of people have atypical symptoms. Women more often present without chest pain and instead have neck pain, arm pain or feel tired. Among those over 75 years old, about 5% have had an MI with little or no history of symptoms. An MI may cause heart failure, an irregular heartbeat, cardiogenic shock or cardiac arrest.

<span class="mw-page-title-main">Cangrelor</span> Chemical compound

Cangrelor, sold under the brand name Kengreal among others, is a P2Y12 inhibitor FDA approved as of June 2015 as an antiplatelet drug for intravenous application. Some P2Y12 inhibitors are used clinically as effective inhibitors of adenosine diphosphate-mediated platelet activation and aggregation. Unlike clopidogrel (Plavix), which is a prodrug, cangrelor is an active drug not requiring metabolic conversion.

Adenosine diphosphate (ADP) receptor inhibitors are a drug class of antiplatelet agents, used in the treatment of acute coronary syndrome (ACS) or in preventive treatment for patients who are in risk of thromboembolism, myocardial infarction or a stroke. These drugs antagonize the P2Y12 platelet receptors and therefore prevent the binding of ADP to the P2Y12 receptor. This leads to a decrease in aggregation of platelets, prohibiting thrombus formation. The P2Y12 receptor is a surface bound protein found on blood platelets. They belong to G protein-coupled purinergic receptors (GPCR) and are chemoreceptors for ADP.

<span class="mw-page-title-main">Management of acute coronary syndrome</span>

Management of acute coronary syndrome is targeted against the effects of reduced blood flow to the affected area of the heart muscle, usually because of a blood clot in one of the coronary arteries, the vessels that supply oxygenated blood to the myocardium. This is achieved with urgent hospitalization and medical therapy, including drugs that relieve chest pain and reduce the size of the infarct, and drugs that inhibit clot formation; for a subset of patients invasive measures are also employed. Basic principles of management are the same for all types of acute coronary syndrome. However, some important aspects of treatment depend on the presence or absence of elevation of the ST segment on the electrocardiogram, which classifies cases upon presentation to either ST segment elevation myocardial infarction (STEMI) or non-ST elevation acute coronary syndrome (NST-ACS); the latter includes unstable angina and non-ST elevation myocardial infarction (NSTEMI). Treatment is generally more aggressive for STEMI patients, and reperfusion therapy is more often reserved for them. Long-term therapy is necessary for prevention of recurrent events and complications.

<span class="mw-page-title-main">Regrelor</span> Chemical compound

Regrelor is an experimental antiplatelet drug that was under investigation by Merck Sharp and Dohme in human clinical trials. Although it was initially found to be well tolerated in healthy subjects, safety concerns led to cessation of clinical trials.


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