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P2Y12 Platelet Inhibitor

Ticagrelor

Approved 6 Feb 2026OralTablet

The FDA lists this product in 37 strengths and forms.

Indications

Ticagrelor tablets are P2Y 12 platelet inhibitor indicated to reduce the risk of a first MI or stroke in patients with coronary artery disease (CAD) at high risk for such events. While use is not limited to this setting, the efficacy of ticagrelor tablets was established in a population with type 2 diabetes mellitus (T2DM). ( 1.2 ) to reduce the risk of stroke in patients with acute ischemic stroke (NIH Stroke Scale score ≤5) or high-risk transient ischemic attack (TIA).

( 1.3 )

1.2Coronary Artery

Disease but No Prior Stroke or Myocardial Infarction Ticagrelor tablets are indicated to reduce the risk of a first MI or stroke in patients with coronary artery disease (CAD) at high risk for such events [see Clinical Studies ( 14.2 )] . While use is not limited to this setting, the efficacy of ticagrelor tablets was established in a population with type 2 diabetes mellitus (T2DM).

1.3Acute Ischemic Stroke or Transient Ischemic Attack (TIA)

Ticagrelor tablets are indicated to reduce the risk of stroke in patients with acute ischemic stroke (NIH Stroke Scale score ≤5) or high-risk transient ischemic attack (TIA) [see Clinical Studies ( 14.3 )] .

Contraindications

History of intracranial hemorrhage. ( 4.1 ) Active pathological bleeding. ( 4.2 ) Hypersensitivity to ticagrelor or any component of the product. ( 4.3 )

4.1History of Intracranial Hemorrhage

Ticagrelor tablets are contraindicated in patients with a history of intracranial hemorrhage (ICH) because of a high risk of recurrent ICH in this population [see Clinical Studies ( 14.2 )].

4.2Active Bleeding

Ticagrelor tablets are contraindicated in patients with active pathological bleeding such as peptic ulcer or intracranial hemorrhage [see Warnings and Precautions (5.1) and Adverse Reactions (6.1)].

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Warnings and precautions

Dyspnea was reported more frequently with ticagrelor than with control agents in clinical trials. Dyspnea from ticagrelor is self-limiting. (5.3) Severe Hepatic Impairment: Likely increase in exposure to ticagrelor. (5.5) Laboratory Test Interference: False negative platelet functional test results have been reported for Heparin Induced Thrombocytopenia (HIT). Ticagrelor tablets are not expected to impact PF4 antibody testing for HIT.

(5.7)

5.1Risk of Bleeding

Drugs that inhibit platelet function including ticagrelor increase the risk of bleeding [see Warnings and Precautions (5.2) and Adverse Reactions (6.1)]. Patients treated for acute ischemic stroke or TIA Patients at NIHSS >5 and patients receiving thrombolysis were excluded from THALES and use of ticagrelor in such patients is not recommended.

5.2Discontinuation of Ticagrelor in Patients Treated for Coronary Artery Disease Discontinuation

of ticagrelor will increase the risk of myocardial infarction, stroke, and death in patients being treated for coronary artery disease. If ticagrelor must be temporarily discontinued (e.g., to treat bleeding or for significant surgery), restart it as soon as possible. When possible, interrupt therapy with ticagrelor for five days prior to surgery that has a major risk of bleeding. Resume ticagrelor as soon as hemostasis is achieved.

5.3Dyspnea

In clinical trials, about 21% (THEMIS) of patients treated with ticagrelor developed dyspnea. Dyspnea was usually mild to moderate in intensity and often resolved during continued treatment but led to study drug discontinuation in 1.0% (THALES) and 6.9% (THEMIS) of patients. If a patient develops new, prolonged, or worsened dyspnea that is determined to be related to ticagrelor, no specific treatment is required; continue ticagrelor without interruption if possible.

In the case of intolerable dyspnea requiring discontinuation of ticagrelor, consider prescribing another antiplatelet agent.

5.4Bradyarrhythmias

Ticagrelor can cause ventricular pauses [see Adverse Reactions ( 6.1 )] . Bradyarrhythmias including AV block have been reported in the postmarketing setting. Patients with a history of sick sinus syndrome, 2 nd or 3 rd degree AV block or bradycardia-related syncope not protected by a pacemaker were excluded from clinical studies and may be at increased risk of developing bradyarrhythmias with ticagrelor.

5.5Severe Hepatic Impairment

Avoid use of ticagrelor in patients with severe hepatic impairment. Severe hepatic impairment is likely to increase serum concentration of ticagrelor. There are no studies of ticagrelor patients with severe hepatic impairment [see Clinical Pharmacology ( 12.3 )].

5.6Central Sleep Apnea

Central sleep apnea (CSA) including Cheyne-Stokes respiration (CSR) has been reported in the post-marketing setting in patients taking ticagrelor, including recurrence or worsening of CSA/CSR following rechallenge. If central sleep apnea is suspected, consider further clinical assessment.

5.7Laboratory Test Interferences

False negative functional tests for Heparin Induced Thrombocytopenia (HIT) Ticagrelor has been reported to cause false negative results in platelet functional tests (including, the heparin-induced platelet aggregation (HIPA) assay) for patients with Heparin Induced Thrombocytopenia (HIT). This is related to inhibition of the P2Y 12 -receptor on the healthy donor platelets in the test by ticagrelor in the affected patient's serum/plasma.

Information on concomitant treatment with ticagrelor is required for interpretation of HIT functional tests. Based on the mechanism of ticagrelor interference, ticagrelor is not expected to impact PF4 antibody testing for HIT.

Interactions

Avoid use with strong CYP3A inhibitors or CYP3A inducers. (7.1, 7.2) Opioids: Decreased exposure to ticagrelor. Consider use of parenteral antiplatelet agent. (7.3) Patients receiving more than 40 mg per day of simvastatin or lovastatin, or more than 20 mg per day of rosuvastatin may be at increased risk of statin-related adverse effects. (7.4) Monitor digoxin levels with initiation of or any change in ticagrelor. (7.5)

7.1Strong CYP3A Inhibitors Strong

CYP3A inhibitors substantially increase ticagrelor exposure and so increase the risk of dyspnea, bleeding, and other adverse events. Avoid use of strong inhibitors of CYP3A (e.g., ketoconazole, itraconazole, voriconazole, clarithromycin, nefazodone, ritonavir, saquinavir, nelfinavir, indinavir, atazanavir and telithromycin) [see Clinical Pharmacology ( 12.3 )] .

7.2Strong CYP3A Inducers Strong

CYP3A inducers substantially reduce ticagrelor exposure and so decrease the efficacy of ticagrelor. Avoid use with strong inducers of CYP3A (e.g., rifampin, phenytoin, carbamazepine and phenobarbital) [see Clinical Pharmacology ( 12.3 )] .

7.3 Opioids As with other oral P2Y 12 inhibitors, co-administration of opioid agonists delay and reduce the absorption of ticagrelor and its active metabolite presumably because of slowed gastric emptying [see Clinical Pharmacology ( 12.3 )] . Consider the use of a parenteral anti-platelet agent in acute coronary syndrome patients requiring co-administration of morphine or other opioid agonists.

7.4Simvastatin, Lovastatin, Rosuvastatin

Ticagrelor increases serum concentrations of simvastatin and lovastatin because these drugs are metabolized by CYP3A4. Avoid simvastatin and lovastatin doses greater than 40 mg [see Clinical Pharmacology (12.3)]. Ticagrelor increases serum concentration of rosuvastatin because rosuvastatin is a BCRP substrate. Avoid rosuvastatin doses greater than 20 mg [see Clinical Pharmacology (12.3)]. In patients at increased risk for rhabdomyolysis, consider rosuvastatin dosages less than 20 mg per day.

7.5Digoxin

Ticagrelor inhibits the P-glycoprotein transporter; monitor digoxin levels with initiation of or change in ticagrelor therapy [see Clinical Pharmacology ( 12.3 )].

Pregnancy and breastfeeding

8.1Pregnancy Risk Summary

Available data from case reports with ticagrelor use in pregnant women have not identified a drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes. Ticagrelor given to pregnant rats and pregnant rabbits during organogenesis caused structural abnormalities in the offspring at maternal doses about 5 to 7 times the maximum recommended human dose (MRHD) based on body surface area.

When ticagrelor was given to rats during late gestation and lactation, pup death and effects on pup growth were seen at approximately 10 times the MRHD (see Data). The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively.

Data Animal Data In reproductive toxicology studies, pregnant rats received ticagrelor during organogenesis at doses from 20 to 300 mg/kg/day. 20 mg/kg/day is approximately the same as the MRHD of 90 mg twice daily for a 60 kg human on a mg/m 2 basis. Adverse outcomes in offspring occurred at doses of 300 mg/kg/day (16.5 times the MRHD on a mg/m2 basis) and included supernumerary liver lobe and ribs, incomplete ossification of sternebrae, displaced articulation of pelvis, and misshapen/misaligned sternebrae.

At the mid-dose of 100 mg/kg/day (5.5 times the MRHD on a mg/m 2 basis), delayed development of liver and skeleton was seen. When pregnant rabbits received ticagrelor during organogenesis at doses from 21 to 63 mg/kg/day, fetuses exposed to the highest maternal dose of 63 mg/kg/day (6.8 times the MRHD on a mg/m 2 basis) had delayed gall bladder development and incomplete ossification of the hyoid, pubis and sternebrae occurred.

In a prenatal/postnatal study, pregnant rats received ticagrelor at doses of 10 to 180 mg/kg/day during late gestation and lactation. Pup death and effects on pup growth were observed at 180 mg/kg/day (approximately 10 times the MRHD on a mg/m 2 basis). Relatively minor effects such as delays in pinna unfolding and eye opening occurred at doses of 10 and 60 mg/kg (approximately one-half and 3.2 times the MRHD on a mg/m 2 basis).

Adverse reactions

The following adverse reactions are also discussed elsewhere in the labeling: Bleeding [see Warnings and Precautions ( 5.1 )] Dyspnea [see Warnings and Precautions ( 5.3 )] Most common adverse reactions (>5%) are bleeding and dyspnea. ( 5.1 , 5.3 , 6.1 ) To report SUSPECTED ADVERSE REACTIONS, contact Lifestar Pharma LLC at 1-888-995-4337 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

6.1Clinical Trials Experience

Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice. Ticagrelor has been evaluated for safety in more than 58,000 patients. Bleeding in THEMIS (Prevention of major CV events in patients with CAD and Type 2 Diabetes Mellitus) The Kaplan-Meier curve of time to first TIMI Major bleeding event is presented in Figure 3.

Figure 3 - Time to first TIMI Major bleeding event (THEMIS) T = Ticagrelor; P = Placebo; N = Number of patients The bleeding events in THEMIS are shown below in Table 6. Table 6 – Bleeding events (THEMIS) Ticagrelor N=9562 Placebo N=9531 Events / 1000 patient years Events / 1000 patient years TIMI Major 9 4 TIMI Major or Minor 12 5 TIMI Major or Minor or Requiring medical attention 46 18 Fatal bleeding 1 0 Intracranial hemorrhage 3 2 Bleeding in THALES (Reduction in risk of stroke in patients with acute ischemic stroke or TIA) The Kaplan-Meier curve of time course of GUSTO severe bleeding events is presented in Figure 4.

Figure 4 - Time course of GUSTO severe bleeding events KM%: Kaplan-Meier percentage evaluated at Day 30; T = Ticagrelor; P = placebo; N = Number of patients GUSTO Severe : Any one of the following: fatal bleeding, intracranial bleeding (excluding asymptomatic hemorrhagic transformations of ischemic brain infarctions and excluding microhemorrhages < 10 mm evident only on gradient-echo magnetic resonance imaging), bleeding that caused hemodynamic compromise requiring intervention (eg, systolic blood pressure <90 mmg Hg that required blood or fluid replacement, or vasopressor/inotropic support, or surgical intervention).

Intracranial bleeding and fatal bleeding in THALES: In total, there were 21 intracranial hemorrhages (ICHs) for ticagrelor and 6 ICHs for placebo. Fatal bleedings, almost all ICH, occurred in 11 for ticagrelor and in 2 for placebo. Bradycardia THEMIS and THALES excluded patients at increased risk of bradycardic events (e.g., patients who have sick sinus syndrome, 2 nd or 3 rd degree AV block, or bradycardic-related syncope and not protected with a pacemaker).

6.2Postmarketing Experience

The following adverse reactions have been identified during post-approval use of ticagrelor. Because these reactions are reported voluntarily from a population of an unknown size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. Blood and lymphatic system disorders: Thrombotic Thrombocytopenic Purpura (TTP) has been rarely reported with the use of ticagrelor.

TTP is a serious condition which can occur after a brief exposure (<2 weeks) and requires prompt treatment. Immune system disorders: Hypersensitivity reactions including angioedema [see Contraindications (4.3)] . Respiratory Disorders: Central sleep apnea, Cheyne-Stokes respiration Skin and subcutaneous tissue disorders: Rash figure3 figure4