platelet aggregation at the sites of atherosclerotic plaque rupture initiates the cascade leading to atherothrombosis resulting in myocardial infarction , stroke etc . , thus , anti - platelet therapy remains cornerstone of antithrombotic therapy in patients suffering from acute coronary syndrome ( acs ) . different pharmacotherapeutic agents acting through different mechanism of action can be used , as platelet activation is a multifaceted process . now a days , a dual antiplatelet therapy of clopidrogel and aspirin is widely used for synergistic platelet inhibition . however , thienopyridine i.e. , clopidrogel , the most widely used p2y12-type adenosine diphosphate ( adp ) receptor inhibitor has number of limitations  being irreversible inhibitor of p2y12 receptors , it carries increase risk of bleeding ; being a prodrug , it requires hepatic conversion to an active metabolite resulting in delayed onset of action and inter - individual variability . prasugel , a new thienopyridine agent , is more efficiently metabolized to its active metabolite , however , the risk of major bleeding episodes and life - threatening hemorrhages are higher for patients taking prasugrel compared to those taking clopidrogel . to overcome the drawbacks of the thienopyridine group of antiplatelet agents , ticagrelor first drug of a new chemical class called cyclopentyl - triazolo - pyrimidine is designed . it has unique pharmacological properties : it is a reversible inhibitor of p2y12 receptor , so the effects can be reversed more easily ; it is not a prodrug , therefore , does not require metabolic activation resulting in rapid onset of action with less inter - individual variation ; it also inhibits non - platelet p2y12 receptor present on vascular smooth muscles , where they cause vasoconstriction and increases myocardial perfusion.[57 ] adp plays an important role in platelet aggregation by acting on p2y1 and p2y12 receptors on the surface of platelets . ticagrelor binds to an area distinct from the adp binding site , and inhibits adp - induced receptor activation in a non - competitive manner . as compared to ticagrelor , clopidrogel binds covalently to adp binding site and renders the receptor permanently inactivated . whereas , ticagrelor leaves the receptor intact upon dissociation , thus inhibition of platelet aggregation is reversible . these effects are not seen with thienopyridines , as they can not penetrate vascular wall owing to their physical and chemical properties . in addition , ticagrelor increases myocardial blood flow by inhibiting uptake of adenosine by erythrocytes and provides additional benefit to the patients of acs . ticagrelor is rapidly absorbed from the gut after oral administration and reaches peak plasma concentration in around 1.5 hours . its bioavailability is around 36% . it is mainly metabolized to active metabolite via cytochrome enzymes . the pharmacokinetics of ticagrelor and its active metabolite are predictable up to 1260 mg dose ( seven fold daily dose ) . both ticagrelor and its active metabolite show plasma protein binding greater than 99.7% , and the efficacy and safety of ticagrelor have been evaluated by platelet inhibition and patient outcomes ( plato ) phase - iii trial . the plato trial was performed in patients with either non - st elevation or st - elevation acs . a total of 18,624 patients were randomly assigned to receive either ticagrelor ( 180 mg loading dose , 90 mg twice daily thereafter ) or clopidrogel ( 300 - 600 mg loading dose , 75 mg thereafter ) along with aspirin ( 75 - 100 mg per day ) for 12 months . myocardial infarction or stroke was significantly reduced among patients who received ticagrelor compared with those who took clopidrogel ( 9.8% versus 11.7% ; hazard ratio ( hr ) 0.84 , p < 0.001 ) . however , one group of patients enrolled in united states fared worse with ticagrelor as compared of clopidrogel ( hazard ratio 1.27 as compared to hazard ratio for non us patients : 0.81 ) . plato data showed that aspirin dosage was 300 mg in this subgroup of patients and that might be reason for this type of response . it is thought this effect may be due to its action on uptake of adenosine . various types of bleeds , i.e. , gastrointestinal , intracranial , and dermal , had been seen . rate of major bleed was similar between the ticagrelor and clopidrogel groups ( p = 0.43 ) , but rate of major bleeding not related to coronary artery bypass graft surgery was higher with ticagrelor ( p = 0.03 ) . furthermore , ticagrelor was reported to have higher incidences of ventricular pauses in the first week of treatment but difference did not persist by 30 days . other adverse effects reported with ticagrelor were headache , nausea , dyspepsia , insomnia , dizziness , syncope , and hypotension . in addition , ticagrelor and its active metabolite are both substrate as well as inhibitor of p - glycoprotein . it has been shown to significantly increase plasma digoxin concentration by inhibiting p - glycoprotein . ticagrelor has been approved by fda in july 2011 in patients suffering from acs , it is available as 90 mg tablet ; given as single 180 mg oral loading dose followed by a twice - daily 90 mg maintenance dose along with maintenance dose of 75 - 100 mg aspirin . it has been approved for marketing in india by drug controller general in may 2012 .