Catalog No.S4079 Synonyms: AZD 6140

Ticagrelor Chemical Structure

Molecular Weight(MW): 522.57

Ticagrelor is the first reversibly binding oral P2Y12 receptor antagonist with Ki of 2 nM.

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In DMSO USD 130 In stock
USD 97 In stock
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  • Effect of antiplatelet drugs on platelet aggregation in healthy individuals. Samples from healthy individuals were preincubated with anti-platelet drugs (n = 3). Curves and columns show mean platelet aggregation and the relationship between platelet aggregation and drug concen-tration. Bars represent standard deviations. *P < 0.05 as compared with platelet aggregation with the same agonist but no drugs added; pairedStudent’s t-test. (A-C) The drugs tested were abciximab (A), ticagrelor (B), and vorapaxar (C).

    J Thromb Haemost, 2017, 15(6):1191-1202. Ticagrelor purchased from Selleck.

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Biological Activity

Description Ticagrelor is the first reversibly binding oral P2Y12 receptor antagonist with Ki of 2 nM.
Features First-in-class of a new type of P2Y12 antagonist known as cyclopentyl-triazolo-pyrimidines.
P2Y12 [1]
2 nM(Ki)
In vitro

Ticagrelor is an active drug which, does not require metabolic activation after intestinal absorption. It does not compete directly with ADP at the ADP binding site but occupies an adjacent binding site and acts in an allosteric way, resulting in a reversible conformational change of the receptor. Ticagrelor binds reversibly to the receptor and exhibits rapid onset and offset of effect. Binding studies in rh-P2Y12 receptor-transfected CHO-K1 cells indicate that ticagrelor exhibits potent, rapid, and reversible binding, with a Kd of 10.5 nM, a kon (association constant) of 0.00011/(nM•s), a koff (dissociation constant) of 0.00087/s, and half-life values of 4 min for binding and 14 min for unbinding, indicating that the magnitude of platelet inhibition is dependent on concentrations of drug available to bind platelets. [1] Ticagrelor moderately inhibits CYP2C9 activity in human liver microsomes, while exhibiting little or no inhibition of CYP1A2, CYP2B6, CYP2C8, CYP2C19, CYP2D6, and CYP2E1. In human liver microsomes, ticagrelor inhibits midazolam 4-hydroxylation, while activating 1_-hydroxylation of midazolam. Evaluated in fresh human hepatocytes, ticagrelor is not an inducer of CYP1A2 or CYP3A4. [3]

In vivo Absorption of ticagrelor is rapid with t max of 1.3-2 h. And the Cmax and area under the plasma concentration-time curve from time 0 to infinity increases in an apparently dose-proportional manner over the dose range studied, indicating linear pharmacokinetics. The mean terminal-phase half-life (t1/2) is approximately 7-8.5 h for ticagrelor. Inhibition of platelet aggregation (IPA) is dose related and is nearly complete at 2 h at doses of 100-400 mg. Ticagrelor is well tolerated, with no serious or doserelated adverse events or notable changes in laboratory values observed. [2]


Solubility (25°C)

In vitro DMSO 100 mg/mL (191.36 mM)
Ethanol 53 mg/mL (101.42 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order:
2% DMSO+30% PEG 300+5% Tween 80+ddH2O
For best results, use promptly after mixing.

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 522.57


CAS No. 274693-27-5
Storage powder
in solvent
Synonyms AZD 6140

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03027934 Not yet recruiting Diabetes Mellitus CirQuest Labs, LLC February 28, 2017 Phase 4
NCT03016611 Not yet recruiting Acute Coronary Syndrome|STEMI Sheba Medical Center February 2017 Phase 4
NCT02866175 Not yet recruiting Atrial Fibrillation Daiichi Sankyo Inc.|European Cardiovascular Research Institute|Kompetenznetz Vorhofflimmern e.V.|Chiltern International Inc. February 2017 Phase 3
NCT02663713 Recruiting Myocardial Infarction|Diabetes Mellitus|Renal Disease|Coronary Artery Disease University of Patras|AstraZeneca January 2017 Phase 4
NCT02617290 Not yet recruiting Coronary Artery Disease|Myocardial Ischemia|Myocardial Infarction|Stent Thrombosis|Cardiovascular Diseases Assistance Publique - Hôpitaux de Paris|Action Research Group December 2016 Phase 3
NCT02989558 Not yet recruiting Aortic Valve Stenosis University of Athens December 2016 Phase 3

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID