For research use only.

Catalog No.S4079 Synonyms: AZD 6140

7 publications

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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10mM (1mL in DMSO) USD 130 In stock
USD 97 In stock
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Selleck's Ticagrelor has been cited by 7 publications

2 Customer Reviews

  • 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.

    Washed platelets were incubated with varying concentrations of ticagrelor using a thrombin EC80. IC50s were calculated.

    J Thromb Haemost, 2018, doi:10.1111/jth.14318. 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]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
H9c2 MVrGeY5kfGmxbjDhd5NigQ>? NVTq[4x5OC5zLDCwMFMh[W6mIEGg{txO NVzGWpNbOjRiaB?= M2\IPYVn\mWldHn2[UBqdiC{ZXT1Z4lv\yCQQ2ixJJJmfmW{c3WgZYN1cX[rdImge4hmdiCub4fldkBkd26lZX70doF1cW:wcx?= NH2wVlg{ODd{MUewOC=>
EAhy926 NXKzTlBZSXCxcITvd4l{KGG|c3H5 M1TDNlQxKM7:TTDhcoQhPjBizszN NWXrW3dQ\GWlcnXhd4Uhd3hvTFTMMYlv\HWlZXSgZZBweHSxc3nzMEBx[XK2aXP1cIFzdHliYYSgZUBpcWeqZYKgZ49v[2WwdILheIlwdg>? M3nUUFMxPTl{Mkex
AsPC-1 NFPsW5ZHfW6ldHnvckBie3OjeR?= M{P0eFExKM7:TR?= MVKyJIg> MlXheIlk[We{ZXzvdkBv\WejdHXkJJRp\SCybHH0[YxmfCC{ZXzlZZNifGViZX\m[YN1KG:wIFHreEwhTXKtIHHjeIl3[XSrb36gZY5lKFOudXegeZBz\We3bHH0bY9v MlXINlkxPjR|OEi=
BxPC-3 MXjGeY5kfGmxbjDhd5NigQ>? MoPpNVAh|ryP NVjkb291OiCq NXnydZQ3fGmlYXfy[YxweiCwZXfheIVlKHSqZTDwcIF1\WyndDDy[Yxm[XOjdHWg[YZn\WO2IH;uJGFsfCxiRYLrJIFkfGm4YYTpc44h[W6mIGPseYchfXC{ZXf1cIF1cW:w NHziTnkzQTB4NEO4PC=>

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot

PubMed: 27694321     

Representative immunoblots showing VASP-P, VASP, and α-tubulin (internal control) levels in washed platelets after preincubation at 37°C with the following: Ticagrelor (10 µM) for 0, 0.5, 5, 10, 15, 30, and 60 minutes.

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(Data is from Selleck tests instead of citations):
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
Smiles CCCSC1=NC2=C(N=N[N]2C3CC(OCCO)C(O)C3O)C(=N1)NC4CC4C5=CC(=C(F)C=C5)F

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04286438 Recruiting Drug: PB2452 Infusion Hemorrhage|Urgent Surgery|Invasive Procedure PhaseBio Pharmaceuticals Inc. March 27 2020 Phase 3
NCT04206176 Recruiting Drug: Ticagrelor Platelet Dysfunction Due to Drugs The University of The West Indies October 1 2019 Phase 1|Phase 2
NCT04088123 Not yet recruiting Drug: Ticagrelor Oral Tablet [Brilinta] Thrombosis; Artery George Washington University|National Institute on Minority Health and Health Disparities (NIMHD)|Shenandoah University|The GW Medical Faculty Associates October 2019 --
NCT02302508 Withdrawn Drug: Clopidogrel Prasugrel Ticagrelor Diabetes Centre hospitalier de l''Université de Montréal (CHUM)|Centre de Recherche du Centre Hospitalier de l''Université de Montréal September 1 2019 Phase 4

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID