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    Ticagrelor (AZD6140)
    Ticagrelor (AZD6140)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1303
    CAS #: 274693-27-5Purity ≥98%

    Description: Ticagrelor (formerly AZD-6140; AR-C 126532XX; AZD6140; AR-C126532XX; Trade name: Brilinta; Brilique; Possia) is the first reversibly binding, potent and orally bioactive P2Y12 receptor antagonist used as an antiplatelet and anticoagulant. It inhibits P2Y12 receptor with a Ki of 2 NM. Ticagrelor was approved in 2011 by FDA as an antiplatelet drug 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. 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.

    References: J Thromb Haemost. 2009 Sep;7(9):1556-65; Eur J Clin Pharmacol. 2010 May;66(5):487-96. 

    Related CAS#:1251765-07-7 (Ticagrelor metabolite M5)

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    Molecular Weight (MW)522.57
    CAS No.274693-27-5
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 105 mg/mL (200.9 mM)
    Water:<1 mg/mL
    Ethanol: 53 mg/mL (101.4 mM)
    Other infoChemical Name: (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
    InChi Code: 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
    SMILES Code: O[[email protected]]1[[email protected]@H](O)[[email protected]](N2N=NC3=C(N[[email protected]]4[[email protected]](C5=CC=C(F)C(F)=C5)C4)N=C(SCCC)N=C32)C[[email protected]@H]1OCCO 
    SynonymsAZD 6140; AZD 6140; AR-C 126532XX; AR-C-126532XX; AZD-6140; AZD6140; AR-C126532XX; Ticagrelor; brand name: Brilinta; Brilique; Possia

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    In Vitro

    In vitro activity: 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. 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.

    Kinase Assay: Ticagrelor promotes a greater inhibition of adenosine 5′-diphosphate (ADP)–induced Ca2+ release in ished platelets vs other P2Y12R antagonists. This additional effect of ticagrelor beyond P2Y12R antagonism is in part as a consequence of ticagrelor inhibiting the equilibrative nucleoside transporter 1 (ENT1) on platelets, leading to accumulation of extracellular adenosine and activation of Gs-coupled adenosine A2A receptors. B16-F10 cells exhibit decreased interaction with platelets from ticagrelor-treated mice compared to saline-treated mice.

    In VivoIn B16-F10 melanoma intravenous and intrasplenic metastasis models, mice treated with a clinical dose of ticagrelor (10 mg/kg) exhibits marked reductions in lung (84%) and liver (86%) metastases. Furthermore, ticagrelor treatment improves survival compared to saline-treated animals. A similar effect is observed in a 4T1 breast cancer model, with reductions in lung (55%) and bone marrow (87%) metastases following ticagrelor treatment. Single oral administration of ticagrelor (1-10 mg/kg) causes dose-related inhibitory effect on platelet aggregation. Ticagrelor, at the highest dose (10 mg/kg) significantly inhibits platelet aggregation at 1 h after dosing and the peak inhibition is observed at 4 h after dosing.
    Animal modelMice bearing B16-F10 melanoma tumor
    Formulation & DosageMice: Female BALB/c mice are inoculated subcutaneously in the fourth mammary pad with 4T1 breast cancer cells. Once a tumor is palpable, mice receive daily injections of PBS or ticagrelor (10 mg/kg). One week later, mice undergo primary tumor resection. At 28 days mice are sacrificed and lungs, femurs and tibiae harvested. Dissociated cells from lung and bone marrow are plated in medium containing 60 μM 6-thioguanine. After 14 days, culture plates are fixed with methanol and stained with 0.03% methylene blue to enumerate metastatic 4T1 colonies. 
    ReferencesJ Thromb Haemost. 2009 Sep;7(9):1556-65; Eur J Clin Pharmacol. 2010 May;66(5):487-96; Int J Cancer. 2015 Jan 1;136(1):234-40.

    These protocols are for reference only. InvivoChem does not independently validate these methods.

     ADP-induced platelet aggregation using human washed platelet suspension. J Thromb Haemost. 2009 Sep;7(9):1556-65. 
     Determination of the inhibition of rh-P2Y12 signaling by ticagrelor. J Thromb Haemost.2009 Sep;7(9):1556-65. 
     Kinetics for 3H-ticagrelor binding to rh-P2Y12. J Thromb Haemost. 2009 Sep;7(9):1556-65. 


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