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    Prasugrel (PCR 4099; CS-747)
    Prasugrel (PCR 4099; CS-747)

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    This product is for research use only, not for human use. We do not sell to patients.
    Number: - + Pieces(InventoryPieces)
    InvivoChem Cat #: V1300
    CAS #: 150322-43-3Purity ≥98%

    Description: Prasugrel (formerly CS-747, PCR-4099; LY-640315; trade name Effient; Prasita), a piperazine derivative, is an irreversible and thienopyridine-based ADP receptor (P2Y12) antagonist approved as an antiplatelet and anticoagulant drug used for the reduction of thrombotic cardiovascular events. As a platelet aggregation inhibitor, it is used to prevent thrombosis in patients with acute coronary syndrome; unstable angina and myocardial infarction, as well as in those undergoing percutaneous coronary interventions. Prasugrel was also approved for use in Europe in February 2009 and On July 10, 2009 in the US for for the reduction of thrombotic cardiovascular events in patients with acute coronary syndrome who are to be managed with PCI. 

    References: Biochem Pharmacol. 2007;74:1003-9; Eur J Pharmacol. 2009;612:29-34.

    Related CAS#: 389574-19-0 (HCl salt); 150322-43-3 (free base); 389574-20-3 (Prasugrel Maleic acid)

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    Molecular Weight (MW)373.44
    CAS No.150322-43-3
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 30 mg/mL (80.3 mM)
    Water: <1 mg/mL
    Ethanol: <1 mg/mL
    Other infoChemical Name: 5-(2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl)-4,5,6,7-tetrahydrothieno[3,2-c]pyridin-2-yl acetate
    InChi Code: InChI=1S/C20H20FNO3S/c1-12(23)25-18-10-14-11-22(9-8-17(14)26-18)19(20(24)13-6-7-13)15-4-2-3-5-16(15)21/h2-5,10,13,19H,6-9,11H2,1H3
    SMILES Code: CC(OC(S1)=CC2=C1CCN(C(C3=CC=CC=C3F)C(C4CC4)=O)C2)=O
    SynonymsCS-747; LY-640315; PCR-4099; CS747; LY640315; PCR4099; CS 747; LY 640315; PCR 4099; trade name Effient; Prasita

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    In Vitro

    In vitro activity: Prasugrel is a novel orally active thienopyridine with faster, higher and more reliable inhibition of platelet aggregation than clopidogrel reflecting its metabolism in vivo to an active metabolite with selective P2Y(12) antagonistic activity.

    In VivoPrasugrel shows platelet inhibition that was 8.2 times more potent than clopidogrel in WT mice. rasugrel (3 and 10 mg/kg) dose-relatedly and significantly reduces thrombus-mediated cerebral infarction 24 hours after the irradiation in rat models of cerebral and peripheral arterial occlusive diseases. Prasugrel (0.3-3 mg/kg) reduces incidence, total area, and total number of cerebral infarcts in a dose-related manner 24 hours after the vascular injury in an embolic infarction rats model. Prasugrel (0.03-3 mg/kg/day) administered from the day before the lauric acid injection for 11 successive days inhibits the progression of the disease in a dose-related manner in rats with lauric acid-induced peripheral arterial occlusive diseases. Prasugrel administrated in dogs (0.03-0.3 mg/kg/day) and monkeys (0.1 and 0.3 mg/kg/day) once a day for 14 days results in potent, dose-related and cumulative inhibition of ADP-induced platelet aggregation. Prasugrel (0.1-1 mg/kg/day, p.o.) significantly prolongs the time to arterial occlusion and increases the duration of arterial patency in a rat model of electrically-induced arterial thrombosis.
    Animal modelMice and rats
    Formulation & Dosage0.03-3 mg/kg/day; p.o.
    ReferencesBiochem Pharmacol. 2007 Oct 1;74(7):1003-9; Eur J Pharmacol. 2009 Jun 10;612(1-3):29-34.

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

    Early prasugrel use by ACTION predicted risk quintile. J Am Heart Assoc. 2014 Apr; 3(2): e000849.


    Prasugrel use by predicted mortality and bleeding risk. J Am Heart Assoc. 2014 Apr; 3(2): e000849.


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