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    Milrinone (Win47203; Primacor)
    Milrinone (Win47203; Primacor)

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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 #: V0795
    CAS #: 78415-72-2Purity ≥98%

    Description: Milrinone (formerly known as Win-47203; Win 47203; trade name Primacor) is a potent and selective phosphodiesterase 3 (PDE3) inhibitor that is used as a pulmonary vasodilator to increase the heart's contractility. Milrinone has shown the effect of concentration-dependent inhibition of PDE3 on the photolabelling with a IC50 value of 56±12nM. In addition, Milrinone has been reported to increase the accumulation of [3H] cAMP with a EC50 value of 5329±970nM in platelets.

    References: J Cardiovasc Pharmacol. 1999 Oct;34(4):497-504; Br J Pharmacol. 1996 Oct;119(3):609-15.

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    Molecular Weight (MW)211.22
    CAS No.78415-72-2
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 42 mg/mL (198.8 mM)
    Water:<1 mg/mL
    Ethanol: <1 mg/mL
    Other info

    Chemical Name: 6-methyl-2-oxo-5-pyridin-4-yl-1H-pyridine-3-carbonitrile


    InChi Code: InChI=1S/C12H9N3O/c1-8-11(9-2-4-14-5-3-9)6-10(7-13)12(16)15-8/h2-6H,1H3,(H,15,16)

    SMILES Code: N#CC1=CC(C2=CC=NC=C2)=C(C)NC1=O

    SynonymsWin 47203; Win47203; Milrinone, Primacor, Corotrop, Milrila, Win-47203

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    In Vitro

    In vitro activity: Milrinone causes a concentration-dependent increase in the cAMP level in rabbit and human platelets with similar potency. Milrinone inhibits human platelet aggregation with a median inhibitory concentration (IC50) of 2 mM.Milrinone concentration-dependently increases left ventricular developed pressure (LVDP) and contractility. Milrinone concentration-dependently increases cAMP in rabbit coronary smooth muscle cells. Milrinone increases intracellular cyclic adenosine monophosphate by inhibiting Type III phosphodiesterase. Milrinone is a potent (IC50 = 0.16-0.90 mM) and selective (100 times peak III relative to peak I) peak III inhibitor. Milrinone significant increases in cAMP content accompany significant vasorelaxation.

    Kinase Assay: Milrinone (1 µM) increases PKA activity in hypoxic myocytes to normoxic levels. Milrinone (50 nM) normalizes TP receptor sensitivity in hypoxic myocytes by restoring PKA-mediated regulatory TP receptor phosphorylation. Milrinone significantly reduces NE-induced vasoconstriction, attenuating both NE sensitivity and maximal tension generation. Inhibition of ATP-sensitive K+ channels or voltage-gated K+ channels do not prevent the milrinone-induced attenuation of NE responses

    In VivoMilrinone inhibits PDE4 in addition to PDE3 activity in the rabbit heart. Milrinone (>10 microM) causes greater elevations in intracellular cAMP and calcium than cilostazol. Milrinone causes similar increases in heart rate, cardiac output, and left ventricular +dP/dt and decreases in end-diastolic pressure and systemic vascular resistance in anaesthetized dogs. Milrinone leads to significant increases in right ventricular function as well as significant improvements in pulmonary vascular resistance, pulmonary blood flow, and left ventricular filling in mongrel dogs underwent pulmonary artery catheterization.
    Animal modelRabbit 
    Formulation & Dosage>10 microM

    J Cardiovasc Pharmacol. 1999 Oct;34(4):497-504; Br J Pharmacol. 1996 Oct;119(3):609-15.

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


    Influence of milrinone on cGMP/NO-signaling in PVs with and without pre-constriction. PLoS One. 2014; 9(1): e87685.


    Impact of K+channels on milrinone-induced relaxation in PVs. PLoS One. 2014; 9(1): e87685.


    Vascular effects of milrinone in PAs and PVs with and without BP0104-induced pre-constriction. PLoS One. 2014; 9(1): e87685.


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