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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.
Chemical Name: 6-methyl-2-oxo-5-pyridin-4-yl-1H-pyridine-3-carbonitrile
InChi Key: PZRHRDRVRGEVNW-UHFFFAOYSA-N
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
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2
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
J Cardiovasc Pharmacol. 1999 Oct;34(4):497-504; Br J Pharmacol. 1996 Oct;119(3):609-15.
Purity ≥ 98%
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