Catalog No.S2484 Synonyms: Win 47203
Molecular Weight(MW): 211.22
Milrinone is a phosphodiesterase 3 (PDE3) inhibitor, used to increase the heart's contractility.
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Viability of H9c2 cells incubated with MRN-HSA-NPs (black bars) compared with MRN-Lactate (grey bars) at different MRN concentrations, at (a) 4 hours, (b) 24 hours and (c) 48 hours. The graph shows a representative result of mean±SD (n=3). ****P<0.0001, ***P<0.001, **P<0.01 and *P<0.05 were considered significant based on Sidak’s posthoc analysis.
Mol Pharm, 2017. Milrinone purchased from Selleck.
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|Description||Milrinone is a phosphodiesterase 3 (PDE3) inhibitor, used to increase the heart's contractility.|
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. 
|In vivo||Milrinone 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. |
-  Cone J, et al. J Cardiovasc Pharmacol, 1999, 34(4), 497-504.
-  Shipley JB, et al. Am J Med Sci, 1996, 311(6), 286-291.
-  Silver PJ, et al. J Pharmacol Exp Ther, 1988, 247(1), 34-42.
|In vitro||DMSO||42 mg/mL (198.84 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02951130||Not yet recruiting||Congenital Diaphragmatic Hernia|Persistent Pulmonary Hypertension of the Newborn|Hypoxemic Respiratory Failure|Pulmonary Hypoplasia||NICHD Neonatal Research Network|Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)||February 2017||Phase 2|
|NCT02726620||Recruiting||Hypotension||Vanderbilt University Medical Center|UMC Utrecht||January 2017||--|
|NCT02712788||Recruiting||Cerebral Vasospasm||Indiana University||April 2016||Phase 2|
|NCT02644057||Recruiting||Cardiorenal Syndrome||Maimonides Medical Center||March 2016||Phase 2|
|NCT02549066||Recruiting||Complication of Extracorporeal Circulation|Kidney Circulation Disorder|Renal Function Disorder||Sahlgrenska University Hospital, Sweden||January 2016||--|
|NCT02640846||Recruiting||Septic Shock|Cardiomyopathy||Sahlgrenska University Hospital, Sweden||December 2015||Phase 4|
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