Olprinone Hydrochloride - CAS 119615-63-3
Catalog number: 119615-63-3
Category: Inhibitor
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Molecular Formula:
C14H11ClN4O
Molecular Weight:
286.72
COA:
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Targets:
Phosphodiesterase (PDE)
Description:
Olprinone is a selective phosphodiesterase 3 (PDE3) inhibitor. Olprinone is used as cardiotonic agent with positive inotropic and vasodilating effects. Olprinone has been reported to improve microcirculation and attenuate inflammation. Olprinone is often used to increase cardiac output after cardiopulmonary bypass (CPB). Olprinone was infused at a rate of 0.2 μg/kg/min when weaning from CPB was started. Olprinone has also shown potent antioxidative and anti-inflammatory effects in the meconium-induced oxidative lung injury.
Purity:
>98%
Synonyms:
1,2-Dihydro-5-(imidazo[1,2-a]pyridin-6-yl)-6-methyl-2-oxo-3-pyridinecarbonitrile hydrochloride, Loprinone hydrochloride
MSDS:
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InChIKey:
PWTBMBAQRAOAFF-UHFFFAOYSA-N
InChI:
InChI=1S/C14H10N4O.ClH/c1-9-12(6-11(7-15)14(19)17-9)10-2-3-13-16-4-5-18(13)8-10;/h2-6,8H,1H3,(H,17,19);1H
Canonical SMILES:
CC1=C(C=C(C(=O)N1)C#N)C2=CN3C=CN=C3C=C2.Cl
1.[Effects of olprinone hydrochloride in patients undergoing off-pump coronary artery bypass grafting].
Arai T1, Kamishima K, Terauchi T, Enomoto Y, Shimazaki M, Inoue H, Okuda Y. Masui. 2006 Feb;55(2):158-63.
BACKGROUND: Olprinone hydrochloride (OLP) is a new phosphodiesterase III inhibitor with positive inotropic and vasodilator properties. It is characterized by strong inotropic effect and relatively weak vasodilating effect. Although the method for administration of OLP has been reasonably optimized, no studies have examined the administration mode for patients with off-pump coronary artery bypass grafting (OPCAB).
2.Neuroprotective effects of olprinone after cerebral ischemia/reperfusion injury in rats.
Genovese T1, Mazzon E, Paterniti I, Esposito E, Cuzzocrea S. Neurosci Lett. 2011 Oct 3;503(2):93-9. doi: 10.1016/j.neulet.2011.08.015. Epub 2011 Aug 17.
Olprinone hydrochloride, a specific phosphodiesterase III inhibitor, has anti-inflammatory effects in addition to its inotropic and vasodilatory effects. The purpose of this study was to examine the beneficial effects of olprinone on cerebral ischemia reperfusion injury. In the present study, we examined the detailed mechanisms underlying the inhibitory effects of olprinone on inflammatory and apoptotic responses induced by middle cerebral artery occlusion (MCAo) in rats. Focal cerebral ischemia was induced by transient MCAo in the right hemisphere, via the external carotid artery into the internal carotid to block the origin of the median carotid artery. The rats were subjected to artery occlusion (2 h) followed by reperfusion (22 h). Olprinone was administered 5 min before reperfusion. MCAo-induced cerebral ischemia was associated with an increase in inducible nitric oxide synthase expression, nitrotyrosine formation, as well as IL-1β expression and ICAM-1 expression in ischemic regions.
3.Olprinone, a PDE3 inhibitor, modulates the inflammation associated with myocardial ischemia-reperfusion injury in rats.
Di Paola R1, Mazzon E, Paterniti I, Impellizzeri D, Bramanti P, Cuzzocrea S. Eur J Pharmacol. 2011 Jan 15;650(2-3):612-20. doi: 10.1016/j.ejphar.2010.10.043. Epub 2010 Oct 27.
Coronary ischemia and subsequent reperfusion result in deleterious effects, one of the principal ones being vascular and myocardial inflammation. Olprinone hydrochloride, a specific phosphodiesterase III inhibitor, has anti-inflammatory effects in addition to its inotropic and vasodilator effects. The purpose of this study was to examine the beneficial effects of olprinone on myocardial ischemia-reperfusion injury. Myocardial ischemia-reperfusion injury was caused by clamping the LAD (left anterior descending) coronary artery for 25 min followed by a release of the clamp allowing reperfusion for 1 h. Olprinone i.p. (0.2 mg/kg, i.p.) was administrated 15 min after ischemia. The olprinone administration significantly reduced the: (1) histological evidence of myocardial injury, (2) pro-inflammatory cytokines: tumor necrosis factor-α (TNF-α) and Interleukin-1β (IL-1β), (3) adhesion molecules: Inter-Cellular Adhesion Molecule 1 (ICAM-1) and P-Selectin, (4) nitrotyrosine formation, (5) nuclear factor kappa-B (NF-κB) expression, (6) Poly (ADP-ribose) (PAR) formation, and (7) apoptosis (Bax, Bcl-2, Fas-L and terminal deoxynucleotidyl transferase-mediated UTP end labeling (TUNEL).
4.The enhancement of cellular cAMP with olprinone protects autotransplanted rat kidney against cold ischemia-reperfusion injury.
Zhang Y1, Ma Q. Transplant Proc. 2006 Jun;38(5):1580-3.
The administration of a cyclic nucleotide analog improves cold ischemia/reperfusion injury in several organs. The type 3 phosphodiesterase inhibitor olprinone is a potent stimulus that enhances cellular cAMP levels. The present study was performed to investigate the protective effects of enhanced intracellular cAMP levels by olprinone in rat orthotopic kidney transplantation. Autotransplantation and immediate contralateral nephrectomy were performed in Lewis rats after 18 hours of graft storage at 4 degrees C in University of Wisconsin (UW) solution with or without 25 microg/mL olprinone hydrochloride. At 2 hours after reperfusion, serum and urinary biochemical indicators of renal dysfunction and injury were measured: serum creatinine, fractional excretion of Na+ and urinary N-acetyl-D-glucosaminidase. Additionally, intracellular cAMP in kidney tissues was measured by a radioimmunology method. Compared to the only UW solution group, olprinone hydrochloride significantly reduced the increased in serum creatinine, FENa and NAG caused by renal ischemia/reperfusion injury, after 2 hours of reperfusion.
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CAS 119615-63-3 Olprinone Hydrochloride

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