Olprinone hydrochloride hydrate
Based on 1 publication(s) in Google Scholar
Olprinone (Loprinone) hydrochloride hydrate is a potent and selective phosphodiesterase 3 (PDE3) inhibitor, with IC50 values of 150, 100, 0.35, and 14 μM against PDE1, PDE2, PDE3, and PDE4, respectively. Olprinone hydrochloride hydrate exerts comprehensive protective effects including anti-inflammatory, antioxidant, and anti-apoptotic activities by elevating intracellular cAMP levels and inhibiting the NF-κB and MAPK signaling pathways. Olprinone hydrochloride hydrate can be used in studies related to lung injury, spinal cord injury, myocardial ischemia-reperfusion injury, and cerebral ischemic injury.
For research use only. We do not sell to patients.
- CAS No.: 2072803-95-1
- Formula: C14H13ClN4O2
- Molecular Weight:304.73
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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- References
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Publications Citing Use of MedChemExpress (MCE) Olprinone hydrochloride hydrate
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Biological Activity
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PDE1 150 μM (IC50) |
PDE2 100 μM (IC50) |
PDE3 0.35 μM (IC50) |
PDE4 14 μM (IC50) |
Olprinone (Loprinone) hydrochloride (10 mM; 48-72 h) hydrate inhibits LPS (HY-D1056)-induced production of TNF-α and IL-6, and promotes the production of IL-10, in isolated rat alveolar macrophages[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Primary rat alveolar macrophages
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Concentration:10 mM
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Incubation Time:48, 72 h
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Result:Significantly suppressed the levels of TNF-α and IL-6 at 48 h and 72 h.
Augmented the production of IL-10 at 48 h and 72 h.
Olprinone (0.2 mg/kg; i.p.; administered at 1 h and 6 h post-injury, followed by daily administration until day 9 post-injury; observation for 10 days) hydrochloride hydrate exerts effects of alleviating spinal cord inflammation, reducing cell apoptosis and improving hindlimb motor function in a mouse model of spinal cord injury[3].
Olprinone (0.2 mg/kg; i.v.; single administration; observation for 5 h) hydrochloride hydrate exerts effects of alleviating pulmonary oxidative stress, reducing pulmonary edema and inflammatory cell infiltration in a rabbit model of acute lung injury induced by meconium aspiration syndrome[4].
Olprinone (0.2 mg/kg; i.p.; single administration) hydrochloride hydrate exerts effects of reducing myocardial infarction size, anti-inflammation and anti-apoptosis in a rat model of myocardial ischemic injury[5].
Olprinone (0.2 mg/kg; i.p.; single administration; 5 minutes before reperfusion) hydrochloride hydrate exerts effects of reducing cerebral infarction volume, improving neurological deficits, anti-inflammation and anti-apoptosis in a rat model of cerebral ischemia/reperfusion injury[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar rats (male, 180-220 g, acute lung injury model via intravenous Escherichia coli serotype 055:B5 lipopolysaccharide injection at 5 mg/kg)[2]
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Dosage:0.2 mg/kg
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Administration:i.p.; single dose (30 minutes prior to LPS exposure); 6 h
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Result:Significantly inhibited the LPS-induced neutrophil influx into the lungs.
Suppressed inflammatory cytokines TNF-α and IL-6 in the serum.
Augmented the production of the anti-inflammatory cytokine IL-10 in the serum.
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Animal Model:CD1 mice (male adult, 25-30 g, spinal cord injury induced by extradural compression of T5-T8 spinal cord with 24 g closing force for 1 min after four-level T5-T8 laminectomy)[3]
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Dosage:0.2 mg/kg
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Administration:i.p.; 1 h and 6 h post-injury, then daily until day 9 post-injury (motor function assessment); 10 days
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Result:Reduced the degree of spinal cord inflammation and tissue injury.
Attenuated neutrophil infiltration (reduced myeloperoxidase activity) and nitrotyrosine formation.
Decreased the expression of pro-inflammatory cytokines (TNF-α, IL-1β) and adhesion molecules (ICAM-1, P-selectin).
Inhibited NF-κB expression, p-ERK1/2, and p-p38 MAP kinase activation.
Decreased apoptosis, evident by reduced TUNEL staining, Fas ligand, and Bax expression, alongside preserved Bcl-2 expression.
Ameliorated the recovery of hind-limb function (BMS score).
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Animal Model:Chinchilla rabbit (adult, 2.7 kg; meconium aspiration syndrome model via intratracheal meconium instillation)[4]
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Dosage:0.2 mg/kg
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Administration:i.v.; single dose; 5 h
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Result:Reduced the numbers of neutrophils and eosinophils in the BAL fluid.
Decreased the formation of oxidation markers (conjugated dienes, TBARS, dityrosine, and lysine-lipid peroxidation products) in lung mitochondria.
Reduced lung edema (decreased wet/dry weight ratio) and prevented a decrease in total antioxidant status (TAS) in the lung homogenate and plasma.
Decreased TBARS levels in blood plasma and preserved cytochrome coxidase (COX) activity in the lung.
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Animal Model:Wistar (male, 270-290 g, transient right hemisphere middle cerebral artery occlusion for 2 hours followed by 22 hours of reperfusion)[6]
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Dosage:0.2 mg/kg
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Administration:i.p.; single dose; 5 minutes before reperfusion
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Result:Reduced the infarct volume and improved the neurological deficit score.
Blocked the acute turning behavior significantly.
Suppressed the formation of nitrotyrosine and the expression of iNOS, IL-1β, and ICAM-1 in ischemic tissues.
Reduced levels of apoptosis (decreased TUNEL-positive cells and Bax expression, and maintained Bcl-2 expression).
Chemical Information
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CAS No. 2072803-95-1
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Molecular Weight 304.73
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Formula C14H13ClN4O2
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SMILES
CC(N1)=C(C=C(C#N)C1=O)C2=CN3C(C=C2)=NC=C3.Cl.O
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Synonyms
Loprinone hydrochloride hydrate
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
Purity & Documentation
References
[1].
Sugioka M, et al. Identification and characterization of isoenzymes of cyclic nucleotide phosphodiesterase in human kidney and heart, and the effects of new cardiotonic agents on these isoenzymes. Naunyn Schmiedebergs Arch Pharmacol. 1994 Sep;350(3):284-93.
[Content Brief]
[2]. Koike T, et al. Pretreatment with olprinone hydrochloride, a phosphodiesterase III inhibitor, attenuates lipopolysaccharide-induced lung injury via an anti-inflammatory effect. Pulmonary pharmacology & therapeutics. 2008;21(1):166-71. [Content Brief]
[4]. Mokra D, et al. Selective phosphodiesterase 3 inhibitor olprinone attenuates meconium-induced oxidative lung injury. Pulmonary pharmacology & therapeutics. 2012 Jun;25(3):216-22. [Content Brief]
[5]. Di Paola R, et al. Olprinone, a PDE3 inhibitor, modulates the inflammation associated with myocardial ischemia-reperfusion injury in rats. European journal of pharmacology. 2011 Jan 15;650(2-3):612-20. [Content Brief]
[6]. Genovese T, et al. Neuroprotective effects of olprinone after cerebral ischemia/reperfusion injury in rats. Neuroscience letters. 2011 Oct 03;503(2):93-9. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Olprinone hydrochloride hydrate Related Classifications
HY-14254B Related Classifications
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- Olprinone hydrochloride
- 2072803-95-1
- Loprinone hydrochloride
- Phosphodiesterase (PDE)
- Apoptosis
- NF-κB
- p38 MAPK
- male Wistar rats
- macrophage activation
- myocardial ischemia-reperfusion injury
- intracellular cAMP
- spinal cord injury
- pro-inflammatory cytokines
- phosphodiesterase III
- rat alveolar macrophages
- neutrophil influx
- Inhibitor
- inhibitor
- inhibit