Olprinone
(Synonyms: 奥普力农; Loprinone) 目录号 : GC36803
An inhibitor of PDE3
Cas No.:106730-54-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Olprinone is an inhibitor of phosphodiesterase 3 (PDE3; IC50 = 0.35 μM for human cardiac enzyme).1 It is selective for PDE3 over PDE1 and PDE2 (IC50s = 150 and 100 μM, respectively). Olprinone induces relaxation of precontracted isolated rabbit renal and carotid arterial rings (IC50s = 40 and 103 nM, respectively).2 It reduces infarct size and improves cardiac function in a rat model of myocardial ischemia-reperfusion injury when administered at a dose of 0.6 mg/kg twice per day.3 Olprinone (0.2 mg/kg) reduces cortical and striatal damage, as well as reduces injured cerebral tissue nitrotyrosine formation, apoptosis, and levels of inducible nitric oxide synthase (iNOS), IL-1β, and intercellular adhesion molecule 1 (ICAM-1) in a rat model of cerebral ischemia-reperfusion injury.4 It inhibits neutrophil infiltration into the lungs and inhibits increases in serum levels of TNF-α and IL-6 in a rat model of LPS-induced lung inflammation when administered at a dose of 0.2 mg/kg.5
1.Sugioka, M., Masuoka, H., Ichikawa, K., 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 isoenzymesNaunyn. Schmiedebergs. Arch. Pharmacol.350(3)284-293(1994) 2.Minonishi, T., Ogawa, K., Tokinaga, Y., et al.Differential vasodilation response to olprinone in rabbit renal and common carotid arteriesJ. Anesth.24(1)61-66(2010) 3.Han, M.-X., Xu, X.-W., Lu, S.-Q., et al.Effect of olprinone on ischemia-reperfusion induced myocardial injury in ratsBiomed. Pharmacother.1111005-1012(2019) 4.Genovese, T., Mazzon, E., Paterniti, I., et al.Neuroprotective effects of olprinone after cerebral ischemia/reperfusion injury in ratsNeurosci. Lett.503(2)93-99(2011) 5.Koike, T., Nadeen Qutab, M., Tsuchida, M., et al.Pretreatment with olprinone hydrochloride, a phosphodiesterase III inhibitor, attenuates lipopolysaccharide-induced lung injury via an anti-inflammatory effectPulm. Pharmacol.21(1)166-171(2008)
| Cas No. | 106730-54-5 | SDF | |
| 别名 | 奥普力农; Loprinone | ||
| Canonical SMILES | CC(N1)=C(C=C(C#N)C1=O)C2=CN3C(C=C2)=NC=C3 | ||
| 分子式 | C14H10N4O | 分子量 | 250.26 |
| 溶解度 | DMSO : 50mg/mL | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.9958 mL | 19.9792 mL | 39.9584 mL |
| 5 mM | 0.7992 mL | 3.9958 mL | 7.9917 mL |
| 10 mM | 0.3996 mL | 1.9979 mL | 3.9958 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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Olprinone: a phosphodiesterase III inhibitor with positive inotropic and vasodilator effects
Cardiovasc Drug Rev 2002 Fall;20(3):163-74.PMID:12397365DOI:10.1111/j.1527-3466.2002.tb00085.x.
Olprinone is a newly developed phosphodiesterase III inhibitor characterized by several properties. First, Olprinone has positive inotropic and vasodilator actions and improves myocardial mechanical efficiency. Second, Olprinone augments cerebral blood flow by a direct vasodilatory effect on cerebral arteries. The cerebrovascular reactivity to Olprinone is marked in patients with impaired cerebral circulation. Third, Olprinone selectively improves carotid artery distensibility, which may be attributable to differences in the arterial structural components or the reactivity of smooth muscle cells to Olprinone. Fourth, Olprinone improves inadequate redistribution of brain perfusion and may prevent cerebral metabolic abnormalities in heart failure.
[Research status of Olprinone in cardiovascular diseases]
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue 2018 Dec;30(12):1209-1212.PMID:30592961DOI:10.3760/cma.j.issn.2095-4352.2018.012.022.
First marketed in Japan in the 1990s, Olprinone is a newly developed phosphodiesterase III (PDE III) inhibitor. It can not only increase cardiac contractility and also reduce peripheral vascular resistance without affecting mean arterial pressure and heart rate. At present, Olprinone is mainly used in the treatment of acute heart failure and postoperative acute cardiac insufficiency. Through selectively inhibiting the activity of PDE III and increasing the concentration of cyclic adenosine monophosphate (cAMP) by blocking its degradation, Olprinone accelerates the influx of Ca2+ in cardiac myocytes, leading to enhancement of myocardial contractility; and on the other hand, decreases the influx of Ca2+ in vascular smooth muscle cells, resulting in dilation of peripheral blood vessels. Recently, a considerable amount of research has been conducted on Olprinone in terms of pulmonary hypertension, myocardial ischemia/reperfusion (I/R) injury, and arrhythmia. In this review, we summarize the application of olprinione in acute heart failure, pulmonary hypertension, myocardial I/R injury, and arrhythmia, and analyze its application value and related progress in cardiovascular diseases.
The effects of Olprinone, a phosphodiesterase 3 inhibitor, on systemic and cerebral circulation
Curr Vasc Pharmacol 2006 Jan;4(1):1-7.PMID:16472171DOI:10.2174/157016106775203072.
Olprinone, a phosphodiesterase (PDE) 3 inhibitor, is used to treat heart failure due to its positive inotropic and vasodilative effects. Selective inhibition of the PDE 3 isozyme increases intracellular adenosine 3;5;-cyclic monophosphate and enhances Ca(2+) influx into cardiac muscle cells. The most significant advantage of PDE 3 inhibitors is their ability not only to enhance myocardial contraction, but to reduce, through vasodilatory action, the stress to which the heart is subjected. In peripheral vessels, the decrease of cytosolic free Ca(2+) induces the vasorelaxation of vascular smooth muscle cells. In this way, Olprinone reduces mean aortic and pulmonary artery pressures. Additionally, Olprinone exerts differential vasodilatory effects on peripheral vessels in each organ, based on the differences in the distribution of PDE 3 among the organs. With respect to the cerebral circulation, Olprinone augments blood flow in the cerebral cortex through direct vasodilatory effects on small cerebral arteries or arterioles. Olprinone increases hepatosplanchnic blood flow and improves oxygen supply. While long-term therapy with PDE 3 inhibitors in patients with chronic heart failure may accelerate the progress of the underlying disease and provoke serious ventricular arrhythmia, Olprinone shows good potential for short-term treatment in patients who have experienced severe heart failure or patients who have undergone cardiac surgery.
Effect of Olprinone on ischemia-reperfusion induced myocardial injury in rats
Biomed Pharmacother 2019 Mar;111:1005-1012.PMID:30841413DOI:10.1016/j.biopha.2019.01.010.
Aims: This study investigated the effect of Olprinone on ischemia-reperfusion (I/R) induced cardiac injury, and the underlying mechanism. Main methods: Male Sprague-Dawley rats were subjected to a 30-min coronary arterial occlusion followed by 24 h reperfusion. After the start of reperfusion, rats were respectively treated with Olprinone in three different dosages (0.2, 0.6, 2 mg/kg, intraperitoneal injection, i.p./12 h). Twenty-four hours later, a mean arterial pressure (MAP) heart function analysis system was used to monitor hemodynamic parameters; TTC staining method was used to detect the myocardial infarct size; 24-hour mortality of rats was recorded; western blot was used to detect the protein expressions of Caspase-3, Bax, Bcl-2, Beclin-1 and LC3-II/LC3-I. Results: Cardiac function in I/R group was lower than that in sham group (dp/dt max: 1348.29 ± 266.01 vs. 3333.73 ± 1258.03, -dp/dt max: 1163.23 ± 588.18 vs. 3198.93 ± 1416.00, P < 0.05), which was significantly improved by treatment with high dosage of Olprinone (dp/dt max: 1348.29±266.01 vs. 2022.43±493.39, -dp/dt max: 1163.23±588.18 vs. 1784.50±418.92, P < 0.05). The percentage of myocardial infarct size in medium and high dosages of Olprinone group was lower than that in I/R group (42.67 ± 2.94, 22.33 ± 3.63 vs. 63.67 ± 5.86, P < 0.05). There was no significant difference in mortality among each group within 24 h. Compared with sham group, the expression of Caspase-3 was significantly up-regulated in I/R group (3.44±0.47-fold of sham, P < 0.05), which was inhibited by medium dosage of Olprinone treatment (2.00±0.52-fold of sham, P < 0.05 vs. I/R group); also, expression of Bax was increased compared with sham group (4.06±0.25-fold of sham, P < 0.05), which was markedly inhibited by all dosages of Olprinone treatment (low: 2.16±0.61-fold, medium: 2.74±0.66-fold, high 1.65±0.55-fold, P < 0.05 vs. I/R group). Expression of Bcl-2 was increased after I/R (1.17±0.06-fold, P < 0.05), which was further elevated in all dosages of Olprinone treatment (low: 1.62 ± 0.13-fold, medium: 1.46 ± 0.13-fold, high: 1.82 ± 0.39-fold, P < 0.05 vs. I/R group). In addition, compared with sham group, the expression of Beclin-1 was up-regulated to 1.44±0.05-fold of sham in I/R group (P < 0.05), which was further increased in low and medium dosages of Olprinone group (low: 2.46±0.44-fold, medium: 2.80±0.75-fold, P < 0.05 vs. I/R group). Moreover, expression of LC3-II was elevated in low dosage of Olprinone treated group (low: 4.50±0.47-fold, P < 0.05 vs. I/R group). Conclusions: Olprinone improves the cardiac function in response to myocardial I/R injury by regulation of anti-apoptotic, pro-apoptotic. In addition, autophagic signal pathways may also play a role in Olprinone's therapeutic effect.
Retraction
Fukushima J Med Sci 2017;63(2):126.PMID:28794319DOI:10.5387/fms.63_126.
The below article has been retracted. Article title 「EFFECTS OF Olprinone ON NEUROMUSCULAR BLOCKADE CAUSED BY VECURONIUM」Author Takaaki Katayama , Yuhji Saitoh , Chiaki Nemoto , Takahiro Hirama , Tsuyoshi Isosu , Masahiro Murakawa Journal title FUKUSHIMA JOURNAL OF MEDICAL SCIENCE Vol.53, No.2 2007:61-69 Fukushima Medical SocietyEditorial CommitteeJuly 5 , 2017.