Pranidipine
(Synonyms: 普拉地平,OPC-13340) 目录号 : GC38230
Pranidipine (Acalas, OPC 13340) is a new 1,4-dihydropyridine calcium channel blocker. Pranidipine can enhance cyclic GMP-independent nitric oxide-induced relaxation of the rat aorta.
Cas No.:99522-79-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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Pranidipine (Acalas, OPC 13340) is a new 1,4-dihydropyridine calcium channel blocker. Pranidipine can enhance cyclic GMP-independent nitric oxide-induced relaxation of the rat aorta.
[1] Mori T, et al. Mol Cell Biochem. 1998 Jan;178(1-2):335-43.
| Cas No. | 99522-79-9 | SDF | |
| 别名 | 普拉地平,OPC-13340 | ||
| Canonical SMILES | O=C(C1=C(C)NC(C)=C(C(OC/C=C/C2=CC=CC=C2)=O)C1C3=CC=CC([N+]([O-])=O)=C3)OC | ||
| 分子式 | C25H24N2O6 | 分子量 | 448.47 |
| 溶解度 | DMSO: 270 mg/mL (602.05 mM) | 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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1 mg | 5 mg | 10 mg |
| 1 mM | 2.2298 mL | 11.149 mL | 22.298 mL |
| 5 mM | 0.446 mL | 2.2298 mL | 4.4596 mL |
| 10 mM | 0.223 mL | 1.1149 mL | 2.2298 mL |
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Pranidipine, a 1,4-dihydropyridine calcium channel blocker that enhances nitric oxide-induced vascular relaxation
Cardiovasc Drug Rev 2001 Spring;19(1):1-8.PMID:11314598DOI:10.1111/j.1527-3466.2001.tb00179.x.
Pranidipine, a long acting 1,4-dihydropyridine calcium channel blocker, prolongs nitric oxide (NO)-mediated relaxation of rat aorta; it prolongs acetylcholine-induced relaxation in presence of endothelium as well as nitroglycerin-induced relaxation in absence of endothelium. In rat aorta the effect of Pranidipine on NO-mediated relaxation is cyclic guanosine monophosphate (cGMP)-independent, but in guinea pig carotid artery the same effect of Pranidipine is cGMP-dependent. It has been reported that in co-cultured human endothelial and smooth muscle cells Pranidipine, at a higher concentration (10(-6) M), enhances vasorelaxant effect of NO by blocking NO decomposition. The enhancement of NO action by Pranidipine differs from the direct NO-releasing action of other 1,4-dihydropyridines. It is expected that enhancement of NO-induced vasodilatation will lead to a venodilator action in vivo and less peripheral edema. The target organ protective effects of Pranidipine are also reviewed in this article.
Pranidipine enhances the action of nitric oxide released from endothelial cells
Hypertension 2000 Jan;35(1 Pt 1):82-5.PMID:10642279DOI:10.1161/01.hyp.35.1.82.
Nitric oxide (NO) synthesis in vascular endothelium of patients with hypertension is altered. Calcium antagonists have been shown to improve endothelial function in hypertensive patients. Here we report that Pranidipine, one of the latest long-acting calcium antagonists in the dihydropyridine group, enhances the actions of NO released from endothelial cells (ECs). Pranidipine significantly enhanced cGMP accumulation in vascular smooth muscle cells cocultured with ECs, whereas amlodipine and nifedipine had no significant effects. In addition, Pranidipine also suppressed basal and thrombin-stimulated endothelin-1 production from ECs. Pranidipine also enhanced cGMP accumulation in rat aortic segments with endothelium but not in endothelium-denuded vessels. In contrast, Pranidipine had no effect in the presence of N(G)-monomethyl-L-arginine, an inhibitor of NO synthesis. Pranidipine did not affect the basal expression of endothelial NO synthase in ECs. However, Pranidipine upregulated the activity of superoxide dismutase in ECs. These findings suggest that Pranidipine enhances NO action through inhibition of superoxide-induced NO decomposition in the vessel wall. Thus, Pranidipine may be useful in the treatment of impaired endothelial function in patients with hypertension.
Comparative effects of Pranidipine with amlodipine in rats with heart failure
Pharmacology 2006;77(1):1-10.PMID:16508340DOI:10.1159/000091746.
The aim of the present study was to compare the cardioprotective properties of long-acting calcium channel antagonist Pranidipine with amlodipine in rat model of heart failure induced by autoimmune myocarditis. Twenty-eight days after immunization the surviving rats were randomized for the oral administration of low-dose amlodipine (1 mg/kg/day), high-dose amlodipine (5 mg/kg/day), Pranidipine (0.3 mg/kg/day) or vehicle (0.5% methylcellulose). After oral administration for 1 month, the animals underwent echocardiography and hemodynamic analysis. Histopathology, immunohistochemistry, and Western immunoblotting were carried out in the heart samples. Both Pranidipine and high-dose amlodipine increased survival rate. Although the heart rate did not differ among the four groups, left ventricular end-diastolic pressure was significantly decreased and +/-dP/dt was increased in the pranidipine- and high-dose amlodipine-treated rats, but not in low-dose amlodipine-treated rats. In comparison to amlodipine treatment, Pranidipine treatment significantly reduced myocyte size and central venous pressure. Furthermore, both Pranidipine and high-dose amlodipine treatment significantly reduced myocardial protein levels of atrial natriuretic peptide and inducible nitric oxide synthase, whereas Pranidipine only significantly decreased tumor necrosis factor-alpha, and improved sarcoplasmic reticulum Ca2+ ATPase2 protein levels. We conclude that Pranidipine ameliorates the progression of left ventricular dysfunction and cardiac remodeling in rats with heart failure after autoimmune myocarditis in a lower dose when compared to amlodipine and which may be a clinically potential therapeutic agent for the treatment of heart failure.
Inhibitory effect of Pranidipine on N-type voltage-dependent Ca2+ channels in mice
Neurosci Lett 2004 Aug 26;367(1):118-22.PMID:15308311DOI:10.1016/j.neulet.2004.05.092.
We investigated the N-type voltage-dependent calcium channel blocking action of Pranidipine, a novel dihydropyridine (DHP) derivative. Pranidipine significantly suppressed KCl-induced intracellular calcium changes ([Ca(2+)](i)) in a dose-dependent fashion in dorsal root ganglion neurons. A patch-clamp investigation revealed a dose-dependent blocking effect on N-type currents. Intrathecal injection of Pranidipine significantly shortened the licking time in the late phase of the formalin test, as occurs with cilnidipine and amlodipine, which act on L- and N-type channels. Conversely, nicardipine, which acts exclusively on L-type channels, had no antinociceptive effect. Our results indicate that Pranidipine inhibits N-type calcium channels. Furthermore, it exerts an antinociceptive effect, which might be related to an attenuation of synaptic transmission by nociceptive neurons due to the blocking effect of Pranidipine on N-type calcium channels in primary nociceptive afferent fibers.
Pranidipine, a novel calcium antagonist, once daily, for the treatment of hypertension: a multicenter, double-blind, placebo-controlled dose-finding study
Cardiovasc Drugs Ther 1996 Mar;10(1):59-66.PMID:8723171DOI:10.1007/BF00051131.
The antihypertensive effects and tolerance of once-daily (od), Pranidipine, a novel dihydropyridine derivative with a long duration of action, were evaluated in a double-blind, placebo-controlled, parallel-group dose-finding study. A total of 199 patients, with a diastolic blood pressure (BP) of 95-115 mmHg, were included in the trial. After 4 weeks on placebo, patients were randomly assigned to either placebo or Pranidipine at 1, 2, 4, or 8 mg od for a further 4 weeks. A dose response was seen in the reduction (delta) of diastolic BP: placebo, delta 1.7 mm Hg; 1 mg, delta 6.4 mmHg; 2 mg, delta 7.5 mmHg, p < 0.01; 4 mg, delta 11.5 mmHg, p < 0.01; and 8 mg, delta 10.6 mmHg, p < 0.01. There were no meaningful changes in heart rate. The number of responders (decrease of diastolic blood pressure to < 90 mmHg and by 10 mmHg or more from baseline value) in each group also revealed a dose-response relationship: placebo = 9%; 1 mg = 25%, n.s.; 2 mg = 27%, n.s.; 4 mg = 41.5%, p < 0.01; and 8 mg = 41%, p < 0.01 (compared with placebo). Plasma concentrations of Pranidipine also demonstrated linear dose-response relationships. An increase in adverse events was observed within the 8 mg group. The degree of reduction in BP and the number of responders were not greater in the 8 mg group compared with the 4 mg group, although the plasma concentration (mean values, ng/dl) of pranidine in the 8 mg group was higher (2.2 on day 42; 2.3 on day 56) compared with the 4 mg group (1.4 on day 42; 1.6 on day 56). In conclusion, Pranidipine is a well-tolerated and 24-hour effective novel calcium antagonist that reduces BP in a dose-related manner up to 4 mg od.