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Dipyridamole

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Chemical Structure| 58-32-2 同义名 : NSC 515776;NSC 619103;Dipyridamol;Dipyridamine;RA 8
CAS号 : 58-32-2
货号 : A619148
分子式 : C24H40N8O4
纯度 : 98%
分子量 : 504.626
MDL号 : MFCD00010555
存储条件：

粉末 Keep in dark place,Sealed in dry,Room Temperature

液体 -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 50 mg/mL(99.08 mM)，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：
生物活性
靶点

  • PDE
描述 Intracellular cyclic nucleotide levels can be controlled through regulation of either synthesis via respective cyclases or degradation via the phosphodiesterases (PDEs)[3]. Dipyridamole inhibits the phosphodiesterase enzyme that degrades cyclic AMP to 5’-AMP, resulting in the intraplatelet accumulation of cyclic AMP[4]. Inhibition of the erythrocytic nucleoside transport system by dipyridamole (10 μM) evokes the antiaggregatory action of adenosine in whole blood (IC50 congruent to 2 μM)[5]. In an in situ perfused rabbit lung model in which the pulmonary vascular resistance (PVR) was elevated, 0.06 μM dipyridamole reduced elevated PVR by 8.2 +/- 2.8%, and the EC50 for dipyridamole was approximately 0.2 μM[6]. In newborn lambs with persistent pulmonary hypertension of the newborn (PPHN), dipyridamole infused at 0.02 mg/kg/min for 45 min alone significantly decreased pulmonary and systemic blood pressure, decreased pulmonary vascular resistance, and increased pulmonary blood flow[7]. Some potent dipyridamole derivatives are able to increase the primary immune response in mice immunized with sheep red blood cells (SRBC). 10 mg/kg/day of the most potent substance administered in the drinking water increased the number of plaque forming cells (PFC) in spleens of these mice by a factor of about 2 when the treatment was started after immunization[8].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

1.98mL

0.40mL

0.20mL

9.91mL

1.98mL

0.99mL

19.82mL

3.96mL

1.98mL
参考文献

[1]Klabunde RE. Dipyridamole inhibition of adenosine metabolism in human blood. Eur J Pharmacol. 1983 Sep 16;93(1-2):21-6.

[2]Best LC, McGuire MB, et al. Mode of action of dipyridamole on human platelets. Thromb Res. 1979;16(3-4):367-79.

[3]Glass WF 2nd, Moore JB Jr. Inhibition of human lung cyclic GMP and cyclic AMP phosphodiesterases by certain nucleosides, nucleotides, and pharmacological phosphodiesterase inhibitors. Biochem Pharmacol. 1979 Apr 1;28(7):1107-12. doi: 10.1016/0006-2952(79)90313-7. PMID: 87197.

[4]FitzGerald GA. Dipyridamole. N Engl J Med. 1987 May 14;316(20):1247-57. doi: 10.1056/NEJM198705143162005. PMID: 3553945.

[5]Dawicki DD, Agarwal KC, Parks RE Jr. Potentiation of the antiplatelet action of adenosine in whole blood by dipyridamole or dilazep and the cAMP phosphodiesterase inhibitor, RA 233. Thromb Res. 1986 Jul 15;43(2):161-75. doi: 10.1016/0049-3848(86)90057-5. PMID: 3016942.

[6]Clarke WR, Uezono S, Chambers A, Doepfner P. The type III phosphodiesterase inhibitor milrinone and type V PDE inhibitor dipyridamole individually and synergistically reduce elevated pulmonary vascular resistance. Pulm Pharmacol. 1994 Apr;7(2):81-9. doi: 10.1006/pulp.1994.1009. PMID: 8081075.

[7]Dukarm RC, Morin FC 3rd, Russell JA, Steinhorn RH. Pulmonary and systemic effects of the phosphodiesterase inhibitor dipyridamole in newborn lambs with persistent pulmonary hypertension. Pediatr Res. 1998 Dec;44(6):831-7. doi: 10.1203/00006450-199812000-00002. PMID: 9853914.

[8]Lichtner R, Wedderburn N. Enhancement of the immune response to sheep erythrocytes in mice by phosphodiesterase-inhibiting dipyridamole derivatives. J Immunopharmacol. 1984;6(1-2):43-55. doi: 10.3109/08923978409026457. PMID: 6088639.