Cilostazol is a potent cyclic nucleotide phosphodiesterase type 3 (PDE3) inhibitor with IC50 of 0.2 μM and inhibitor of adenosine uptake.
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HazMat fee for 500 gram (Estimated)
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Type 3 cyclic nucleotide phosphodiesterase (PDE-3) isoforms exhibit a high affinity ("low K(m)") for cAMP and are specifically inhibited by cGMP and a number of pharmacological agents. The PDE-3 family consists of at least two isozymes, PDE-3A (cardiac type) and PDE-3B (adipocyte type), with distinct tissue-specific distributions[3]. Cilostazol is a 2-oxo-quinoline derivative with antithrombotic, vasodilator, antimitogenic and cardiotonic properties. The compound is a potent inhibitor of phosphodiesterase (PDE) 3A, the isoform of PDE 3 in the cardiovascular system (IC50: 0.2 μM). There is no relevant effect by cilostazol on PDE 1, 2 and 4 at comparable concentrations, and only a minor effect on PDE 5 (IC50: 5 ± 8 mM). In addition, there was inhibition of adenosine uptake, eventually resulting in changes in cAMP levels[4]. In vitro, cilostazol inhibited adenosine uptake into cardiac myocytes, coronary artery smooth muscle cells and endothelial cells, with a median effective concentration of 10 μM, which might result from stimulation of adenosine A1 receptors and might counteract the increase of cAMP via PDE-inhibition[4]. Cilostazol inhibits platelet aggregation and has considerable antithrombotic effects in vivo. The compound relaxed vascular smooth muscle and inhibited mitogenesis and migration of vascular smooth muscle cells and decreaseed levels of serum triglycerides and caused some increase in HDL-cholesterol levels[4]. In the rat carotid injury model, single local application of cilostazol resulted in a marked inhibition of intima proliferation. Interestingly, the tissue concentration of cilostazol in the carotid artery and muscle around the carotid artery was considerably higher than in plasma, which was probably related to its highly lipophilic nature. There was also suppression of neointimal formation in dog grafted veins, which appeared to be related to inhibition of angiotensin II forming enzymes[4].
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