Cilostazol (OPC 13013) is a potent and selective inhibitor of phosphodiesterase (PDE) 3A, the isoform of PDE 3 in the cardiovascular system, with an IC50 of 0.2 μM.
性状
Solid
IC50 & Target[1][2]
IC50: 0.2 μM ( PDE 3A)
体外研究(In Vitro)
Cilostazol selectively inhibits cGMP-inhibited phosphodiesterase (PDE 3) and is a potent inhibitor of platelet aggregation induced by various agonists.
Cilostazol inhibits stress-induced human platelet aggregation (SIPA) dose-dependently, with an IC50 of 15 μM for SIPA, and with a similar IC50 of 12.5 μM for ADP-induced platelet aggregation.
Cilostazol directly and effectively inhibits the activation of HSC but not of Kupffer cells.
Medlife has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究(In Vivo)
Cilostazol (clinically used doses; p.o.; for 2 weeks) could alleviate CCl4 -induced hepatic fibrogenesis in vivo, presumably due to its direct effect to suppress HSC activation.
Cilostazol (intraperitoneal injection; 10 mg/kg; 7 consecutive days after ischemia) attenuates neurological dysfunctions, brain atrophy and infarct volume, and inhibits astrocyte proliferation/glial scar formation and accelerated the angiogenesis in the ischemic boundary zone 7 and 28 days after ischemia.
Medlife has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Male C57BL/6J mice
Dosage:
0.1% w/w, 0.3% w/w
Administration:
Oral administration; fed a normal diet for 2 weeks
Result:
Exhibited a lesser fibrotic area than control groups.
Animal Model:
Male ICR mice
Dosage:
10 mg/kg
Administration:
Intraperitoneal injection; 7 consecutive days after ischemia