JavaScript seems to be disabled in your browser. For the best experience on our site, be sure to turn on Javascript in your browser.
Tel: +1-832-696-8203
Email: [email protected]
Worldwide Distributors
In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Cilostazol is specific inhibition of cyclic nucleotide phosphodiesterase 3 (PDE3) with IC50 value of 200 nM.[1] PDE3 is one of phosphodiesterase. PDE3 plays an important role in regulating vascular smooth muscle, heart muscle and platelet aggregation, so, it is clinically significant. The PDE3 family consists of two members including PDE3A and PDE3B. PDE3A is mainly related cardiovascular function and PDE3B is mainly related to lipolysis. The activity of PDE3 is regulated by phosphorylation pathways. PDE 3 is activited via phosphorylation at different phosphorylation sites by protein kinase A and protein kinase B. PDE3 enzymes also are involved in regulation of vascular and cardiac smooth muscle contractility.Cilostazol prevents platelet aggregation by specifically and selectively inhibiting PDE3 in platelets with IC50 value of 200 nM. Cilostazol also cause intracellular cAMP levels increasing by inhibiting adenosine uptake leading to increased adenosine levels in cells. Cilostazol also inhibits the expression of platelet surface P-selectin, platelet factor 4 (PF4), thromboxane B2 production release. Cilostazol also cause decrease in triglyceride levels and an increase in high-density lipoprotein. [1] Cilostazol may has effective function in dementia. Cilostazol has beneficial effects on learning impairment induced by Aβ25-35 in mice. Cilostazol attenuated the impairment induced by Aβ25-35 at 100 mg/kg.[2]References: [1]. Rondina MT, Weyrich AS: Targeting phosphodiesterases in anti-platelet therapy. Handb Exp Pharmacol 2012(210):225-238.[2]. Hiramatsu M, Takiguchi O, Nishiyama A, Mori H: Cilostazol prevents amyloid beta peptide(25-35)-induced memory impairment and oxidative stress in mice. Br J Pharmacol 2010, 161(8):1899-1912.