Cilostazol

그림문자(GHS)

• 그림문자(GHS)

  

• 신호 어

  Warning

• 예방조치문구

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Cilostazol MSDS

• 6-[4-(1-Cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2(1H)-quinolinone Additional name: 6-[4-(1-Cyclohexyl-5-tetrazolyl)butoxy]-1,2,3,4- tetrahydro-2-oxoquinolinone

Cilostazol 화학적 특성, 용도, 생산

• 개요

  Cilostazol is a platelet aggregation inhibitor with cerebral vasodilating activity, indicated for use in stroke and myocardial infarction. In patients with cerebral thrombosis, transient ischemia and cerebral arteriosclerosis, cilostazol significantly inhibits ADP-, collagenand epinephrine-induced platelet aggregation. Side effects include headache and tachycardia.

• 화학적 성질

  Colourless Needles

• 용도

  A potent phosphodiesterase III A (PDE3A) inhibitor (IC50=0.2uM) and inhibitor of adenosine uptake. Has antimitogeni, antithrombotic, vasodilatory and cardiotonic properties in vivo. Also affects lipid levels in vivo

• 정의

  ChEBI: A lactam that is 3,4-dihydroquinolin-2(1H)-one in which the hydrogen at position 6 is substiuted by a 4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxy group.

• 일반 설명

  Cilostazol is a potent cyclic nucleotide phosphodiesterase inhibitor. It is mainly used as antiplatelet agent.

• 생물학적 활성

  Potent phosphodiesterase III A (PDE3A) inhibitor (IC 50 = 0.2 μ M) and inhibitor of adenosine uptake. Has antimitogenic, antithrombotic, vasodilatory and cardiotonic properties in vivo . Also affects lipid levels in vivo .

• Mechanism of action

  Cilostazol exhibits greater selectivity than dipyridamole as an inhibitor of PDE3A. The drug does not affect the other PDEs (PDEs 1, 2, or 4). Cilostazol reversibly inhibit platelet aggregation induced by a number of stimuli, such as thrombin, ADP, collagen, or stress from exercise. Additionally, cilostazol inhibits adenosine uptake, leading to increased activity of adenosine at A1 and A2 receptors.

• Clinical Use

  Cilostazol, a quinolinone derivative, is a potent orally active antiplatelet drug approved for the treatment of intermittent claudication (a peripheral artery disease resulting from blockage of blood vessels in the limbs).

• 신진 대사

  Cilostazol is rapidly absorbed after oral administration, particularly with a high-fat meal, which greatly increases its bioavailability to approximately 90%. It is extensively metabolized in the liver by various cytochromes. The most important cytochromes appear to be CYP3A4 and, to lesser extent, by CYP2C19, with an elimination half-life of approximately 11 to 13 hours. Among the various metabolites produced (11 metabolites are known), the two major metabolites are 3,4-dehydrocilostazol and 4′-trans-hydroxycliostazol. These two metabolites are pharmacologically active. Studies indicate that the concomitant administration of cilostazol with CYP3A inhibitors can greatly increase cilostazol blood concentrations, and a dose reduction may be required. Similar results are seen when CYP2C19 is inhibited, leading to decreased formation of 4-trans-hydroxycliostazol and significant increases in cilostazol and 3,4-dehydrocilostazol.

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