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Acyclovir

阿昔洛韋

Mechanism of action:

在病毒感染的細胞內,acyclovir 先被病毒的胸苷激酶(thymidine kinase)磷酸化為阿昔洛韋單磷酸(acyclovir monophosphate),再由鳥苷酸激酶(guanylate kinase)轉成二磷酸形式,最後經過多種細胞的激酶轉換成阿昔洛韋三磷酸(acyclovir triphosphate),之後競爭性抑制病毒 DNA 聚合酶,並在被摻入病毒 DNA 後,由於缺乏 3'-OH 基團,導致 DNA 延長終止。此選擇性機制使其對感染細胞具較高抑制作用,而對正常細胞的影響相對較低。

​Reference(s):

1. Nies AT et al. (2012). Multidrug and toxin extrusion proteins as transporters of antimicrobial drugs. Expert Opin Drug Metab Toxicol. 


2. Yonezawa A et al. (2011). Importance of the multidrug and toxin extrusion MATE/SLC47A family to pharmacokinetics, pharmacodynamics/toxicodynamics and pharmacogenomics. Br J Pharmacol.

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