據估計全球約有2%~3%的人口感染C型肝炎病毒，感染C型肝炎病毒患者，在感染該病毒的二十年間，大約有4%~5%的患者會演變成肝硬化和肝癌而死亡1,2,3。目前治療C型肝炎是使用interferon結合ribavirin，雖然對非基因型1的病患有較好的療效3，但是嚴重的副作用加上價格昂貴使得治療上有一定的瓶頸，因此，發展擁有價格低、副作用少的全新藥物來改善藥效與這些治療上的限制。
C型肝炎病毒之非結構型5B是一RNA依賴RNA複製酶4，它擔任病毒RNA複製的重任，因此，我們選擇C型肝炎病毒基因型1b NS5B為藥物標靶，以分子對接藥物篩選分別對非競爭型與非核甘酸型抑制劑作用部位找出新的前導化合物。針對非競爭型抑制劑的部份，我們已經完成了藥物篩選工作，並篩選出一百個作用向量與位置相異或不盡相異於原配體的化合物，並以能量評分與藥效基團多寡作降冪排列，選出計算結果最好的前五十名與次佳的五十名，目前該部分已經在做活性測試。另一部份非核甘酸型抑制劑，我們也篩選出一百個在作用走向與原子相異或不盡相異於原配體的化合物，並將這些做活性測試。
據估計全球約有2%~3%的人口感染C型肝炎病毒，感染C型肝炎病毒患者，在感染該病毒的二十年間，大約有4%~5%的患者會演變成肝硬化和肝癌而死亡1,2,3。目前治療C型肝炎是使用interferon結合ribavirin，雖然對非基因型1的病患有較好的療效3，但是嚴重的副作用加上價格昂貴使得治療上有一定的瓶頸，因此，發展擁有價格低、副作用少的全新藥物來改善藥效與這些治療上的限制。
C型肝炎病毒之非結構型5B是一RNA依賴RNA複製酶4，它擔任病毒RNA複製的重任，因此，我們選擇C型肝炎病毒基因型1b NS5B為藥物標靶，以分子對接藥物篩選分別對非競爭型與非核甘酸型抑制劑作用部位找出新的前導化合物。針對非競爭型抑制劑的部份，我們已經完成了藥物篩選工作，並篩選出一百個作用向量與位置相異或不盡相異於原配體的化合物，並以能量評分與藥效基團多寡作降冪排列，選出計算結果最好的前五十名與次佳的五十名，目前該部分已經在做活性測試。另一部份非核甘酸型抑制劑，我們也篩選出一百個在作用走向與原子相異或不盡相異於原配體的化合物，並將這些做活性測試。

It is estimated that there are 170 million chronically infected HCV carriers worldwide（2%~3% of the global population）. Within 20 years of infection, about 4~5% of them will develop cirrhosis and hepatocellular carcinoma, often resulting in death. Current HCV therapy consists of injectable, α-interferon used alone or in combination with ribavirin. Although effective in certain patient populations, interferon therapy has several limitations including high cost and significant side effects that often require does adjustment or discontinuation of therapy. Moreover, while not will understood, interferon therapy has been shown to be most effective against genotype 2 and 3 HCV infections and least effective against genotype 1 infections. The lack of an effective and well-tolerated treatment has therefore spurred intense research efforts to develop affordable, oral and novel anti-HCV agents.
We chose HCV genome type 1b as a drug target using the approach of virtual docking screening to find the potential drug candidates both of noncompetitive and nonnucleoside inhibitor binding site. According to the dimension of noncompetitive inhibitor, we had finished the task of drug screening, and screened out one hundred compounds whose ligands were different or not exactly different on orientation and binding site. Besides, we sorted those compounds from the best to the worst by the method of energy score and the numbers of pharmacophore to select the first fifty good ones and secondary fifty good ones by the calculating result. All above as we had mentioned are in the procedure of biotest. In another portion,the dimension of nonnucleoside inhibitor, we had also chosen one hundred compounds whose ligands were different or not exactly different on orientation and binding site to perform the biotest.

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