Department of Biochemistry , Vanderbilt University School of Medicine , Nashville , Tennessee 37232 , United States.
Synchrotron Research Center, Life Science Collaborative Access Team , Northwestern University , Argonne , Illinois 60439 , United States.
J Med Chem. 2019 Nov 27;62(22):10391-10401. doi: 10.1021/acs.jmedchem.9b01485. Epub 2019 Nov 11.
Sterol 14α-demethylases (CYP51) are the cytochrome P450 enzymes required for biosynthesis of sterols in eukaryotes, the major targets for antifungal agents and prospective targets for treatment of protozoan infections. Human CYP51 could be and, for a while, was considered as a potential target for cholesterol-lowering drugs (the role that is now played by statins, which are also in clinical trials for cancer) but revealed high intrinsic resistance to inhibition. While microbial CYP51 enzymes are often inhibited stoichiometrically and functionally irreversibly, no strong inhibitors have been identified for human CYP51. In this study, we used comparative structure/functional analysis of CYP51 orthologs from different biological kingdoms and employed site-directed mutagenesis to elucidate the molecular basis for the resistance of the human enzyme to inhibition and also designed, synthesized, and characterized new compounds. Two of them inhibit human CYP51 functionally irreversibly with their potency approaching the potencies of azole drugs currently used to inhibit microbial CYP51.
甾醇 14α-脱甲基酶(CYP51)是真核生物甾醇生物合成所必需的细胞色素 P450 酶,也是抗真菌药物的主要靶点,也是治疗原生动物感染的潜在靶点。人 CYP51 可能是(并且有一段时间被认为是)降低胆固醇药物(现在由他汀类药物发挥作用,他汀类药物也在临床试验中用于癌症)的潜在靶点,但对抑制具有很高的内在抗性。虽然微生物 CYP51 酶通常被化学计量和功能不可逆地抑制,但尚未鉴定出人 CYP51 的强抑制剂。在这项研究中,我们使用来自不同生物王国的 CYP51 同源物的比较结构/功能分析,并采用定点突变来阐明人酶对抑制的抗性的分子基础,还设计、合成和表征了新化合物。其中两种以接近目前用于抑制微生物 CYP51 的唑类药物的效力不可逆地抑制人 CYP51。