Department of Pharmaceutical and Biological Chemistry, School of Pharmacy, University of London, 29-39 Brunswick Square, London WC1N 1AX, United Kingdom.
Bioorg Med Chem. 2010 Nov 1;18(21):7475-85. doi: 10.1016/j.bmc.2010.08.055. Epub 2010 Sep 18.
Acetylenic fatty acids are known to display several biological activities, but their antimalarial activity has remained unexplored. In this study, we synthesized the 2-, 5-, 6-, and 9-hexadecynoic acids (HDAs) and evaluated their in vitro activity against erythrocytic (blood) stages of Plasmodium falciparum and liver stages of Plasmodium yoelii infections. Since the type II fatty acid biosynthesis pathway (PfFAS-II) has recently been shown to be indispensable for liver stage malaria parasites, the inhibitory potential of the HDAs against multiple P. falciparum FAS-II (PfFAS-II) elongation enzymes was also evaluated. The highest antiplasmodial activity against blood stages of P. falciparum was displayed by 5-HDA (IC(50) value 6.6 μg/ml), whereas the 2-HDA was the only acid arresting the growth of liver stage P. yoelii infection, in both flow cytometric assay (IC(50) value 2-HDA 15.3 μg/ml, control drug atovaquone 2.5 ng/ml) and immunofluorescence analysis (IC(50) 2-HDA 4.88 μg/ml, control drug atovaquone 0.37 ng/ml). 2-HDA showed the best inhibitory activity against the PfFAS-II enzymes PfFabI and PfFabZ with IC(50) values of 0.38 and 0.58 μg/ml (IC(50) control drugs 14 and 30 ng/ml), respectively. Enzyme kinetics and molecular modeling studies revealed valuable insights into the binding mechanism of 2-HDA on the target enzymes. All HDAs showed in vitro activity against Trypanosoma brucei rhodesiense (IC(50) values 3.7-31.7 μg/ml), Trypanosoma cruzi (only 2-HDA, IC(50) 20.2 μg/ml), and Leishmania donovani (IC(50) values 4.1-13.4 μg/ml) with generally low or no significant toxicity on mammalian cells. This is the first study to indicate therapeutic potential of HDAs against various parasitic protozoa. It also points out that the malarial liver stage growth inhibitory effect of the 2-HDA may be promoted via PfFAS-II enzymes. The lack of cytotoxicity, lipophilic nature, and calculated pharmacokinetic properties suggests that 2-HDA could be a useful compound to study the interaction of fatty acids with these key P. falciparum enzymes.
炔酸脂肪酸已知具有多种生物活性,但它们的抗疟活性尚未得到探索。在这项研究中,我们合成了 2-、5-、6-和 9-十六炔酸(HDAs),并评估了它们对恶性疟原虫(Plasmodium falciparum)红细胞(血液)阶段和间日疟原虫(Plasmodium yoelii)肝期感染的体外活性。由于 II 型脂肪酸生物合成途径(PfFAS-II)最近被证明对肝期疟原虫是必不可少的,因此还评估了 HDAs 对多种 PfFAS-II(PfFAS-II)延伸酶的抑制潜力。5-HDA 对恶性疟原虫血液阶段显示出最高的抗疟活性(IC50 值 6.6 μg/ml),而 2-HDA 是唯一一种能阻止间日疟原虫肝期感染生长的酸,在流式细胞术测定(IC50 值 2-HDA 15.3 μg/ml,对照药物阿托伐醌 2.5 ng/ml)和免疫荧光分析(IC50 值 2-HDA 4.88 μg/ml,对照药物阿托伐醌 0.37 ng/ml)中均如此。2-HDA 对 PfFAS-II 酶 PfFabI 和 PfFabZ 显示出最好的抑制活性,IC50 值分别为 0.38 和 0.58 μg/ml(对照药物的 IC50 值分别为 14 和 30 ng/ml)。酶动力学和分子建模研究揭示了 2-HDA 与靶酶结合机制的有价值的见解。所有 HDAs 对布氏锥虫(Trypanosoma brucei rhodesiense)(IC50 值 3.7-31.7 μg/ml)、克氏锥虫(仅 2-HDA,IC50 值 20.2 μg/ml)和杜氏利什曼原虫(Leishmania donovani)(IC50 值 4.1-13.4 μg/ml)均具有体外活性,对哺乳动物细胞一般没有或没有显著的毒性。这是第一项表明 HDAs 对各种寄生原生动物具有治疗潜力的研究。它还指出,2-HDA 对恶性疟原虫肝期生长的抑制作用可能是通过 PfFAS-II 酶促进的。缺乏细胞毒性、亲脂性和计算的药代动力学特性表明,2-HDA 可能是一种有用的化合物,可用于研究脂肪酸与这些关键 PfFAS-II 酶的相互作用。