Degardin Mélissa, Wein Sharon, Duckert Jean-Frédéric, Maynadier Marjorie, Guy Alexandre, Durand Thierry, Escale Roger, Vial Henri, Vo-Hoang Yen
UMR 5247 CNRS-UMI-UMII-ENSCM, Institut des Biomolecules Max Mousseron (IBMM), Faculté des Sciences Pharmaceutiques et Biologiques, Université de Montpellier I/II, 15 Avenue Charles Flahault, 34093 Montpellier (France).
ChemMedChem. 2014 Feb;9(2):300-4. doi: 10.1002/cmdc.201300419. Epub 2014 Jan 8.
Plasmodium falciparum is responsible of the most severe form of malaria, and new targets and novel chemotherapeutic scaffolds are needed to fight emerging multidrug-resistant strains of this parasite. Bis-alkylguanidines have been designed to mimic choline, resulting in the inhibition of plasmodial de novo phosphatidylcholine biosynthesis. Despite potent in vitro antiplasmodial and in vivo antimalarial activities, a major drawback of these compounds for further clinical development is their low oral bioavailability. To solve this issue, various modulations were performed on bis-alkylguanidines. The introduction of N-disubstituents on the guanidino motif improved both in vitro and in vivo activities. On the other hand, in vivo pharmacological evaluation in a mouse model showed that the N-hydroxylated derivatives constitute the first oral bioprecursors in bis-alkylguanidine series. This study paves the way for bis-alkylguanidine-based oral antimalarial agents targeting plasmodial phospholipid metabolism.
恶性疟原虫引发最严重形式的疟疾,对抗这种寄生虫新出现的多重耐药菌株需要新的靶点和新型化学治疗骨架。双烷基胍类化合物的设计旨在模拟胆碱,从而抑制疟原虫的从头磷脂酰胆碱生物合成。尽管这些化合物具有强大的体外抗疟活性和体内抗疟活性,但它们进一步临床开发的一个主要缺点是口服生物利用度低。为了解决这个问题,对双烷基胍类化合物进行了各种修饰。在胍基上引入N-二取代基提高了体外和体内活性。另一方面,在小鼠模型中的体内药理学评估表明,N-羟基化衍生物是双烷基胍系列中的首个口服生物前体。这项研究为靶向疟原虫磷脂代谢的基于双烷基胍的口服抗疟药物铺平了道路。