Division of Medicinal Chemistry, Amsterdam Institute for Molecules, Medicines and Systems, Vrije Universiteit Amsterdam, 1081 HZ Amsterdam, The Netherlands.
School of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.
Bioorg Med Chem. 2019 Sep 15;27(18):4013-4029. doi: 10.1016/j.bmc.2019.06.026. Epub 2019 Jul 5.
Inhibitors against Trypanosoma brucei phosphodiesterase B1 (TbrPDEB1) and B2 (TbrPDEB2) have gained interest as new treatments for human African trypanosomiasis. The recently reported alkynamide tetrahydrophthalazinones, which show submicromolar activities against TbrPDEB1 and anti-T. brucei activity, have been used as starting point for the discovery of new TbrPDEB1 inhibitors. Structure-based design indicated that the alkynamide-nitrogen atom can be readily decorated, leading to the discovery of 37, a potent TbrPDEB1 inhibitor with submicromolar activities against T. brucei parasites. Furthermore, 37 is more potent against TbrPDEB1 than hPDE4 and shows no cytotoxicity on human MRC-5 cells. The crystal structures of the catalytic domain of TbrPDEB1 co-crystalized with several different alkynamides show a bidentate interaction with key-residue Gln874, but no interaction with the parasite-specific P-pocket, despite being (uniquely) a more potent inhibitor for the parasite PDE. Incubation of blood stream form trypanosomes by 37 increases intracellular cAMP levels and results in the distortion of the cell cycle and cell death, validating phosphodiesterase inhibition as mode of action.
抗布氏锥虫磷酸二酯酶 B1(TbrPDEB1)和 B2(TbrPDEB2)抑制剂作为治疗人类非洲锥虫病的新方法引起了关注。最近报道的炔丙酰胺四氢酞嗪酮对 TbrPDEB1 具有亚微摩尔活性和抗 T. brucei 活性,已被用作发现新型 TbrPDEB1 抑制剂的起点。基于结构的设计表明,炔丙酰胺-氮原子可以很容易地修饰,从而发现了 37,这是一种有效的 TbrPDEB1 抑制剂,对 T. brucei 寄生虫具有亚微摩尔活性。此外,37 对 TbrPDEB1 的抑制作用强于 hPDE4,对人 MRC-5 细胞无细胞毒性。与几种不同的炔丙酰胺共结晶的 TbrPDEB1 催化结构域的晶体结构显示与关键残基 Gln874 形成双齿相互作用,但与寄生虫特异性 P 袋没有相互作用,尽管它是寄生虫 PDE 的更有效的抑制剂。37 孵育血液阶段锥虫会增加细胞内 cAMP 水平,并导致细胞周期扭曲和细胞死亡,验证了磷酸二酯酶抑制作用作为作用模式。