Suzuki Nobutaka, Ito Tatsuo, Matsui Hisanori, Takizawa Masayuki
Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, 26-1 Muraoka-Higashi 2-chome, Fujisawa, Kanagawa 251-8555 Japan.
Springerplus. 2016 Aug 30;5(1):1429. doi: 10.1186/s40064-016-3125-1. eCollection 2016.
TAK-475 (lapaquistat acetate) and its active metabolite-I (TAK-475 M-I) inhibit squalene synthase, which catalyzes the conversion of farnesyl diphosphate (FPP) to squalene. FPP is a substrate for synthesis of other mevalonate-derived isoprenoids (MDIs) such as farnesol (FOH), geranlygeranyl diphosphate (GGPP), and geranylgeraniol. In patients with MKD, a rare autosomal recessive disorder, defective activity of mevalonate kinase leads to a shortage of MDIs. MDIs especially GGPP are required for prenylation of proteins, which is a posttranslation modification necessary for proper functioning of proteins like small guanosine triphosphatases. Malfunction of prenylation of proteins results in upregulation of the inflammatory cascade, leading to increased production of proinflammatory cytokines like interleukin-1β (IL-1β), eventually leading to episodic febrile attacks. In vitro, TAK-475 M-I incubation in a concentration dependent manner increased levels of FPP, GGPP, and FOH in human monocytic THP-1 cells. In subsequent experiments, THP-1 cells or human peripheral blood mononuclear cells (PBMCs) were incubated with simvastatin, which inhibits hydroxymethylglutaryl-coenzyme A reductase and thereby decreases levels of the precursors of MDIs, leading to the depletion of MDIs as expected in MKD patients. Increased levels of GGPP and FPP attenuated lipopolysaccharide (LPS)-induced IL-1β production in THP-1 cells and human PBMCs in statin-treated conditions. The MDIs also significantly reduced the damaged cell ratio in this active MKD-like condition. Moreover, TAK-475 M-I directly inhibited LPS-induced IL-1β production from statin-treated THP-1 cells. These results show anti-inflammatory and cytoprotective effects of MDIs via TAK-475 M-I treatment in statin-treated immune cells, suggesting that possible therapeutic effects of TAK-475 treatment in MKD patients.
TAK - 475(醋酸拉帕喹他)及其活性代谢物 - I(TAK - 475 M - I)可抑制角鲨烯合酶,该酶催化法尼基二磷酸(FPP)转化为角鲨烯。FPP是合成其他甲羟戊酸衍生类异戊二烯(MDIs)的底物,如法尼醇(FOH)、香叶基香叶基二磷酸(GGPP)和香叶基香叶醇。在患有MKD(一种罕见的常染色体隐性疾病)的患者中,甲羟戊酸激酶活性缺陷会导致MDIs短缺。蛋白质的异戊二烯化需要MDIs,尤其是GGPP,而异戊二烯化是小GTP酶等蛋白质正常功能所必需的翻译后修饰。蛋白质异戊二烯化功能失调会导致炎症级联反应上调,导致促炎细胞因子如白细胞介素 - 1β(IL - 1β)的产生增加,最终导致发作性发热。在体外,以浓度依赖的方式在人单核细胞THP - 1细胞中孵育TAK - 475 M - I会增加FPP、GGPP和FOH的水平。在随后的实验中,将THP - 1细胞或人外周血单核细胞(PBMCs)与辛伐他汀一起孵育,辛伐他汀抑制羟甲基戊二酰辅酶A还原酶,从而降低MDIs前体的水平,导致如MKD患者预期的那样MDIs耗竭。在他汀治疗的条件下,GGPP和FPP水平的增加减弱了脂多糖(LPS)诱导的THP - 1细胞和人PBMCs中IL - 1β的产生。在这种类似MKD的活跃状态下,MDIs也显著降低了受损细胞比例。此外,TAK - 475 M - I直接抑制了他汀治疗的THP - 1细胞中LPS诱导的IL - 1β产生。这些结果表明,在他汀治疗的免疫细胞中,通过TAK - 475 M - I治疗,MDIs具有抗炎和细胞保护作用,提示TAK - 475治疗对MKD患者可能具有治疗效果。