Khalaf Juhienah K, Bowen William S, Bazin Hélène G, Ryter Kendal T, Livesay Mark T, Ward Jon R, Evans Jay T, Johnson David A
GlaxoSmithKline Vaccines, 553 Old Corvallis Road, Hamilton, MT 59840, USA.
Institute for Cellular Therapeutics, University of Louisville School of Medicine, Donald E. Baxter Biomedical Research Building, 570 South Preston Street, Louisville, KY 40202, USA.
Bioorg Med Chem Lett. 2015 Feb 1;25(3):547-53. doi: 10.1016/j.bmcl.2014.12.024. Epub 2014 Dec 17.
TLR4 agonists that favor TRIF-dependent signaling and the induction of type 1 interferons may have potential as vaccine adjuvants with reduced toxicity. CRX-547 (4), a member of the aminoalkyl glucosaminide 4-phosphate (AGP) class of lipid A mimetics possessing three (R)-3-decanoyloxytetradecanoyl groups and d-relative configuration in the aglycon, selectively reduces MyD88-dependent signaling resulting in TRIF-selective signaling, whereas the corresponding secondary ether lipid 6a containing (R)-3-decyloxytetradecanoyl groups does not. In order to determine which secondary acyl groups are important for the reduction in MyD88-dependent signaling activity of 4, the six possible ester/ether hybrid derivatives of 4 and 6a were synthesized and evaluated for their ability to induce NF-κB in a HEK293 cell reporter assay. An (R)-3-decanoyloxytetradecanoyl group on the 3-position of the d-glucosamine unit was found to be indispensable for maintaining low NF-κB activity irrespective of the substitutions (decyl or decanoyl) on the other two secondary positions. These results suggest that the carbonyl group of the 3-secondary lipid chain may impede homodimerization and/or conformational changes in the TLR4-MD2 complex necessary for MyD88 binding and pro-inflammatory cytokine induction.
有利于依赖TRIF的信号传导和1型干扰素诱导的TLR4激动剂可能具有作为毒性降低的疫苗佐剂的潜力。CRX-547(4)是氨基烷基葡糖胺4-磷酸(AGP)类脂多糖模拟物的成员,在糖苷配基中具有三个(R)-3-癸酰氧基十四烷酰基和d-相对构型,选择性地降低依赖MyD88的信号传导,导致TRIF选择性信号传导,而含有(R)-3-癸氧基十四烷酰基的相应仲醚脂质6a则不然。为了确定哪些仲酰基对于降低4的依赖MyD88的信号传导活性很重要,合成了4和6a的六种可能的酯/醚杂化衍生物,并在HEK293细胞报告基因测定中评估了它们诱导NF-κB的能力。发现d-葡糖胺单元3位上的(R)-3-癸酰氧基十四烷酰基对于维持低NF-κB活性是必不可少的,而与其他两个仲位上的取代基(癸基或癸酰基)无关。这些结果表明,3-仲脂质链中的羰基可能会阻碍MyD88结合和促炎细胞因子诱导所需的TLR4-MD2复合物中的同二聚化和/或构象变化。