Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.
Bioorg Med Chem Lett. 2010 Mar 1;20(5):1712-7. doi: 10.1016/j.bmcl.2010.01.079. Epub 2010 Jan 21.
Suppression of vitamin D receptor (VDR)-mediated transcription is expected be of therapeutic value in Paget's disease. Once an agonist activates VDR, recruitment of additional coactivator proteins is essential for transcription. Neither non-secosteroidal VDR antagonists nor non-peptide coactivator binding inhibitors for VDR have been reported so far. Based on the X-ray structure of VDR and an LXXLL-containing peptide fragment of the coactivator (where L is leucine and X is any amino acid), which adopts a partially alpha-helical conformation, benzodiazepine molecules were rationally designed as non-peptide coactivator mimetics. TR-FRET assay showed that the synthesized compounds inhibited the interaction between VDR and a coactivator peptide fragment. Compound 2 showed an IC(50) of 20microM. Compound 2 also inhibited VDR-mediated transcription, and this activity was independent of the concentration of co-existing agonist. Furthermore, compound 2 did not inhibit estrogen receptor alpha-mediated transcription, indicating that it is not a non-selective inhibitor of other nuclear receptors.
抑制维生素 D 受体(VDR)介导的转录有望成为治疗 Pagets 病的一种有价值的方法。一旦激动剂激活 VDR,募集额外的共激活蛋白对于转录是必不可少的。到目前为止,尚未报道非甾体 VDR 拮抗剂或非肽类 VDR 共激活剂结合抑制剂。基于 VDR 的 X 射线结构和共激活剂的含有 LXXLL 的肽片段(其中 L 是亮氨酸,X 是任何氨基酸),该肽片段采用部分α-螺旋构象,苯并二氮杂䓬分子被合理设计为非肽共激活剂模拟物。TR-FRET 测定表明,合成的化合物抑制了 VDR 与共激活肽片段之间的相互作用。化合物 2 的 IC50 为 20μM。化合物 2 还抑制了 VDR 介导的转录,并且这种活性不依赖于共存激动剂的浓度。此外,化合物 2 不抑制雌激素受体α介导的转录,表明它不是其他核受体的非选择性抑制剂。