Department of Medicinal Chemistry, The Institute for Structural Biology, Drug Discovery and Development, School of Pharmacy, Virginia Commonwealth University, Richmond, VA 23298, USA.
Vertex Pharmaceutical Incorporated, Boston, MA 02210, USA.
Molecules. 2022 Oct 12;27(20):6835. doi: 10.3390/molecules27206835.
Sickle cell disease (SCD) is caused by a single-point mutation, and the ensuing deoxygenation-induced polymerization of sickle hemoglobin (HbS), and reduction in bioavailability of vascular nitric oxide (NO), contribute to the pathogenesis of the disease. In a proof-of-concept study, we successfully incorporated nitrate ester groups onto two previously studied potent antisickling aromatic aldehydes, TD7 and VZHE039, to form TD7-NO and VZHE039-NO hybrids, respectively. These compounds are stable in buffer but demonstrated the expected release of NO in whole blood in vitro and in mice. The more promising VZHE039-NO retained the functional and antisickling activities of the parent VZHE039 molecule. Moreover, VZHE039-NO, unlike VZHE039, significantly attenuated RBC adhesion to laminin, suggesting this compound has potential in vivo RBC anti-adhesion properties relevant to vaso-occlusive events. Crystallographic studies show that, as with VZHE039, VZHE039-NO also binds to liganded Hb to make similar protein interactions. The knowledge gained during these investigations provides a unique opportunity to generate a superior candidate drug in SCD with enhanced benefits.
镰状细胞病 (SCD) 是由单点突变引起的,随之而来的脱氧诱导镰状血红蛋白 (HbS) 聚合,以及血管一氧化氮 (NO) 的生物利用度降低,导致了疾病的发病机制。在一项概念验证研究中,我们成功地将硝酸酯基团结合到之前研究过的两种强效抗镰状芳香醛 TD7 和 VZHE039 上,分别形成 TD7-NO 和 VZHE039-NO 杂合体。这些化合物在缓冲液中稳定,但在体外和小鼠中表现出预期的全血中 NO 释放。更有前途的 VZHE039-NO 保留了母体 VZHE039 分子的功能和抗镰状活性。此外,与 VZHE039 不同,VZHE039-NO 显著减弱了 RBC 与层粘连蛋白的黏附,表明该化合物具有体内 RBC 抗黏附特性,与血管阻塞事件相关。晶体学研究表明,与 VZHE039 一样,VZHE039-NO 也与配体结合的 Hb 结合,从而产生类似的蛋白相互作用。在这些研究中获得的知识为 SCD 提供了一个独特的机会,可以生成一种具有增强效益的更优候选药物。