Zhang Xia, Amin Elizabeth Ambrose
Department of Medicinal Chemistry, College of Pharmacy, University of Minnesota, 717 Delaware St. SE, Minneapolis, MN 55414-2959, United States.
Department of Medicinal Chemistry, College of Pharmacy, University of Minnesota, 717 Delaware St. SE, Minneapolis, MN 55414-2959, United States; Minnesota Supercomputing Institute for Advanced Computational Research, 117 Pleasant St SE, Minneapolis, MN, United States.
J Mol Graph Model. 2016 Jan;63:22-8. doi: 10.1016/j.jmgm.2015.11.008. Epub 2015 Nov 17.
Anthrax is a highly lethal, acute infectious disease caused by the rod-shaped, Gram-positive bacterium Bacillus anthracis. The anthrax toxin lethal factor (LF), a zinc metalloprotease secreted by the bacilli, plays a key role in anthrax pathogenesis and is chiefly responsible for anthrax-related toxemia and host death, partly via inactivation of mitogen-activated protein kinase kinase (MAPKK) enzymes and consequent disruption of key cellular signaling pathways. Antibiotics such as fluoroquinolones are capable of clearing the bacilli but have no effect on LF-mediated toxemia; LF itself therefore remains the preferred target for toxin inactivation. However, currently no LF inhibitor is available on the market as a therapeutic, partly due to the insufficiency of existing LF inhibitor scaffolds in terms of efficacy, selectivity, and toxicity. In the current work, we present novel support vector machine (SVM) models with high prediction accuracy that are designed to rapidly identify potential novel, structurally diverse LF inhibitor chemical matter from compound libraries. These SVM models were trained and validated using 508 compounds with published LF biological activity data and 847 inactive compounds deposited in the Pub Chem BioAssay database. One model, M1, demonstrated particularly favorable selectivity toward highly active compounds by correctly predicting 39 (95.12%) out of 41 nanomolar-level LF inhibitors, 46 (93.88%) out of 49 inactives, and 844 (99.65%) out of 847 Pub Chem inactives in external, unbiased test sets. These models are expected to facilitate the prediction of LF inhibitory activity for existing molecules, as well as identification of novel potential LF inhibitors from large datasets.
炭疽是一种由杆状革兰氏阳性细菌炭疽芽孢杆菌引起的高致死性急性传染病。炭疽毒素致死因子(LF)是该杆菌分泌的一种锌金属蛋白酶,在炭疽发病机制中起关键作用,主要负责炭疽相关的毒血症和宿主死亡,部分原因是通过使丝裂原活化蛋白激酶激酶(MAPKK)失活从而破坏关键的细胞信号通路。氟喹诺酮类等抗生素能够清除杆菌,但对LF介导的毒血症无效;因此,LF本身仍然是毒素失活的首选靶点。然而,目前市场上没有作为治疗药物的LF抑制剂,部分原因是现有LF抑制剂支架在疗效、选择性和毒性方面存在不足。在当前的工作中,我们提出了具有高预测准确性的新型支持向量机(SVM)模型,旨在从化合物库中快速识别潜在的新型、结构多样的LF抑制剂化学物质。这些SVM模型使用508种具有已发表的LF生物活性数据的化合物和存放在Pub Chem生物测定数据库中的847种无活性化合物进行训练和验证。其中一个模型M1,通过正确预测外部无偏测试集中41种纳摩尔水平的LF抑制剂中的39种(95.12%)、49种无活性化合物中的46种(93.88%)以及847种Pub Chem无活性化合物中的844种(99.65%),对高活性化合物表现出特别良好的选择性。这些模型有望促进对现有分子的LF抑制活性的预测,以及从大型数据集中识别新型潜在的LF抑制剂。