β‐Thalassemia is an inherited hematologic disorder caused by various mutations of the β‐globin gene, thus resulting in a significant decrease in adult hemoglobin (HbA) production. An increase in fetal hemoglobin (HbF) levels by drug molecules is considered of great potential in β‐thalassemia treatment and is expected to counterbalance the impaired production of HbA. In this work, based on a set of 129 experimentally tested biological inhibitors, we developed and validated a computational model for the prediction of K562 functional inhibition, possibly associated with HbF induction. To facilitate future advancements in the field, we incorporated our model into Enalos Cloud Platform, which enabled online access to our computational scheme (http://enalos.insilicotox.com/K562) through a user‐friendly interface. This web service is offered to the wider community to promote in silico drug discovery through fast and reliable predictions.

中文翻译：

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通过Enalos云平台抑制人K562细胞生长的共识预测模型

β-地中海贫血是由β-珠蛋白基因的各种突变引起的遗传性血液病，因此导致成人血红蛋白（HbA）产量显着下降。药物分子增加胎儿血红蛋白（HbF）的水平被认为在β地中海贫血治疗中具有巨大潜力，并有望抵消HbA产生受损。在这项工作中，基于一组129种经过实验测试的生物抑制剂，我们开发并验证了预测K562功能抑制（可能与HbF诱导相关）的计算模型。为了促进该领域的未来发展，我们将模型整合到Enalos Cloud Platform中，该平台允许通过用户友好的界面在线访问我们的计算方案（http://enalos.insilicotox.com/K562）。