Overcoming multidrug resistance (MDR) of cancer cells can be accomplished using drug delivery systems in large-molecular-weight ATP-binding cassette transporters before entry into phagolysosomes and by particle–cell-surface interactions. However, these hypotheses do not address the intratumoral heterogeneity in cancer. Anti-MDR must be related to alterations of drug targets, expression of detoxification, as well as altered proliferation. In this study, it is shown that the excellent efficacy and sustainability of anti-MDR is due to a stable ES complex because of the allosteric facilities of artificial enzymes when they are used as supermolecular complexes. The allosteric effect of supermolecular drugs can be explained by the induced-fit model and can provide stable feedback control systems through the loop transfer function of the Hill equation.

克服癌细胞的多药耐药性（MDR）可以在进入吞噬溶酶体之前，通过大分子ATP结合盒转运蛋白中的药物输送系统，以及通过颗粒-细胞-表面相互作用来完成。但是，这些假设并未解决癌症中的肿瘤内异质性。抗MDR必须与药物靶标的改变，解毒的表达以及增殖的改变有关。在这项研究中，研究表明抗MDR的出色功效和可持续性归因于稳定的ES复合物，这是因为人工酶用作超分子复合物时具有变构作用。超分子药物的变构作用可以通过诱导拟合模型来解释，并且可以通过希尔方程的循环传递函数提供稳定的反馈控制系统。