This study explores the interesting effect of p-sulfonatocalix[n]arene hosts (SCXn) on the excited-state tautomeric equilibrium of Chrysazine (CZ), a model antitumour drug molecule. Detailed photophysical investigations reveal that conversion of CZ from its more dipolar, excited normal form (N*) to the less dipolar, tautomeric form (T*) is hindered in SCXn-CZ host–guest complexes, which is quite unexpected considering the nonpolar cavity of the hosts. The atypical effect of SCXn is proposed to arise due to the partial inclusion or external binding of CZ with the hosts, which facilitates H-bonding interactions between CZ and the sulfonate groups present at the portals of the hosts. The intermolecular H-bonding subsequently leads to weakening of the pre-existing intramolecular H-bond network within CZ, and thus hinders the tautomerizaion process. Our results suggest that rather than the binding affinity, it is the orientation of CZ in the SCXn-CZ complexes, and its proximity to the portals of the host that plays a predominant role in influencing the tautomeric equilibrium. These observations are supported by quantum chemical calculations. Thermodynamic studies validate that SCXn-CZ interaction is essentially enthalpy driven and accompanied by small entropy loss, which is consistent with the binding mechanisms.

中文翻译：

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通过在chrysazine的质子互变异构现象的抑制p -sulfonatocalixarene主机†

本研究探讨的有趣的效果p -sulfonatocalix [ Ñ ]芳烃主机（SCX Ñ上Chrysazine（CZ），模型的抗肿瘤药物分子的激发态互变异构平衡）。详细的光物理研究表明，在SCX n -CZ宿主-客体复合物中，阻碍了CZ从偶极激发态的正态（N *）转变为偶极互变异构体（T *）的转变，考虑到非极性，这是非常出乎意料的宿主的腔。SCX n的非典型效应提出由于CZ与主体的部分包含或外部结合而出现，这促进了CZ与存在于主体的门户处的磺酸酯基团之间的H键相互作用。分子间的H键随后导致CZ内预先存在的分子内H键网络的弱化，因此阻碍了互变异构过程。我们的结果表明，SCX n -CZ络合物中CZ的取向而不是结合亲和力，以及它与宿主门户的接近程度在影响互变异构平衡中起主要作用。这些观察得到量子化学计算的支持。热力学研究验证了SCX n-CZ相互作用本质上是由焓驱动的，并且伴随着小的熵损失，这与结合机制是一致的。