Warshel Institute for Computational Biology, School of Medicine, The Chinese University of Hong Kong, Shenzhen, Guangdong 518172, P. R. China.
Department of Pharmacology and Pharmacy, The University of Hong Kong, Pokfulam 999077, Hong Kong SAR, P. R. China.
J Am Chem Soc. 2024 Nov 6;146(44):30117-30125. doi: 10.1021/jacs.4c07937. Epub 2024 Oct 23.
Paclitaxel (PTX, or Taxol), a chemotherapeutic agent widely employed in the treatment of various cancers, undergoes metabolic transformations through the cytochrome P450 enzymes CYP3A4 and CYP2C8. CYP3A4 catalyzes the aromatic hydroxylation reaction of PTX, whereas CYP2C8 demonstrates a distinct reactivity pattern, producing 6α-hydroxypaclitaxel via alkane hydroxylation. Despite the significant impact of PTX metabolism on its anticancer efficacy, the detailed mechanisms underlying these transformations have remained largely unclear. In this study, we employed hybrid quantum mechanics and molecular mechanics (QM/MM) calculations to elucidate the mechanism of PTX metabolism by human CYP2C8. Our QM/MM results reveal that the hydroxylation of PTX by CYP2C8 follows an atypical rebound mechanism. Either of the two hydrogen atoms at the C6 position of PTX can be abstracted, leading to a common radical intermediate. Although the subsequent rebound barrier is unusually high, stereochemical scrambling is unlikely, as the rebound barrier for the formation of the 6α-hydroxylated PTX─the actual product─is significantly lower than that for the 6β-hydroxylated metabolite. Thus, product selectivity is determined by the non-rate-determining rebound step. Furthermore, the hydroxyl group at the C7 position of PTX plays a catalytic role by facilitating the hydrogen abstraction and rebound steps. Our study also confirms a pronounced stability of the transition state in the high-spin sextet spin state, enabled by the enzyme's specific substrate positioning.
紫杉醇(PTX,或 Taxol)是一种广泛用于治疗各种癌症的化疗药物,它通过细胞色素 P450 酶 CYP3A4 和 CYP2C8 进行代谢转化。CYP3A4 催化 PTX 的芳香族羟化反应,而 CYP2C8 则表现出独特的反应性模式,通过烷烃羟化作用生成 6α-羟基紫杉醇。尽管 PTX 代谢对其抗癌疗效有重大影响,但这些转化的详细机制在很大程度上仍不清楚。在这项研究中,我们采用混合量子力学和分子力学(QM/MM)计算方法阐明了人 CYP2C8 代谢 PTX 的机制。我们的 QM/MM 结果表明,CYP2C8 对 PTX 的羟化作用遵循非典型回弹机制。PTX 的 C6 位的两个氢原子中的任一个都可以被提取,导致一个共同的自由基中间体。尽管随后的回弹势垒异常高,但立体化学的重排不太可能发生,因为形成 6α-羟基化 PTX(实际产物)的回弹势垒明显低于形成 6β-羟基化代谢物的回弹势垒。因此,产物选择性由非速率决定的回弹步骤决定。此外,PTX 的 C7 位的羟基通过促进氢提取和回弹步骤起到催化作用。我们的研究还证实了在高自旋 sextet 自旋态中过渡态的显著稳定性,这得益于酶的特定底物定位。