前列腺癌是全球男性患病率和死亡率的主要原因。在本研究中，我们采用了无机萃取方法对报道的用于前列腺癌表观遗传学靶点的几种新化合物及其衍生物的可能作用机制进行了预测，并通过ADMET评估、药物相似性和分子对接分析来进行详尽研究。选中的化合物：芥子硫苷、水飞蓟素、3,3'-二碘甲烷基化合物（DIM）和染料木酚，大多符合了ADMET和药物相似性规则，包括Lipinski的规则。对接研究揭示了芥子硫苷与HDAC6的强大结合能量（-4.2千卡/摩尔），DIM与HDAC2的结合能量（-5.2千卡/摩尔），染料木酚与HDAC6的结合能量（-4.1千卡/摩尔）以及水飞蓟素对HDAC1的结合能量（-7.0千卡/摩尔），衍生后的这些化合物具有更好的结合亲和力和生物化学稳定性。本研究的发现可能揭示了这些化合物对前列腺癌的潜在表观基因重编程机制，并可能为前列腺癌植物治疗的成功之路铺平了道路。©本文作者（或其他权利人）与Springer-Verlag GmbH Germany 公司或其授权方（例如学会或其他合作伙伴）签订了独家出版协议。本文作者自行归档已接受的手稿版本仅受此类出版协议和适用法律的约束。

Prostate cancer is a leading cause of morbidity and mortality among men globally. In this study, we employed an in silico approach to predict the possible mechanisms of action of selected novel compounds reported against prostate cancer epigenetic targets and their derivatives, exhausting through ADMET profiling, drug-likeness, and molecular docking analyses. The selected compounds: sulforaphane, silibinin, 3, 3'-diindolylmethane (DIM), and genistein largely conformed to ADMET and drug-likeness rules including Lipinski's. Docking studies revealed strong binding energy of sulforaphane with HDAC6 (- 4.2 kcal/ mol), DIM versus HDAC2 (- 5.2 kcal/mol), genistein versus HDAC6 (- 4.1 kcal/mol), and silibinin against HDAC1 (- 7.0 kcal/mol) coupled with improved binding affinities and biochemical stabilities after derivatization. Findings from this study may provide insight into the potential epigenetic reprogramming mechanisms of these compounds against prostate cancer and could pave the way toward more success in prostate cancer phytotherapy.© The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.