本研究尝试通过有机钯催化的 C-C 键形成对黄酮框架（位置 7）进行结构调整。还评估了具有不同电子效应的取代基（苯环，苯并吡喃支架的2位）对抗肿瘤特性的影响。结果，这些努力产生了具有 4-氟苯环（位置 2）的呋喃基苯并吡喃臂 (14)，通过 PARP 和微管蛋白的双重抑制介导，对 Ishikawa 细胞系表现出出色的抗肿瘤作用 [(IC50 (PARP1) = 74 nM，IC50 (PARP2) = 109 nM) 和微管蛋白 (IC50 = 1.4 μM)]。进一步的研究证实了 14 能够诱导细胞凋亡和自噬，并导致细胞周期停滞在 G2/M 期。总体而言，该研究的结果最终产生了一种易于处理的双 PARP-微管蛋白抑制剂，该抑制剂具有令人印象深刻的抗子宫内膜癌活性。

Structural tailoring of the flavone framework (position 7) via organopalladium-catalyzed C-C bond formation was attempted in this study. The impact of substituents with varied electronic effects (phenyl ring, position 2 of the benzopyran scaffold) on the antitumor properties was also assessed. Resultantly, the efforts yielded a furyl arm bearing benzopyran possessing a 4-fluoro phenyl ring (position 2) (14) that manifested a magnificent antitumor profile against the Ishikawa cell lines mediated through dual inhibition of PARP and tubulin [(IC50 (PARP1) = 74 nM, IC50 (PARP2) = 109 nM) and tubulin (IC50 = 1.4 µM)]. Further investigations confirmed the ability of 14 to induce apoptosis as well as autophagy and cause cell cycle arrest at the G2/M phase. Overall, the outcome of the study culminated in a tractable dual PARP-tubulin inhibitor endowed with an impressive activity profile against endometrial cancer.