Flavonoids are phenolic substances that appear to exert beneficial effects in several chronic diseases, including cancer. Structure-activity relationships of the cytotoxic activity of a series of flavonols and their 3-methyl ether derivatives established that 3′-hydroxy-3,4′-dimethoxyflavone (flavonoid 11) displayed strong cytotoxicity against human leukaemia cell lines (HL-60, U-937 and MOLT-3), and cells that over-express the anti-apoptotic proteins, Bcl-2 and Bcl-x_L, and against P-glycoprotein-overexpressing K-562/ADR cells. This compound induced G₂-M cell cycle arrest and it was a potent apoptotic inducer on HL-60, MOLT-3, U-937 and U-937/Bcl-2 cell lines. Cell death was (i) mediated by caspase activation, since it was prevented by the non-specific caspase inhibitor z-VAD-fmk and reduced by a selective caspase-9 inhibitor, (ii) associated with cytochrome c release, the dissipation of the inner mitochondrial membrane potential (ΔΨ_m) and the activation of the mitogen-activated protein kinase pathway and (iii) partially blocked by the inhibition of c-jun NH₂ terminal kinases/stress activated protein kinases (JNK/SAPK) signalling and by the free-radical scavenger N-acetyl-l-cysteine.

黄酮类化合物是酚类物质，似乎在包括癌症在内的几种慢性疾病中发挥有益作用。一系列黄酮醇及其3-甲醚衍生物的细胞毒性活性与结构-活性的关系建立了3'-羟基-3,4'-二甲氧基黄酮（类黄酮11）对人白血病细胞系（HL-60， U-937和MOLT-3），以及过表达抗凋亡蛋白Bcl-2和Bcl-x _L以及对抗过表达P-糖蛋白的K-562 / ADR细胞的细胞。该化合物诱导G ₂-M细胞周期停滞，它是HL-60，MOLT-3，U-937和U-937 / Bcl-2细胞系的有效凋亡诱导剂。细胞死亡是由（i）caspase激活介导的，因为它被非特异性caspase抑制剂z-VAD-fmk阻止，并被选择性caspase-9抑制剂减少，（ii）与细胞色素c释放相关，内线粒体膜电位（ΔΨ_米）和丝裂原活化蛋白激酶途径和（iii）由C-抑制部分阻断的活化君NH ₂末端激酶/应激活化蛋白激酶（JNK / SAPK）信令和由自由基清除剂N-乙酰基-1-半胱氨酸。