和厚朴酚及厚朴酚是疏水性烯丙基联苯酚类结构的同分异构体，均有抗肺癌药理作用。和厚朴酚能抑制肺癌A549细胞、H1299细胞和Lewis细胞移植瘤在小鼠体内的生长和转移，而厚朴酚能预防乌拉坦诱导小鼠发生肺癌和抑制A549细胞移植瘤在小鼠体内生长。和厚朴酚及厚朴酚在体外能浓度相关地抑制人小细胞肺癌N446细胞、H446细胞，非小细胞肺癌中的肺腺癌A549、H1299、H441、H1975、Calu3、A2、PC、SPC-A-1、95D细胞，大细胞肺癌H460细胞，人肺鳞癌H226、H520、CH27细胞以及小鼠肺癌Lewis细胞增殖，并诱导其凋亡和坏死。和厚朴酚及厚朴酚抑制肺癌的主要机制是：（1）抑制I型去乙酰化酶的表达和酶活性，上调死亡受体-5（DR5）的表达，激活肿瘤坏死因子相关的凋亡诱导配体（TRAIL）信号通路；（2）激活与半胱天冬酶无关的凋亡通路；（3）阻滞癌细胞中的微管聚合，破坏微管结构；（4）阻滞蛋白激酶B（AKT）/哺乳动物雷帕霉素靶蛋白（mTOR）信号通路，诱导癌细胞自噬；（5）阻滞磷脂酰肌醇-3激酶（PI3K）/AKT信号通路而抑制癌细胞转移。

Honokiol and magnolol are hydrophobic isomers of propenyl biphenol-type structure. Honokiol can treat for growth and metastasis of lung cancer A549 cells, H1299cells and Lewis cells transplantation tumor in mice. Magnolol can prevent urethane from inducing lung cancer in mice, and can treat for growth of A549 cells transplantation tumor in mice. In vitro honokiol and magnolol inhibit proliferation and induce apoptosis and necrosis in association with dosage on human small cell lung cancer N446 cells, H446 cells, and human lung adenocarcinoma A549 cells, H1299 cells, H441 cells, H1975 cells, Calu3 cells, A2 cells, PC-9 cells, SPC-A-1 cells, 95D cells, and human large cell lung cancer H460 cells, and human lung squamous carcinoma H226 cells, H520 cells, CH27 cells, and mouse lung cancer Lewis cells. The mechanisms of honokiol and magnolol against lung cancer are inhibiting the expression of class I deacetylase and its enzyme activity to up-regulate the expression of DR5 and to activate TRAIL signaling pathway, and activating caspase-independent apoptosis pathway, and inhibiting microtubule polymerization to destroy microtubule structure, and inhibiting AKT/mTOR signaling pathway to induce autophagy of cancer cells, and inhibiting PI3K/AKT signaling pathway to block metastasis of cancer cells.

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