曼彻斯特大学(the University of Manchester)的研究团队研发了一个新的化学药物能够抑制Aurora B的活性，在细胞的试验中证明能有效的毒杀癌细胞。
Stephen Taylor博士说：「其实最初是Aurora A被作为抗癌标靶的酵素，也由此促成了Aurora B的发现，而且毒杀癌细胞的效果比Aurora A更好。」此研究发表于近期的Cell Science期刊，也引起了全世界抗癌团队对Aurora抑制物的好奇，目前有超过 10家制药公司努力的在探索Aurora抗癌的计划。
虽然抑制Aurora A也看得到潜在的治疗效果，但是这份研究很清楚的显示Aurora B有急起直追的潜力，早期的临床试验已证明Aurora B并没有显著的毒性及副作用，这个结果将有利于Aurora B在短时间内进入下一阶段的临床试验。许多现有的抗癌药虽然效果很好，但却有毒副作用，而Aurora的优势就是其几乎没有毒副作用，因此未来应可成为一个革命性的抗癌新药。
Aurora A以及Aurora B是一种蛋白质激酶(protein kinase)，它们会将其它的蛋白质磷酸化，引发讯息传递诱导癌细胞生长。曼彻斯特研究团队与制药公司AstraZeneca共同研发Aurora B抑制物，早在2003年就指出以Aurora B作为抗癌标靶深具潜力，而最近的实验结果验证了Aurora B抑制物确实能有效的用于癌症治疗。
部分英文原文：
Validating Aurora B as an anti-cancer drug target
The Aurora kinases, a family of mitotic regulators, have received much attention as potential targets for novel anti-cancer therapeutics. Several Aurora kinase inhibitors have been described including ZM447439, which prevents chromosome alignment, spindle checkpoint function and cytokinesis. Subsequently, ZM447439-treated cells exit mitosis without dividing and lose viability. Because ZM447439 inhibits both Aurora A and B, we set out to determine which phenotypes are due to inhibition of which kinase. Using molecular genetic approaches, we show that inhibition of Aurora B kinase activity phenocopies ZM447439. Furthermore, a novel ZM compound, which is 100 times more selective for Aurora B over Aurora A in vitro, induces identical phenotypes. Importantly, inhibition of Aurora B kinase activity induces a penetrant anti-proliferative phenotype, indicating that Aurora B is an attractive anti-cancer drug target. Using molecular genetic and chemical-genetic approaches, we also probe the role of Aurora A kinase activity. We show that simultaneous repression of Aurora A plus induction of a catalytic mutant induces a monopolar phenotype. Consistently, another novel ZM-related inhibitor, which is 20 times as potent against Aurora A compared with ZM447439, induces a monopolar phenotype. Expression of a drug-resistant Aurora A mutant reverts this phenotype, demonstrating that Aurora A kinase activity is required for spindle bipolarity in human cells. Because small molecule-mediated inhibition of Aurora A and Aurora B yields distinct phenotypes, our observations indicate that the Auroras may present two avenues for anti-cancer drug discovery.
