Shakespeare William C, Wang Yihan, Bohacek Regine, Keenan Terry, Sundaramoorthi Raji, Metcalf Chet, Dilauro Anne, Roeloffzen Sonya, Liu Shuangying, Saltmarsh Jennifer, Paramanathan Guru, Dalgarno David, Narula Surinder, Pradeepan Selvi, van Schravendijk Marie Rose, Keats Jeff, Ram Mary, Liou Shuenn, Adams Susan, Wardwell Scott, Bogus Julie, Iuliucci John, Weigele Manfred, Xing Lianping, Boyce Brendan, Sawyer Tomi K
ARIAD Pharmaceuticals, Inc., 26 Landsdowne Street, Cambridge, MA 02139, USA.
Chem Biol Drug Des. 2008 Feb;71(2):97-105. doi: 10.1111/j.1747-0285.2007.00615.x. Epub 2008 Jan 3.
Targeted disruption of the pp60(src) (Src) gene has implicated this tyrosine kinase in osteoclast-mediated bone resorption and as a therapeutic target for the treatment of osteoporosis and other bone-related diseases. Here, we describe structure activity relationships of a novel series of carbon-linked, 2-substituted purines that led to the identification of AP23451 as a potent inhibitor of Src tyrosine kinase with antiresorptive activity in vivo. AP23451 features the use of an arylphosphinylmethylphosphinic acid moiety which confers bone-targeting properties to the molecule, thereby increasing local concentrations of the inhibitor to actively resorbing osteoclasts at the bone interface. AP23451 exhibited an IC50 = 68 nm against Src kinase; an X-ray crystal structure of the molecule complexed with Src detailed the molecular interactions responsible for its Src inhibition. In vivo, AP23451 demonstrated a dose-dependent decrease in PTH-induced hypercalcemia. Moreover, AP23517, a structurally and biochemically similar molecule with comparable activity (IC50 = 73 nm) except devoid of the bone-targeting element, demonstrated significantly reduced in vivo efficacy, suggesting that Src activity was necessary but not sufficient for in vivo activity in this series of compounds.
对pp60(src)(Src)基因进行靶向破坏表明,这种酪氨酸激酶参与破骨细胞介导的骨吸收过程,并且是治疗骨质疏松症和其他骨相关疾病的治疗靶点。在此,我们描述了一系列新型碳连接的2-取代嘌呤的构效关系,这些关系导致鉴定出AP23451作为Src酪氨酸激酶的有效抑制剂,在体内具有抗吸收活性。AP23451的特点是使用了芳基次膦酰基甲基次膦酸部分,该部分赋予分子骨靶向特性,从而增加抑制剂在骨界面处对活跃吸收的破骨细胞的局部浓度。AP23451对Src激酶的IC50 = 68 nM;与Src复合的该分子的X射线晶体结构详细说明了其抑制Src的分子相互作用。在体内,AP23451显示出对甲状旁腺激素诱导的高钙血症的剂量依赖性降低。此外,AP23517是一种结构和生化性质相似、活性相当(IC50 = 73 nM)但缺乏骨靶向元件的分子,其体内疗效显著降低,这表明Src活性对于该系列化合物的体内活性是必要的,但不是充分的。