原肌球蛋白受体激酶A
原肌球蛋白受体激酶B
低亲和力神经生长因子受体
神经营养素
化学
trk受体
变构调节
原肌球蛋白受体激酶C
神经生长因子
药理学
受体
神经营养因子
生物化学
生物
生长因子
血小板源性生长因子受体
作者
Sharan K. Bagal,Kiyoyuki Omoto,David C. Blakemore,Peter J. Bungay,James Bilsland,Philip J. Clarke,Matthew S. Corbett,Ciarán N. Cronin,J. Jean Cui,Rebecca Dias,Neil J. Flanagan,S.E. Greasley,Rachel L. Grimley,Eric F. Johnson,David Fengas,Linda Kitching,Michelle L. Kraus,Indrawan McAlpine,Asako Nagata,Gareth Waldron
标识
DOI:10.1021/acs.jmedchem.8b00280
摘要
Tropomyosin receptor kinases (TrkA, TrkB, TrkC) are activated by hormones of the neurotrophin family: nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4). Moreover, the NGF antibody tanezumab has provided clinical proof of concept for inhibition of the TrkA kinase pathway in pain leading to significant interest in the development of small molecule inhibitors of TrkA. However, achieving TrkA subtype selectivity over TrkB and TrkC via a Type I and Type II inhibitor binding mode has proven challenging and Type III or Type IV allosteric inhibitors may present a more promising selectivity design approach. Furthermore, TrkA inhibitors with minimal brain availability are required to deliver an appropriate safety profile. Herein, we describe the discovery of a highly potent, subtype selective, peripherally restricted, efficacious, and well-tolerated series of allosteric TrkA inhibitors that culminated in the delivery of candidate quality compound 23.
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