Denosumab与破骨细胞RANKL/RANK通路

摘要

Denosumab( 狄诺塞麦) 是一种人工合成、完全人源化、可与RNAKL 结合的单克隆抗体( IgG2 抗体),对人源RANKL 具有很高的亲和力和特异性[1],具有较好的骨吸收抑制作用,是以破骨细胞RANKL/RANK 信号调控通路为靶点的骨质疏松靶向治疗药物,并可降低恶性肿瘤骨转移患者骨骼相关事件( SRE) 的发生、延缓骨痛的进展.本文综述了狄诺塞麦抑制骨吸收的生理作用机制,狄诺塞麦治疗骨质疏松和恶性肿瘤骨转移的研究进展,为狄诺塞麦在临床的应用提供更好的循证医学证据.%Denosumab was a humanized monoclonal antibody that specifically binding to RNAKL,and had a good bone resorption inhibitory effect. It was a osteoporosis targeted therapy drug,which targeted at the RANKL /RANK signaling pathway of osteoclasts,could reduce the occurrence of bone-related events ( SRE) in patients with malignant bone metastases and delay the progression of bone pain. This article reviewed the physiological mechanism of denosumab inhibiting bone resorption,and the research progress of denosumab in the treatment of osteoporosis and malignant tumor bone metastasis. It could provide better evidence-based medical evidence for the clinical application of denosumab.