Abstract
RANK ligand (RANKL) is a key mediator of osteoclast formation, function, and survival. Therefore, RANKL is thought to be responsible for osteoclast-mediated bone resorption in a broad range of disorders such as postmenopausal osteoporosis and cancer-induced bone disease. Moreover, RANKL has been implicated as a primary mediator of bone erosions, a hallmark of rheumatoid arthritis (RA). Denosumab is a fully human monoclonal antibody. This antibody binds to RANKL with high affinity and specificity, and inhibits RANKL-RANK interaction, mimicking the endogenous effects of osteoprotegerin (OPG), a soluble RANKL decoy receptor. Clinical trial data support the continued development of denosumab for the inhibition of bone erosions in RA.
