Romosozumab binds sclerostin, increases bone formation, and decreases bone resorption. Postmenopausal women with osteoporosis were assigned to romosozumab or placebo for 1 year, followed by 1 year of denosumab. Romosozumab was associated with lower vertebral and clinical fracture risk. Osteoporosis can lead to fragility fractures, which result in clinical burden and increased mortality. 1 , 2 Even after a fracture, fewer than 25% of patients receive pharmacologic treatment for osteoporosis. 3 – 5 After the discovery that sclerostin deficiency causes rare genetic conditions that are characterized by high bone mass and resistance to fracture, 6 , 7 sclerostin became a therapeutic target for the treatment of osteoporosis. Sclerostin, a negative regulator of bone formation that is secreted by osteocytes, 8 inhibits Wnt signaling, down-regulating this stimulus for osteoblast development and function. 9 Romosozumab (Amgen and UCB Pharma) is a monoclonal antibody that binds and inhibits sclerostin, with . . .