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Published at www.nejm.org August 11, 2009 (10.1056/NEJMe0905480)

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More than a decade ago, receptor activator of nuclear factor-B ligand (RANKL) was identified as the key molecule mediating osteoclast development, activity, and survival.¹ Since osteoporosis results, in part, from increased osteoclastic bone resorption, the inhibition of RANKL activity has been an obvious therapeutic target. In this issue of the Journal, two articles^2,3 report pivotal studies that reflect more than 10 years of drug development and that establish the efficacy of a human monoclonal antibody to RANKL, denosumab, in reducing fractures.

Cummings et al.² enrolled 7868 postmenopausal women with osteoporosis and randomly assigned them to receive either 60 mg . . . [Full Text of this Article]

Source Information

From the Endocrine Research Unit, College of Medicine, Mayo Clinic, Rochester, MN.

This article (10.1056/NEJMe0905480) was published on August 11, 2009, at NEJM.org.

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