RANK ligand inhibition with denosumab for the management of osteoporosis.
Receptor activator of nuclear factor-kappaB ligand (RANKL) is a cytokine member of the tumour necrosis factor family that is the principal final mediator of osteoclastic bone resorption. It plays a major role in the pathogenesis of postmenopausal osteoporosis, as well bone loss associated with rheumatoid arthritis, metastatic cancer, multiple myeloma, aromatase inhibitor therapy and androgen deprivation therapy. Denosumab (AMG 162) is an investigational fully human monoclonal antibody with a high affinity and specificity for RANKL. By inhibiting the action of RANKL, denosumab reduces the differentiation, activity and survival of osteoclasts, thereby slowing the rate of bone resorption. Denosumab has been shown to increase bone mineral density (BMD) and reduce bone turnover in postmenopausal women with low BMD. Denosumab is a potential treatment for osteoporosis and other skeletal disorders.
Lewiecki
E Michael
EM
New Mexico Clinical Research & Osteoporosis Center, 300 Oak St NE, Albuquerque, New Mexico 87106, USA. LEWIECKI@aol.com
D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D000069448:Denosumab; D019468:Disease Management; D006801:Humans; D010024:Osteoporosis / Q000276:immunology* / Q000378:metabolism / Q000628:therapy*; D053245:RANK Ligand / Q000037:antagonists & inhibitors* / Q000276:immunology / Q000378:metabolism*
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D053245:RANK Ligand; D000069448:Denosumab