NEW GOAL OF OSTEOPOROSIS TARGETED THERAPY — THE RANKL INHIBITOR DENOSUMAB
Summary. Summary. The problem of drug therapy of osteoporosis remains valid, despite the wide range of approved funds. Side effects and low adherence to long-term therapy is the main causes of inefficiency antiosteoporotic therapy. The discovery of the signaling system consisting of a receptor activator of nuclear factor-κB (RANK), its ligand (RANKL), and osteoprotegerin that is a main regulator of the processes of osteoclastic differentiation, function, and apoptosis has broken through in an understanding of the pathophysiology of osteoporosis. Information of a decisive role of RANKL in accelerating bone resorption has given rise to novel drugs, the mechanism of action of which is based on RANKL inhibition. The representative of this drug group is denosumab, the highly specific, fully human antibody against RANKL, which imitates the activity of osteoprotegerin against RANKL.Thus, the pathogenetic therapy of postmenopausal osteoporosis with targeted action on key activation and survival of osteoclasts — signaling pathway RANKL/RANK /OPG — a promising strategy to overcome many of the shortcomings of existing treatments, which implement the invention of innovative molecules denosumab. Clinical studies involving more than 10,000 patients have convincingly proved the effectiveness of denosumab in the prevention of osteoporotic fractures major localizations compared with placebo, more potent antiresorptive effect compared with alendronate, a favorable safety profile and high level of commitment to the treatment of patients. Denosumab has shown full reversibility antiresorptive effects without accumulation in the bone matrix, long-term safety (over 5 years) and adverse events controllability.
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