Halofuginone prevents estrogen-deficient osteoporosis in mice.

Journal of Cellular Biochemistry
Carl J DeSelmSteven L Teitelbaum

Abstract

Osteoporosis is characterized by enhanced activity of osteoclasts relative to that of osteoblasts. Thus, the principal means of treating the most common form of osteoporosis, namely that attending menopause, is inhibition of osteoclast formation or function. We have demonstrated that the inflammatory cytokine, IL-17, mediates estrogen-deficient osteoporosis, in mice, and that genetic blockade of its function prevents ovariectomy-induced bone loss. We herein report that the febrifugine derivative, halofuginone, a small molecule drug, reduces abundance of Th-17 cells in mice and prevents estrogen-deficient osteoporosis by diminishing bone resorption without impacting osteogenesis. In keeping with IL-17 mediating its osteoclastogenic effects by promoting RANK ligand expression by osteoblasts, halofuginone does not directly inhibit the bone resorptive cell. Thus, halofuginone, which is presently FDA-approved for treatment of scleroderma, is a candidate therapeutic for post-menopausal osteoporosis.

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Citations

Sep 17, 2013·European Journal of Clinical Investigation·Renqing Zhao
Feb 7, 2015·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Zachary S BuchwaldRajeev Aurora
Jan 9, 2015·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Mark Pines, Itai Spector
Sep 19, 2018·Current Osteoporosis Reports·Antoine Boulanger PietteJérôme Frenette
Nov 30, 2019·Zeitschrift für Gerontologie und Geriatrie·Zhou-Shan TaoHong-Guang Xu

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