[5] It is a secreted glycoprotein with a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists.

[8] Sclerostin, the product of the SOST gene, located on chromosome 17q12–q21 in humans,[9] was originally believed to be a non-classical bone morphogenetic protein (BMP) antagonist.

[15][16][17] Sclerostin production by osteocytes is inhibited by parathyroid hormone,[17][18] mechanical loading,[19] estrogen[20] and cytokines including prostaglandin E2,[21] oncostatin M, cardiotrophin-1 and leukemia inhibitory factor.

[24] Mutations in the gene that encodes the sclerostin protein are associated with disorders associated with high bone mass, sclerosteosis and van Buchem disease.

[29][30] In a Phase I study, a single dose of anti-sclerostin antibody from Amgen (Romosozumab) increased bone density in the hip and spine in healthy men and postmenopausal women and the drug was well tolerated.

[33] In a Phase III trial, one year of Romosozumab treatment in post-menopausal women reduced the risk of vertebral fractures compared to the placebo group.