1425 San Pablo Street, Los Angeles, CA 90033

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Genetic analysis was used to discover that inactivating mutations in a novel secreted protein, sclerostin, were responsible for causing a very rare, high bone mass disorder known as Sclerosteosis. As such, sclerostin was recognized as being a master negative regulator of bone formation and quickly became viewed as a promising target for potentially increasing bone formation in low bone mass clinical settings, such as post-menopausal osteoporosis.

Sclerostin is primarily expressed by specialized bone cells, and various lines of experimental evidence have now shown that sclerostin acts at the molecular level as an inhibitor of the Wnt signaling pathway. Antibody-mediated sclerostin inhibition in pre-clinical animal models produces marked increases in bone formation, bone mass and bone strength, thus pointing towards the potential of targeting sclerostin in the clinic.

Host: Andy McMahon

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